Fellowship revision > Perioperative > Flashcards
Perioperative Flashcards
What proportion of normal nAChR are left in myasthenia gravis?
30%
What proportion of patients with myasthenia graves have an abnormal thymus?
75%; 85% hyperplasia, 15% thymoma
What proportion of patients with myaesthenia gravis have eye signs only?
15%
What drug is used in the pharmacological test for diagnosis of myasthenia gravis?
edrophonium- acetylcholinesterase inhibitor- improvement in muscle strength 30s after 10mg IV edrophonium; lasts approx 5 mins
What’s one of the medications used to treat myasthenia gravis? it’s half-life? Other treatments?
pyridostigmine anticholinesterase (rapid onset 15-30 mins, peak action 2hrs, t1/2 4hrs, effects last 3-4hrs)- must continue up until & including day of surgery, bearing in mind that it may modify NDNMBAs (delay onset)
IV dose is approx one-30th of the oral dose (ie. 1mg IV is equivalent to 30mg PO)
immunosuppression with corticosteroids (occasional azathioprine, cyclophosphamide)- may require perioperative stress steroid dosing
thymectomy
plasma exchange, IVIg usually reserved preop before thymectomy or other surgery, during myasthenia crisis or periodically to maintain remission for pts with MG that is not otherwise well-controlled.
What are the signs of a cholinergic crisis? treatment?
may occur if anticholinesterase administered to a pt with MG
paradoxical muscle weakness (may get prolonged paralysis)
involuntary twitching, fasciculation
cholinergic sx of sweating, lacrimation, urination, defecation, GI distress, emesis, meiosis
pralidoxime, atropine or glyco
What factors increase the need for postop intubation in myasthenia gravis?
major cavity surgery
preop FEV1 <2.9L
duration of disease >6yrs
Hx co-existing respiratory disease
pyridiostigmine requirement >750mg/day
Also: grade III or IV MG (grade 1= eyes only, IIa= mild generalised responds well to therapy, IIb moderate MG responding less well, III= severe generalised, IV= myaesthetnic crisis)
What’s the conversion pyridostigmine:neostigmine?
30:1
Classify hypothermia
Lowering of core temperature
- mild hypothermia 32 ~ 35°C
- moderate hypothermia 28 ~ 32°C
- severe hypothermia <28°C
What are the components of the CHA(2)DS(2)-Vasc score for AF?
CHF= 1 point
HTN= 1 point
Age <65=0, 65-74=1, >=75=2 points
DM=1 point
Sex F=1 point, Male=0 points
Stroke/TIA/thromboembolism=2 points
Vascular disease history (peripheral vascular disease, prior MI, aortic plaque)= 1 point
What’s the annual risk of ischaemic stroke with CHA(2)DS(2)-Vasc score of 0, 1, 2, 3, 4, 5, 6, 7, 8, 9?
0.2, 0.6, 2.2, 3.2, 4.8, 7.2 9.7, 11.2, 10.8, 12.2%
What CHA2DS2-Vasc score is associated with low, moderate & high perioperative thrombotic risk?
0-3, 4-6, 7-9 (CHADS2 score 0-2, 3-4, 5-6)
What CHA2DS2-Vasc score is associated with low, moderate & high perioperative thrombotic risk?
0-3, 4-6, 7-9 (CHADS2 score 0-2, 3-4, 5-6)
What indications for anticoagulant therapy are considered HIGH thromboembolic risk?
-MECHANICAL HEART VALVE: any mitral, aortic caged-ball or tilting valve prosthesis, recent (within 6/12) stroke or TIA
-ATRIAL FIBRILLATION: CHA2DS2-Vasc score 7-9, recent (within 3/12) TIA/CVA, rheumatic valvular heart disease
-VTE: within 3/12, severe thrombophilia (eg. protein C, S or AT deficiency, antiphospholipid antibodies, multiple abnormalities)
wrt bleeding risk, what is high & low? example procedures?
high bleeding risk is 2-day risk of major bleeding (defined as involving critical site (neuraxial, intracranial, cardiac), lowers Hb >=20g/L, requires transfusion >=2x prbc) 2-4%, low 0-2%.
high risk includes any major operation duration >45mins, endoscopically-guided FNA, kidney biopsy, laminectomy, abdo surgery
what are “critical site” wrt bleeding risk?
intracranial, spinal, neurologic or if neural anaesthesia used
what’s the biologic half-life of warfarin? observed time for INR to fall?
36-42hrs
2-3 days to fall to below 2, 4-6 to normalise- longer in patients with INR 2.5-3.5, older
provided patient able to take PO, when is warfarin restarted postop?
12-24hrs (presuming to unexpected surgical issues increasing bleeding risk and pt taking adequate PO fluids, have prolonged bridging if pt has postop ileus)
what’s the evidence for bridging?
for most patients, bridging doesn’t provide a benefit in lowering thromboembolic risk but consistently increases bleeding risk so avoid in patients on a DOAC or those with low/moderate thromboembolic risk if high thromboembolic risk stop the VKA & initiate bridging
How is bridging initiated?
with a short-acting agent (eg. LMWH therapeutic dose), commenced approx 3/7 before surgery, last preop dose 24hrs before surgery. recommenced 2-3 days after surgery (depending on bleeding risk of the procedure) while awaiting stable warfarin anticoagulation.
What’s prothrombinex?
Sterile freeze-dried powder w purified human coagulation factors II, IX, X, low levels of V & VII. Prepared from pooled human plasma. 500IU vial
What’s FFP?
Blood product obtained either from whole blood collection or apheresis, contains all coagulation factors incl labile factors VIII & V, fibrinogen & vWF, also contains sodium & albumin. Must be frozen to -30 deg within 1 hr of commencement of freezing. Must transfuse immediately once thawed or store 2-6deg for 24hrs. Frozen shelf life 12 months if
Describe the METs study & it’s main findings
Prospective multi centre international cohort study of 1401 patients, published in the Lancet 2018.
Compared the predictive value of subjective assessment of functional capacity (METs poor <4, moderate 4-10 or good >10), CPET to measure peak O2 consumption, scores on the DASI questionnaire & serum N-terminal pro-BNP concentrations for predicting primary outcomes of 30-day death or myocardial infarction after major elective non-cardiac surgery.
Subjective assessment had poor sensitivity for identifying the inability to attain four METs during CPET and did not predict any outcomes.
Only lower DASI scores were associated with predicting the primary outcome (adj OR 0.96), also correlated with death or myocardial injury by 30 days after surgery *DASI 34= threshold for MORBIDITY (MI, MINS, mod-severe compications, new disability). Higher NT pro-BNP [] predicted 30-day death or myocardial injury & 1 year death & lower peak O2 consumption predicted mod/severe postop complications (eg. pulm complications, surgical site infections, unexpected critical care admissions, reoperation).
Main conclusion was that subjectively assessed functional capacity shouldn’t be used for pre-op risk evaluation since it doesn’t accurately identify pts with poor cardiopulmonary fitness nor those @ increased risk for postop M&M- More objective measures, particularly DASI, or NT-Pro-BNP could be used instead to assess perioperative cardiac risk after major elective non-cardiac surgery.
METS study 2018
> 40yrs, major NCS (overnight stay) with at least 1 RF for CVS disease
Compared Subjective assessment DASI and CPET to predict the outcome (each pt had all 3 assessments)
Primary outcome death or MI at 30d
Subjective assessment
20% sensitive; 94% specific to predict VO2max <14mls/kg (METS<4 equivalent)
No association with predicting the primary outcome
AT showed NO association with primary outcome
DASI scores were associated with predicting outcomes and reclassified risk from other measures (RCRI, age and sex)
CPET
VO2max <14ml/kg
Did not predict primary outcome
Did predict secondary outcome complications – mainly respiratory, SSI, ICU admission and re-operation
AT <11ml/kg
Was not predictive
NT-proBNP
Predicted primary outcome
Again, didn’t correlate well with CPET markers suggesting measurement of a different construct
Why did DASI and VO2 max not correlate
Given the only moderate correlation between DASI scores and peak oxygen consumption, a possible explanation is that DASI also measures somewhat different constructs, such as musculoskeletal strength, frailty, and selfimposed physical limitations.29
METS substudy of 6MWT (hence secondary outcomes and theory generating only)
Weak predictor of different outcome: scores of post-op recovery and disability
No correlation of VO2 max with these outcomes
DASI was only predictor of diasbility free survival (albeit with modest performance)
Further METS substudy defined <35 on DASI score – non-linear relationship (equivalent to 5 METS in the Study, although using DASI would calculate 7 METS) as associated with increased risk 30D death or myocardial injury and moderate/severe complications
- risk decreased with OR of ~1 per 1 point scored above 35
- However of note
“efficacious interventions for reducing perioperative risk in patients with low DASI scores remain to be identified. Possible approaches that merit evaluation in future studies include pre-habilitation (i.e. multimodal preoperative exercise training and nutritional supplementation), intensive perioperative haemodynamic management to minimise hypotension, and enhanced postoperative monitoring.”
What happens to plasma [] of BNP & NT-ProBNP in normal subjects & those with LV dysfunction?
similar in normal subjects but in pts with LV dysfunction plasma NT-proBNP rises more than BNP
What’s NT-proBNP? What happens to NT-proBNP with gender, age & renal failure?
A non-active pro-hormone released myocardial cells (same as BNP) in response to myocardial stretch & ischaemia. Values generally higher in older individuals, renal failure & in women. Values are lower in obese. ?higher in HFpEF?
What are the limitations of subjective assessment of METs?
Subjective assessment shows poor agreement with validated questionnaires & inconsistent association with postop complications, the METs study shows it’s got poor prognostic association with 30-day mortality & MI in pts undergoing major non-cardiac surgery
On CPET, what peak O2 consumption is equivalent to 4 METs?
14mL/kg/min
What are some limitations of CPET?
labour intensive, costly, pt risk performing it, many studies supporting its use are older, METS study didn’t find that peak O2 consumption was predictive of 30-day MI or death.
Does the DASI questionnaire have construct validity as a measure of functional capacity?
Yes
In the METs study, did NT-ProBNP correlate well with DASI or peak O2 consumption on CPET?
No
By how much more is the risk of periop MI for emergency vs elective surgery?
3x
What are some of the purposes of pre-op Ax for non cardiac surgery?
1) assessment of perioperative risk (which can be used to inform the timing of or decision to proceed or the choice of surgery and which includes the patient’s perspective- shared decision-making)
2) determination of the need for changes in management, such as further testing, interventions, medication changes, allied health input or intra- and post-op monitoring/disposition
3) identification of cardiovascular conditions or risk factors requiring longer-term management
4) opportunity for clear communication w pt & multi-D team
Does adding NT-ProBNP improve the predictive performance of the RCRI?
Yes
What are the haemodynamic/management issues with HoCM?
reduction in SVR (arterial vasodilators), volume loss, reduction in preload or LV filling may increase the degree of dynamic obstruction & further decrease diastolic filling & CO
Avoid overdiuresis & generally avoid inotropes because of increased LV outflow gradient
What are the ACC/AHA guidelines class 1 recommendations re: preop echo in pts with valvular heart disease? What things should I look for on echo? what other tests are warranted? And for valvular intervention?
do one if there’s clinically suspected moderate or greater degree of valvular stenosis or regurg AND no echo within 1 yr or significant change in clinical status or physical examination since last echo
Quantify the severity of stenosis or regurg, quantify systolic function, estimate right heart pressures. Should also evaluate for concurrent CAD (electrocardiography exercise testing, stress echo, nuclear imaging or angio.
In adults meeting standard indications for valvular replacement & repair on basis of symptoms & severity of stenosis or regard, valvular intervention before elective non-cardiac surgery is effective in reducing perioperative risk
What’s the 30-day mortality for pts having non-emergency non-cardiac surgery with moderate or severe AS? cf those sans AS? What re likely mechanisms for MACE in AS?
2.1% vs 1%
anaesthesia/surg factors–> hypotension, tachycardia which reduce coronary perfusion, risk development of arrhythmias or ischaemia, myocardial injury, cardiac failure & death
What are the options for pts meeting indications for AVR before non cardiac surgery but are considered high risk or ineligible for surgical AVR?
- proceeding with the surgery with invasive haemodynamic monitoring intra-op & optimising the loading conditions
- percutaneous aortic balloon dilatation as a bridging strategy
- transcatheter aortic valve replacement
What are the risks of mortality & stroke with percutaneous aortic balloon dilatation? how about recurrence & mortality by 6/12 after the procedure
2-3%
1-2%
values approach 50% by 6/12
What are the main intraoperative goals for pts with severe MS and AS?
monitor intravascular volume (MUST be sufficient to ensure adequate forward CO without excessive rises in LA pressure & PCWP that could precipitate APO) , avoid tachycardia & hypotension
What are the main intraoperative goals for pts with severe MS and AS?
monitor intravascular volume (MUST be sufficient to ensure adequate forward CO without excessive rises in LA pressure & PCWP that could precipitate APO) , avoid tachycardia & hypotension
Are L)-sided regurgitant or stenotic valvular lesions better tolerated during non cardiac surgery?
regurgitant
Haemodynamic goals for MR & AR?
-
Why do the Canadian guidelines for periop cardiac risk Ax & Mx recommend Lee’s RCRI over the NSQIP calculators?
It’s undergone external validation in studies systematically monitoring troponin after non cardiac surgery
Is NT-pro-BNP available as a point-of-care test?
Yes
In which pts do the Canadian guidelines for pre-op cardiac evaluation for non-cardiac surgery recommend pre-op NTproBNP testing? Why these pts?
Age >=65, 45-64 with significant cardiovascular disease, RCRI >=1
These pts were selected on the basis of considering testing cost & accessibility- restricting testing to those with a baseline clinical risk estimate >5% for cardiovascular death or nonfatal MI @ 30 days after surgery (VISION study, RCRI)
While the Canadian guidelines recommend against routinely obtaining echo before noncardiac surgery to enhance perioperative cardiac risk estimation, which conditions are an exception to this?
exceptions= examination suggests severe undiagnosed obstructive intracardiac abnormality (eg. AS, MS, HOCM) or severe pulmonary HTN which would inform multi D re: the type & degree of disease, also if clinicians suspect undiognosed cardiomyopathy then echo will help optimise long-term cardiac health.
+ What’s HCM?
What proportion of pts with HCM have HOCM?
What prop have SAM & risk dynamic LVOTO?
What’s shown on histopathology?
What’s it characterised by & what are the 4 abnormalities which can develop (depending on the site & extent of cardiac hypertrophy)?
What are some symptoms which may develop with HCM?
What particularly life-threatening complications are pts with HCM at risk of?
What are some potential echo findings in HCM?
what other investigation should pts with HCM undergo?
At what value does LVOT gradient become haemodynamically significant?
Is it an independent predictor of poor prognosis?
What’s sub aortic (LVOT) O caused by in HCM?
What 3 provoking factors may induce or increase LVOTO?
What manoeuvres may reduce/eliminate LVOTO?
What proportion of pts with HCM have exertional chest pain? What’s the possible pathophysiology of this?
In which conditions could you get dynamic LVOTO without HOCM?
What type of murmur is heard in HOCM?
What are the haemodynamic goals for HCM?
What WHO classification is HCM in preg?
When might a B blocker help hypotension?
What are the 3 categories of HOCM?
Treatments in HCM?
A genetically determined (autosomal dominant) heart muscle disease generally caused by mutations in sarcomere genes encoding components of the heart’s contractile apparatus. most common inherited cardiac malformation.
75%
25%
histopath shows hypertrophied & disorganised myocytes with interstitial fibrosis, intramural coronaries have decreased luminal CSA & impaired VD capacity
Characterised by LV hypertrophy
Can develop: LVOTO, diastolic dysfunction, myocardial ischaemia, MR
May be asymptomatic & diagnosed through family screening. May manifest wtih S&S related to heart failure, ischaemia or arrhythmias eg. fatigue, dyspnoea, chest pain, palpitations, pre-syncope or syncope
risk of LVOTO, supra-ventricular & ventricular arrhythmias & sudden cardiac death (annual incidence 1% esp in young- incr risk if FHx SCD, prev cardiac arrest, prev VT, syncope, abN BP response w exercise, LV wall thickness >3cm). arrhythmias may predispose to cardioembolism & CVA. AF poorly tolerated (if diastolic dysfunction more reliant on atrial kick).
-Myocardial hypertrophy (LV wall thickness >=15mm) & diastolic dysfunction
-Systolic function generally preserved (most pts w HCM have normal or hyper-dynamic systolic function). Systolic dysfunction if extensive myocardial involvement
-May get impaired LV emptying due to LVOTO (resulting in incr LVEDP). Severity of LVOT gradient can be assessed. If not at rest, can do with exercise echo.
-With LVOTO, see hyper dynamic LV with under-filled cavity, SAM with prolonged SAM-septal contact ass’d w MR.
-MR (degree can be quantified)
-May get incr LA size
-All pts w HCM should undergo a stress test (ideally exercise)
> =50mmHg at rest (some may develop it with exercise)
Yes- a predictor of poor prognosis
Contact of the MV leaflet with the IV septum in mid-systole
Hypertrophied ventricle, high-velocity blood flows through LVOT, venturi effect created by the high-velocity blood ejected during systole, draws MV leaflet causing systolic anterior motion of the mitral valve leaflet contacting the ventricular septum in midsystole, obstructing LVOT flow
manoeuvres that:
reduce preload (GA, neuraxial, dehydration/sudden blood loss/anaphylaxis, nitrites, sudden upright posture, sepsis, post=epidural, valsalva, diuretics/DHP channel blockers), decrease afterload (vasodilator) & increase LV contractility (fever, exercise, dobutamine/isoprenaline)
ie: conventional HF Rx with nitrates, diuretics & vasodilators may –> further haemodynamic deterioration.
Increasing chamber size (preload) to reduce LVOT obstruction- trendelenberg/legs up/fluid bolus
incr afterload- vasopressors
-ve inotropy: B-blockers, non-DHP Ca++ channel blockers eg. verapamil, REDUCING SNS STIMULATION
30%
La place: wall tension = (transmural pressure x 2wt) / (chamber radius). Myocyte hypertrophy & incr muscle mass & increased wall stress due to elevated diastolic pressures (incr transmural pressure) & increased wall thickness. May increase myocardial O2 demand
reduced supply may occur with early diastolic compression of intramural vessels (reduced radius, reduced capacity to vasodilate)
sepsis, liver failure (hyper-dynamic)
mid-late systolic murmur at the apex
Normal HR 60-80bpm & avoid tachyarrhythmia (for adequate diastolic filling time & coronary perfusion)
Preload: maintain preload & euvolaemia (poorly compliant ventricle)
Afterload: maintain but don’t have excessive afterload which increases myocardial O2 demand
limit excessive contractility
coronary perfusion pressure: important to defend higher DBP (>60mmHg) for myocardial perfusion, as reduced diameter intramural vessels & impaired vasodilatory capacity
if come unstuck? incr preload (fluids, LLs up, trendelenberg) & maintain after load w vasopressor, reduce contractility (blunt SNS response, opioids, adequate DOA)
II (mod incr morbidity, sl incr mort) III (sig incr M&M), depending on the individual. NYHA II + w S/S HF pre-preg higher risk MACE (death, HF, arrhythmia, TE events, esp in T3 or early postpartum)
if it’s due to inadequate diastolic filling time eg. in HOCM
non-obstructive, labile (obstructive only on provocation eg. valsalva, potent inhaled vasodilator, exercise treadmill testing), obstruction @ rest >=30mmHg (the pressure gradient is created by SAM-septal contact at rest or with provocation)
B blockers 1st line if HF to slow rate & -ve inotropy, improve diastolic filling
amiodarone for supravent/vent arrhythmias
ICD to reduce risk SCD in high-risk pts
ETOH septal ablation or surgical myomectomy
What’s the ARISCAT score used for?
predicting risk of postop pulmonary complications incl resp failure
What are the items on the ARISCAT score? (4 pt factors, 3 surgical factors)
Age
Preop SpO2
Resp infection within the last month?
Preop Hb <100g/L
Surgical incision: Thoracic/upper abdo (peripheral no score)
Duration of surgery
Emergency procedure
What are the risks associated with ARISCAT scores?
<26 low risk 1.6% risk postop pulm complications
26-44 intermediate 13.3% risk postop pulm complications
>=45 high risk 42.1% risk postop pulm complications
composite of resp failure, atelectasis on CXR, resp infection, pleural effusion, aspiration pneumonitis, PTx, bronchospasm Rx with bronchodilators
Which have more vasodilatory & -ve inotropic properties among the CCBs?
DHP= vasodilatory
non-DHP= -ve inotropy
According to the Canadian Cardiovascular Society guidelines for non-cardiac surgery, aspirin should NOT be initiated or continued for prevention of periop cardiac events EXCEPT FOR pts with…
coronary arter stent
those who’ll undergo CEA
What’s the risk with performing surgery within 7 days of withholding clopidogrel?
Action of aspirin on COX-1 & clopidogrel’s active metabolite covalently binding the P2Y12 receptor are irreversible- require regeneration of platelets (7-10 days) to lose their full effect
Why do dual anti platelets need to be continued for longer with DES vs BMS?
The anti-mitotic agent (eg. paclitaxel) that prevents stent epithelialisation reduces healing & increases risk of thrombosis within the stent due to the micro-injury caused during insertion. The risk of thrombosis is reduced with 12/12 DAPTs.
What’s the risk of MI, in-stent thrombosis +/- periop death if DAPTs withheld within the recommended continuation timeframes?
5%
What’s the risk of cessation of low-dose aspirin in pts with CAD in the periop period?
2-4 fold incr rate of death & MI
At what level is Thromboxane A2 functioning within 1 hour of aspirin ingestion? what does TXA2 do?
2%
plt aggregation & VC
What equation describes coronary perfusion pressure in HOCM?
CPP= ADP-LVDP
What’s normal FEV1 for a 70kg adult?
4L
What’s normal VC for a 70kg adult? How does it compare with vital capacity?
5L
usually slightly lower than VC due to dynamic airways closure
What’s vital capacity comprised of? what is it’s normal value?
IRV + TV + ERV
usually 70mL/kg
Why is CO used for DLCO measurement? equation for DLCO? what does it relate to? how does it change with increasing age?
It’s diffusion-limited
rate of diffusion/PACO
relates to surface area for gas exchange
reduces linearly with increasing age
What are some factors that may reduce DLCO?
V/Q mismatch
disease processes (eg. emphysema) which change the effective surface area for gas exchange
physical properties of the membrane (eg. pulm oedema)
changes in uptake of gas by the rbc (so should be corrected for Hb)
What’s a situation where you may have reduced DLCO but normal A-a gradient?
Normal gas transfer but chest wall disease (so need to correct the DLCO for VA (lung volume)
Cystic fibrosis: 10 key issues
- Autosomal recessive, mutation CTFR gene on 7q, chloride channels: multisystem chronic suppurative disorder causing increased viscosity of exocrine secretions
- high perioperative M&M- particularly pulmonary- obstructive lung disease & reduced DLCO (parenchymal destruction with bronchiectasis)- difficult to ventilate & extubate (regional vs GA, pulmonary rehab, sputum clearance, multi-D ++: RESPIRATORY PHYSICIAN- inform of admission, need to know tune-up history (pre-op tuneup likely), do OT @ TERTIARY CENTRE with ICU postop)
- High risk infection (reduced ciliary clearance, goblet cell hypertrophy, biofilm & colonisation)
- May have pulmonary HTN or cor pulmonale
- may be on chronic steroids
- possibly on home O2
- transplant consideration
- risk diabetes (first on the list, ENDOCRINE INVOLVEMENT)
- malnourished (pancreatic insufficiency, enzyme supplements & fat-soluble vitamin malabsorption, DIETICIAN INVOLVEMENT)
- thick GI secretions, may get bile duct obstruction–> focal biliary cirrhosis, liver failure, portal HTN
What’s the risk of PTx with paravertebral?
0.5%
What are some red flags on Hx of a pt with CF for higher perioperative risk?
recent admission for flare
transplant waiting list
home O2
current infection
pulm HTN
What is cystic fibrosis & what type of inheritance?
Autosomal recessive
dysfunction of chloride channels
Why may pts with CF have metabolic alkalosis (often mixed resp acidosis & metabolic alkalosis)?
contraction alkalosis (volume contraction & dehydration)
may be due to CF-related diabetes (so may get contraction alkalosis with the diabetes-related polyuria)
Why may pts with CF have metabolic alkalosis (often mixed resp acidosis & metabolic alkalosis)?
contraction alkalosis (volume contraction & dehydration), this may be exacerbated by a CF-related diabetes (so may get contraction alkalosis with the diabetes-related polyuria)
there may be an underlying renal process involving the CFTR
What are some of the features of a pt with CF on examination?
May have clubbing
May have barrel chest, signs of increased WoB
May be on home oxygen
may have signs of right heart failure
may appear malnourished/cachectic
may have signs of corticosteroid excess
What’s an issue with using NSQIP?
If you have a very high risk pt (eg. CF for breast surgery) the calculator may not fully capture the high risk due to a lack of data on such pts
Proportion of pts w OSA undiagnosed?
Has the STOP-BANG score been validated?
80%
Yes. a 2015 meta-analysis & systematic review (Nagappa et al) including >9000 pts demonstrated that STOP-BANG had sensitivity of 90%, 94% & 96%, respectively, for predicting any OSA (AHI >=5), mod-severe OSA (AHI >=15) & severe OSA (AHI >=30. Corresponding NPV was 46%, 75% & 90%.
In surgical patients, the probability of severe OSA with a STOP-Bang score of 3 was 15%.
score 4= 25%
score 5= 35%
score 6= 45%
score 7= 65%
pts w a stopbang of 1-2 have a NPV 100% for severe OSA
Whats an apnoea?
complete cessation of airflow or obstruction lasting 10 seconds or longer.
What’s a hypopnea?
30% or greater reduction in airflow (compared to baseline), and a 3% or greater reduction in Oxygen saturation (a drop in the oxygen level) during a 10 second event
What’s the respiratory disturbance index?
number of apnoea, hypopnoea & respiratory effort-related arousal (RERA, an event not meeting criteria for apnoea or hypopnea but is an arousal event associated with resp effort as noted on the EEG) events per hour.
An indicator of neurocognitive decline from OSA (5, 15, 30)
If serum bicarbonate chronically high in OSA, how may this impact management?
may insert an art line & take serial gases
*serum bicarb improves specificity of STOP-BANG but it’s often detecting OHS vs OSA
What are some perioperative risks associated with smoking?
intra- and post-op risks:
-increasing risk of MACE (eg. myocardial infarction, CVA)
-increasing risk of perioperative respiratory events (eg. laryngospasm, bronchospasm, postop infection, respiratory failure)
-immunosuppression/increased infection risk (poor wound healing)
What are the steps of the 3-point strategy developed by the ASA smoking cessation taskforce?
Ask: if & quantify, ask if they’d considered or attempted, target my education at the point of behavioural change they are at, praise any attempts they’d made, acknowledge challenging (Aust Ca council suggests 12-14 attempts, some studies up to 30- average timescale for overcoming nicotine addiction is 3 months).
Advise (verbal and written) benefits of quitting- increases likelihood of Bx change- surgery a “teachable moment” where many smokers quit or attempt to quit, sometimes permanently- more major surgery= greater impact on smoking cessation
Refer (follow-up, GP and QUIT line, pharmacologic & non-pharmacologic support)
What are the main harmful substances in cigarette smoke & what are their half-lives?
Nicotine: 0.5-1hour
COHb 4-6hrs on RA & 1hr with 100% O2
What’s the pathophysiology of cardiovascular adverse events with smoking?
-nicotine stimulates adrenals–> Adr secretion–> incr SNS tone (HR, BP, SVR, contractility, myocardial O2 demand)
-CO binds cytochrome oxidase in myoglobin which reduces intracellular O2 transport & utilisation–> chronic tissue hypoxia, also Hb has higher affinity for CO than O2, reduces O2-carrying capacity of the blood & it left-shifts the HbO2 dissociation curve, impairing O2 delivery to the tissues
-chronic inflammation promotes atherosclerosis/coronary artery disease (independent risk factor for CAD)
-polycythaemia (from chronic hypoxaemia) & increased viscosity
What’s the pathophysiology of respiratory adverse events with cigarette smoking?
increased mucus secretion + destroy cilia –> reduced tracheobronchial clearance, increased risk of postop respiratory infections
damages epithelium–> airway hyperactivity (bronchial & laryngeal)- coughing with airway instrumentation & risk broncho/laryngospasm
up to 15% COHb (normal 2-3%)
What are some other adverse effects of cigarette smoking (aside from cardiac/respiratory)?
-addictive
-impair humoral activity & cell-mediated immunity–> increased risk infection & malignancy
-SIADH
-induces liver microsomal enzymes incr metabolism opioids, aminosteroid NMBDs
-more postop pain
BUT reduces PONV rates
What’s the time course of physical changes following smoking cessation?
hours: reversal of adverse effects of nicotine on the myocardium
12 hrs: complete elimination of CO
2 weeks: increased sputum volume
potentially a rebound phase of airway hyperactivity + sputum overproduction- emphasise to pts incr sputum volume is a GOOD thing despite more productive cough- cilia working again, defences improving
3 wks: reduced post-op wound-related complications
4 wks: reduced post-op respiratory complications
6-8/52: sputum volume normalises & periop analgesia requirements normalise
6/12: significantly improved immune function
Over time, the airway reactivity & polycythaemia with increased blood viscosity will improve
What does the research tell us about pharmacological & non-pharmacological interventions for smoking cessation?
more intensive intervention= greater abstinence rate so follow-up beyond the pre-anaesthesia consult vital
PHARMACOLOGICAL:
cf placebo for smoking cessation @ 6/12:
-Nicotine replacement therapy= 1st line (patches, gum, oral strips) OR 1.84, combination better than monotherapy. Start high (eg. 21mg 16hr patch) & slowly wean.
-NRT combination OR 2.04
-Varenicline (nicotine partial agonist) OR 2.88, also 1st line therapy, start 2/52 before smoking cessation to occupy receptors. Gradual uptitration, side-effects= nausea, headache, insomnia, avoid in pts with serious psych illness/epilepsy/COPD/IHD, is renally eliminated.
-bupropion OR 1.82, 2nd line: start 1-2 wks b4 smoking cessation, side effects= insomnia, nightmares, poor concentration
-nortryptilline & clonidine aren’t on PBS
NON-PHARMACOLOGICAL:
-individual or group counselling
-rapid smoking aversive therapy- smoke rapidly & hold in mouth for 5-10 secs/puff–> nausea–> reduce desire to smoke through conditioning
combination of pharmacological therapy with multisession F2F counselling significantly improves chances of quitting (RR 10.8 Cochrane 2014)
What does the International Committee for the Advancement of Procedural sedation consensus statement on fasting & aspiration prevention recommendations specific to procedural sedation recommend?
That fasting as currently practiced often substantially exceeds recommended time thresholds & adverse effects (irritability, dehydration, hypoglycaemia) are adverse consequences.
The probability of clinically important aspiration during procedural sedation is negligible.
Pt should be risk-stratified with respect to comorbidities, nature of procedure & anticipated sedation technique. They present a consensus-derived algorithm with graded fasting precautions for liquids & solids for elective procedures based on negligible, mild or.moderate aspiration risk.
What’s ASA 1?
Normal healthy patient- normal BMI, no acute or chronic disease, non-smoker, no or minimal ETOH
What’s ASA II?
mild systemic disease WITHOUT substantive functional limitations
current smoker
social ETOH
normal pregnancy (incl. well-controlled gestational HTN or controlled preeclampsia without severe features, diet-controlled GDM)
obese (BMI 30 to <40)
well-controlled DM/HTN, mild lung disease
oncologic state in remission
asthma without exacerbation
well-controlled epilepsy
What’s ASA IV & examples?
a pt with severe systemic disease that’s a constant threat to life
recent (<3/12) MI, CVA, TIA, CAD/stents
ongoing cardiac ischaemia or severe valve dysfunction
severely reduced EF, shock, sepsis, DIC, ESRD not undergoing regular scheduled dialysis, severe trauma
PET with severe features complicated by HELLP
peripartum cardiomyopathy with EF <40
uncorrected/decompensated heart disease (acquired or congenital)
What’s ASA V & examples?
Moribund patient not expected to survive without the operation
ruptured Tx/abdo aneurysm
massive trauma
intracranial bleed with mass effect
requiring ECMO
resp failure or arrest
malignant hypertension
hepatic encephalopathy
ischaemic bowel in the face of significant cardiac pathology or multiple organ/system dysfunction
uterine rupture
What’s vWF?
a plasma glycoprotein with roles in:
-platelet aggregation & adhesion
-carrier for factor VIII, reducing it’s clearance from plasma
-
0
What’s the most common inherited bleeding disorder? what’s it caused by? transmission? how many major types?
von willebrand disease
caused by a mutation on chromosome 12
autosomal dominant transmission aside from 2N & type 3 which are autosomal recessive
can be acquired
3 major types:
1= quantitative reduction in vWF protein ( [ ] & activity)- mildest & most common phenotype
1C= vicenza- increased clearance of vWF, poor response to DDAVP
2= qualitative defect, dysfunctional, divided into 4 subtypes reflecting specific vWF function affected:
2A= loss of platelet binding function
2B= increased platelet binding by vWF which –> accelerated clearance/sequestration of platelets–> thrombocytopenia
2M= reduced binding of vWF to platelet GPIb or collagen
2N= reduced binding of vWF to factor VIII- similar manifestations to haemophilia A with joint & soft tissue bleeding
3= severe quantitative reduction of vWF & factor VIII
platelet-type: gain of function mutation in GpIb receptor. autosomal dominant.
How are pts with vWF generally managed (prophylactic prior to surgery)? targets? intra-op, how could bleeding be treated?
Depends on the severity of disease & risk of surgery
Generally type 1 & 2A is DDAVP infusion 30-60mins preop (not used if pts has previously had lack of response to a DDAVP trial)
type 2b & 3= vWF replacement (may take 2/52 to reach acceptable vWF & factor VIII levels)
prior to surgery, for high-risk subtypes the target vWF:RCo level is 100 IU/dL, usually achieved with 40-60U/kg (& >50 IU/dL immediate postop), factor VIII activity >50% (but no >200% as risk thrombosis). Generally major surg Rx for 7-14 days, minor 1-5 days.
Rx depends on the severity & site of bleeding, type of vWD & responses to therapy. liaise with haematology.
TxA valuable for bleeding from skin/mucosal surfaces (eg. epistaxis)
vWF concentrates provide excellent haemostasis in many populations- indicated in severe cases, type 3 & qualitative defec ts. From pooled plasma & are virally inactivated- minor bleed 50IU/kg IV expected to raise vWF activity >=50IU/dL. Risk VTE.
DDAVP is only effective for some (approved for type 1, NOT for type 3, discuss use in type 2 with haematologist (variable effect depending on subtype & risk thrombocytopenia)- smaller increases in vVF activity, later onset & shorter duration- so not suitable for major or life-threatening, more suited to minor bleed, 0.3microg/kg (maximum 20microg) IV/subcut infused over 30mins (max dose due to concerns re: toxicity esp hyponatremia & diminishing efficacy @ higher doses) + TxA 15mg/kg.
NOT to be used under 2yo due to risk hyponatremia & seizures. tachyphylaxis develops within a few days. care in pts with risk thrombotic complications. DDAVP= minirin or octostim. If required pre-op, administer 30mins before procedure.
infusion of DDAVP may cause facial flushing, hypotension, hyponatremia (consider fluid restriction). DDAVP may also cause thrombocytopenia, seizures, risk thrombotic complications, tachyphylaxis & diminishing efficacy.
if no concentrate available & active bleed, cryoprecipitate provides vWF (avoid if possible due to risk viral transmission, unpredictable effect).
may require additional haemostat therapies in discussion with haematology if refractory bleed (eg. platelets may be considered if bleeding despite DDAVP & vWF.
adverse effects of DDAVP?
hypnonatremia (due to ADH activity)
seizures (hence not for chn <2yo)
flushing (VD)
headache (reduced with slow infusion rate)
tingling/weakness (may be due to hyponatremia)
thrombosis (rare- not recommended for pts with CV disease)
tachyphylaxis after 48hrs
+What is Duchenne muscular dystrophy? incidence? inheritance? pathophys & presentation? significance for anaesthetics?
most common childhood muscular dystrophy
Becker is a milder form
1:3500 live births
X-linked recessive degenerative disease of skeletal & smooth muscle, post-junctional neuromuscular disease
lack dystrophin, a protein helping anchor muscle cells to the ECM
muscle fibres are replaced with fibrous connective tissue
sarcolemma becomes increasingly permeable with increased intracellular calcium
appears in childhood- boys, from age 3-5
progressive wasting/weakness of usually proximal muscles, presents as wedding gait & calf pseudo hypertrophy
Often wheelchair bound before teens, fatal by adolescence/early adulthood from resp or cardiac failure
Considerations:
High risk- consent discussion/AHD
May have mild cognitive impairment
May be on ACE-I or ARB (digoxin if overt HF), B-blockers or steroids (may be on these to improve motor & pulmonary function, potentially delaying progression of cardiomyopathy, improving survival. Consider stress dose). May be on genetic therapies (may be ass’d w arthralgia, URTI, hypersensitivity reactions, some impact renal function). Heart transplant considered if Beckers & severe DCM but limited skeletal muscle disease.
May be on assisted coughing, nocturnal or daytime assisted ventilation, may have tracheostomy
Airway may be difficult (macroglossia, kyphoscoliosis/contractures–> difficult positioning, aspiration risk (bulbar weakness, reduced gastric motility), risk OSA
Ventilation: restrictive lung disease (kyphoscoliosis/resp muscle weakness), lung protect vent
Circulation: art line, 5-lead ecg, consider CVC depending on comorbidities. Risk cardiomyopathies; 50% have DCM by age 15, ecg may show tall R waves in precordial leads, deep Q in I, aVL, V5-6
Mitral regurg common (consequence of LV dilatation)
conduction defects/arrhythmias common
risk pulm HTN & RV failure (restrictive lung disease)
Bleeding risk (lack of vascular smooth muscle tone, plt dysfunction)
maintain sinus 60-80bpm, maintain preload (relatively fixed CO state), avoid excessive afterload, VERY important to avoid myocardial depression, defend DBP >=60mmHg (cor PP), R) heart considerations esp if RV dilatation
Positioning: risk from contractures/pressure areas
Drugs: succinylcholine & volatiles contraindicated due to anaesthesia-induced rhabdomyolysis & potentially life-threatening hyperkalaemia; not MH, but use use TIVA with clean machine & avoid sux
Female carriers may show elevated CK levels, mild myopathic changes & cardiomyopathy so avoid volatiles & DMRs
Ideally avoid NDMRs (slow onset & offset, may get prolonged block)- if use, monitor TOF
Incr sensitivity to sedatives/hypnotics, risk postop impaired vent response to hypox/hypercapnia, OIVI
Emergence: TOFR>=0.9, awake, upright, only extubate if unequivocally have met criteria
Postop: HDU for ongoing cardioresp monitoring/support while haemodynamics/pulmonary status vulnerable, analgesic titration, chest physio, incentive spirometry +/- cough assist
risk prolonged postop ventilation (risk postop pulmonary complications)
To which type of drug are pts with MS particularly sensitive?
depolarising NMBDs- avoid sux
What’s autonomic dysreflexia? it’s signs/symptoms? causes? risk factors? Rx?
medical emergency
Constellation of S&S of excessive SNS activity in response to a stimulus below the level of a SCI of T6 or higher.
The disordered ANS response is characterised by severe HTN (incr at least 20%, may be >200mmHg) which may–> raised ICP, seizures, intracranial haemorrhage or cardiac complications incl arrhythmias (bracy, tacchy, heart block, sinus arrest), myocardial ischaemia, infarction, acute LV failure & pulm oedema
Other symptoms= headache, nasal congestion, blurred vision, flushing above the lesion & pallor below, sweating, chills, piloerection, splanchnic VC if lesion above T6
Triggered by stimuli below level of lesion, eg. bladder (in 85%)/bowel distension, activation of pain fibres, where there’s a lack of modulation of ascending SC input from higher centres- profound SNS response up to the level of injury, compensatory PSNS response aiming to reduce HTN so get VD/flushing & Brady above the level of the lesion- in tetraplegia therefore you’d see tachycardia, HTN, vasoconstriction below the lesion.
Incr instance with higher & more complete spinal cord lesions, more commonly observed in chronic SCI (10% of pts with lesions above T6 experience ADR within 1st yr of injury)
Mx with immediate removal of stimulus (eg. remove endoscope), deepen anaesthesia, position head up (orthostatic BP drop), FiO2 to 100%, rapid-onset short acting vasodilator medications to prevent complications of severe HTN, eg. GTN (hypotensive effects may be exagg if pt also on sildenafil). longer-acting agents (hydralazine, labetalol) used w caution as hypoT may persist once the AD resolves. Manage any arrhythmias (eg. B block, anticholinergics, ACLS meds), myocardial ischaemia. IABP if ADR doesn’t resolve quickly. consider ICU for post-event management esp if significant complication.
Chronic SCI pts often present for OT (eg. urologic procedures). Since same life expectancy, present for general procedures.
Cord recovers its reflexes, these pts NEED ANAESTHESIA- risk ADR (85% of pts w lesion above T6); with stimulus below the lesion unmodulated by desc inputs, can get overwhelming SNS output.
Neuraxial may be technically difficult (eg. blood clot in epidural space)- patchy block.
Other considerations:
ask pts re: Hx of ADR, inciting events, Rx, prev surg or anaesthesia. Often these pts have had many procedures & know what works well for them (both GA & spinal can effectively prevent ADR)
CNS: chronic pain syndrome common (develop several months to years after SCI). neurogenic pain (burning, stabbing, electrical) often w hyperesthesia; at-level or below-level. musculoskeletal pain (dull/aching/well-localised).
Cardiovascular: CAD more prevalent in SCI, may have atypical chest pain w cardiac ischaemia. Pts w SCI above T6 will have baseline hypotension & bradycardia often hypovolaemic, orthostatic hypotension can persist (care w head up positioning) w reduced SNS & baroreceptor activity. Thorough CV workup (low threshold for pharmacological stress testing periop), consider pre-induction fluid bolus, carefully titrate anaes drugs w vasopressors, use inotropic/chronotropes if injury above cardioaccelerator SNS innervation T1-4. consider art line if sig comorbidities or Hx ADR. goal MAP within 20-25% of pts baseline to maintain spinal cord & coronary perfusion (most neurol recovery after SCI occurs within first 3-6/12, a small proportion have late recovery esp w incomplete SCI)
ADR: manage w vasodilators.
Resp/airway:
potentially difficult airway if prev c-spine fusion or tracheostomy
risk bradycardia w airway manipulation & tracheal suctioning (incr vagal tone common w acute SCI, may persist)
lower lung volumes; desaturate more quickly w apnoea (reduced FRC). may have restrictive lung pattern w RHF.
may be unable to lie flat (resp embarrassment)
More prone to hypotension with PPV (lack of baroreceptor activity)
more prone to periop resp infection
consideration of periop use of any regular assisted ventilation devices (eg. NIPPV, cough assist). Pt may have phrenic nerve or percutaneous diaphragm pacing (liaise w clinician managing the device)
Fully reverse & ensure adequate TVs before extubation.
head-up position assists resp mechanics.
may wean onto Bi-PAP.
Musculoskeletal:
prone to contractures (complicate positioning), muscle spasms common & may be precipitated by cutaneous or proprioceptive stimuli.
pressure ulcers a major concern; examine for at-risk sites preoperatively, meticulously protect bony prominences.
avoid sux for SCI >48hrs.
avoid neuromuscular monitoring in paralysed limb; may use facial nerve monitoring if high SCI & ulnar nerve paralysis.
Temp: impaired thermoregulation from ANS dysfunction, risk for hypothermia or, w warming devices, hyperthermia; monitor & carefully manage throughout periop period.
Haematologic:
50% are anaemic. may be unable to compensate for even modest blood loss with incr SNS activity; diligent replacement of blood loss vital for maintaining adequate CO.
Pts w SCI very high risk VTE (DVT/PE)
Pd: high SCI may be more sensitive to sedative/hypnotics.
Regional/neuraxial: these pts don’t tend to get hypotension from spinal-induced sympathectomy (possibly due to low baseline SNS tone). Epidural less appropriate for SCI (patchy block possible, may fail to prevent AD)
Consider postop HDU if ongoing vasoactives required. pts still @ risk for ADR postop (esp w bladder distension).
ADR particularly a concern in labour, given risk of uteroplacental vasoconstriction & fetal hypoxia (as well as risk of ICH & hypertensive encephalopathy). Lesions below T11 will perceive labour pain, 5-10 may have a painless delivery but may get symptoms of ADR.
Pregnant patients should have antepartum consult w anaes to develop plan; early epidural best but may be challenging because of contractures, spasms or prior spine surgery. CSE or epidural or continuous spinal all appropriate for pts @ risk of ADR. GA or regional for caesarean. continue RA postpartum until haemodynamics stable (postpartum uterine contractions may elicit ADR response).
Pts with high SCI require continuous BP & ECG, low threshold for art line (eg. depending on pts Hx of ADR).
Manage ADR during labour by optimising epidural/intrathecal anaesthesia, head-up (orthostasis), hydralazine 5mg titrated up to 20mg. sublingual nitroglycerin (may decr uterine tone & incr uterine haemorrhage). severe uncontrolled HTN may be an indication for emergency caesarean under GA.
What is myasthenia gravis?
Autoimmune condition where IgG auto-antibodies develop to & attack the nicotinic ACh receptor at the postsynaptic membrane of the neuromuscular junction, preventing ACh binding and producing fatiguable skeletal muscle weakness.
What are the signs & symptoms of myasthenia gravis?
ocular signs (diplopia & ptosis- 15% of pts with MG have isolated eye signs)
weakness & fatiguability of voluntary muscles- generalised- ocular, facial, bulbar (speech, swallow), limbs
resp muscles usually only weakly effected unless myaesthenic crisis where resp failure requiring intubation may occur
What conditions may be associated with myasthenia gravis?
other autoimmune diseases eg. RA, thyroid disease
Anaesthetic considerations for myasthenia gravis?
PRE-OP:
-preparation coordinated with pts neurologist
-time elective surgery with a stable phase of the disease (minimal immunomodulatory medication or glucocorticoid requirement, minimises likelihood of post-op myaesthenic crisis)
-establish:
precise diagnosis- severity, current management (eg. symptomatic Rx with anticholinestarases, chronic immunomodulatory Rx (eg, glucocorticoids) or rapid immunomodulating Rx (eg, plasmapheresis or IVIG. Pts who are refractory may receive monoclonal Abs)
Hx of exacerbations or myasthenia crises, need for endotracheal intubation
associated conditions (eg. RA, thyroid, SLE)
full assessment including
-function (quantify with DASI)
-bulbar dysfunction (symptoms dysphagia, dysarthria, nasal speech, low-intensity speech), which predisposes to aspiration
-respiratory muscle weakness, dyspnoea- pre-op PFTs useful if having GA with NMBAs
-if having thymectomy for thyme mass, may be @ risk airway compromise on induction, review chest CT/other imaging
-optimisation as able (multi-D)
-full discussion with pt/family re: risks/benefits/alternatives of anaesthesia & potential complications (most concerning of which is myasthenia crisis with resp failure)
-careful preop planning:
multi-D discussion including neurologist (eg. major surgery may require plasma exchange/IVIg pre-op which will significantly reduce plasma cholinesterase activity)
Surgery should be at a tertiary centre with experienced surgeon (minimise operative time) & access to postoperative HDU & ideally neurology for consult
schedule surgery early in the day: limit fasting, pt strongest.
-perioperative medication management: must continue anti cholinesterase (pyridostigmine) perioperatively, may require stress steroids
INTRA-OP:
overarching goals= to prevent prolonged effects on resp & bulbar muscles & allow rapid recovery @ end of surgery.
use regional or local where possible- use amides rather than esters for pts taking anticholinesterases (as anticholinesterases may impair hydrolysis of ester LAs, prolonging block), HOWEVER care/avoid mid thoracic or higher neuraxial in pts with preop resp compromise/bulbar weakness. Also, supraclavicular & inter scalene BP blocks paralyse ipsilateral diaphragm in most pts so may not be tolerated by those with resp compromise.
A:
bulbar impairment may predispose to aspiration risk
large thymoma may distort trachea, make intubation difficult
may be associated with RA (neck E, TMJ, VC dysfunction possible)
at higher risk of OSA (poor oropharyngeal tone)
B:
may have restrictive ventilatory defect due to chest wall muscle weakness +/- spinal deformities- FEV1<2.9L increases likelihood pt may require postop ventilation
higher risk postop resp failure, susceptible to OIVI so consider regional/local/opioid sparing but careful consideration of risks/benefits/alternatives of regional if rapidly progressing neurology
C:
cardiac function may be unknown as pt may not stress heart daily
D:
avoid/minimise premeds
level of functional impairment (transfers, positioning, pressure areas)
If sugammadex N/A, avoid NMBAs if at all possible
Unpredictably sensitive to NDNMBDs (& block onset may be delayed in pts taking anticholinesterases) yet resistant to DMRs (as have less ACh receptors)- ED95 for sux in MG is 2.6x normals & Rx with cholinesterase may prolong effect of sux. pts with MG higher risk of phase 2 block.
TOFR to carefully monitor depth of neuromuscular blockade- if paralysis necessary (often it isn’t), higher dose of sux (1.5-2mg/kg) required as lower number functional post-synaptic nAChR (resistant to DMRs) but may get phase II block- highly sensitive to NDMRs so ideally no or very low-dose NMBD (0.1 to 0.2x the ED95, monitor with TOF, reverse with sugammadex). Avoid mivacurium (metabolised by cholinesterase so if taking pyridostigmine it may have prolonged effect) & avoid long-acting agents.
Could consider prop-remi with lignocaine to the cords.
reverse with sugammadex if roc used (neostigmine may precipitate cholinergic crisis)
care to avoid hypothermia or hyponatremia which potentiates neuromuscular blockade
Volatiles may depress neuromuscular transmission- may negate need for (or reduce required dose of) NMBDs
Can consider IV lignocaine, remifentanyl, fentanyl or esmolol to help blunt the reflexes in response to laryngoscopy
AVOID drugs that may exacerbate myasthenia, eg:
aminoglycosides (inhibit ACh release & block ACh receptor postsynaptically)
ciprofloxacin
macrolides
lignocaine may prolong neuromuscular blockade (but could still consider for opioid sparing)
procainamide
gabapentin
phenytoin
lithium
quinine
magnesium
verapamil
B-blockers
Ca++ channel blockers
some opioids
Ultra-short & short-acting sedatives/hypnotics/GA agents to minimise resp depression on emergence. multimodal, opioid sparing (eg. regional)
Postop:
UNSUITABLE for day surgery, HDU or ICU very likely
maximise the possibility of extubation @ the end of surgery
more likely to suffer myasthenia crisis & need postop intubation if:
-major cavity surgery
-vital capacity <2.9L
-pyridostigmine requirement >750mg/day
-duration of disease >6yr
-Hx co-existing respiratory disease (eg, COPD)
-preop bulbar symptoms
-Hx myasthenia crisis
-serum anti-ACh antibody >100nmol/L
-intra-op EBL >1L
short-acting, titratable opioids, multimodal
physio, triflow
recommence anticholinesterases immediately, chronic immunotherapies once taking PO- liaise w neurologist re: medication plan
May require HFNO in PACU, utilise short-acting opioids, consider triflow to limit risk postop pulmonary complications, postop physiotherapy useful
recommence anticholinesterases at reduced dose immediately postop, up-titrate as pt more ambulant
Which medications to avoid as risk exacerbating myasthenia?
aminoglycosides
ciprofloxacin
procainamide
lignocaine (but still consider for multimodal analgesia/opioid sparing)
quinine
Ca++ channel blockers
magnesium
lithium
What’s the most common childhood muscular dystrophy?
Duchenne
What’s the most common myotonic syndrome?
myotonic dystrophy
What are neuromuscular disorders? how to classify? examples?
heterogenous group of diseases affecting skeletal muscle, classified as hereditary and acquired and anatomically wrt site impacted by the disease process
HEREDITARY:
pre-junctional:
-Peripheral neuropathies: Charcot-Marie-Tooth, Fredrichs ataxia
post-junctional:
-Duchenne & Becker’s muscular dystrophy
-Myotonias (myotonic dystrophy, myotonia congenita, hyper/hypokalemic periodic paralysis)
-Metabolic/mitochondrial disorders
ACQUIRED disorders:
pre-junctional:
-Motor neurone disease
-multiple sclerosis
-Guillain-Barre
-peripheral neuropathies (eg. DM)
junctional:
-Myasthenia gravis
-Eaton-Lambert syndrome
post-junctional:
-Inflammatory myopathies
-critical illness polyneuropathy & myopathy
What may increased EtCO2 with unexplained tachycardia signify?
hyperthermic complication, which should be treated aggressively
What’s the concern with using sux in muscle that’s been denervated or immobile for prolonged periods?
extra-junctional receptors can occur, incr number of ACh receptors, may also have foetal gamma isoforms of the nicotinic ACh receptor, massive K efflux can occur with activation of these receptors by sux which may –> fatal hyperK, m fibre swelling, rhabdo
What’s an additional consideration with sux in myotonias?
fasciculation may –> temperomandibular muscle spasm & may prevent I&V
What doses of non-depolarising muscle relaxants should be given to pts with neuromuscular disorders? complications when given to pts with sensitivity to them? which agents are preferred?
10-20% of the recommended dose & degree of neuromuscular block should be monitored
NDMRs may cause respiratory muscle weakness, difficulty weaning from invasive ventilation, sputum retention, dysphagia
rocuronium as short-acting or mivacurium & atracurium due to their relatively short duration & organ-independent degradation
Why avoid anticholinesterases in muscular dystrophies?
like sux, they may lead to hyperkalemia
What are signs of rhabdomyolysis?
metabolic acidosis
hyperkalaemia
myoglobinuria
CK >10,000 U/L
Which neuromuscular disorders MAY actually have an association with MH?
central core disease
hypokalaemic periodic paralysis
What is the management of rhabdomyolysis?
cease offending agent
manage hyperkalaemia
aggressive volume resus to remove myoglobin & maintain urine output >1mL/kg/hr
may alkalinise the urine using sodium bicarbonate
consider dantrolene if pt hyperthermic
general considerations of autonomic dysfunction with neuromuscular disorders?
gastric dysmotility may increase aspiration risk
may develop severe hypotension on induction & after regional anaesthesia
sympathomimetic drug doses may need to be reduced (increased sensitivity of alpha & beta receptors)
What is the mechanism & triggers for myotonic contractures, which may occur with the dystrophic & non-dystrophic myotonia?
repeated action potentials –> permanent Na influx or Cl efflux, rendering muscle membrane hyper excitable
triggers= sux, anticholinesterases, opioids, temp changes, acidosis, shivering
What is the management of a myotonic contracture?
correct environmental or physiological precipitant
consider sodium channel blockers (eg. LA), anti-arrhythmias
they are not classically responsive to neuromuscular block, regional or peripheral nerve blockade
What’s Charcot-Marie-Tooth?
hereditary pre-junctional disorder
may be X-linked, AD or AR
chronic peripheral neuromuscular denervation
results in atrophy of muscles –> spinal & limb deformity
motor weakness & sensory disturbance
Orthopaedic intervention often required for foot deformities (per caves)
Spinal deformities may result in restrictive lung disease
AVOID DMRs (denervation & hyperkalaemia risk)
NDMR action may be prolonged
respiratory compromise (restrictive) may warrant postop ventilation
note neurological deficits prior to regional anaesthesia
What’s Fredrich’s ataxia?
hereditary pre-junctional disorder, peripheral neuropathy
autosomal recessive inheritance
skeletal muscle weakness, progressive limb ataxia
myocardial degeneration often occurs–> myocardial failure & death
Anaes considerations:
aspiration risk
diaphragm often impaired–> resp failure risk
myocardial failure common–> care with -ve inotropic drugs
Avoid DMRs due to denervation
What is Becker’s muscular dystrophy? incidence? inheritance? presentation? significance for anaesthetics?
X-linked recessive inherited neuromuscular disorder where dystrophin protein (which anchors muscle cells to ECM) is only partially absent
1:30,000 men
milder symptoms vs Duchenne, runs a more protracted course- initial presentation generally in teens. slowly progressive muscle weakness of legs & pelvis. death due to cardiac (usually manifests as DCM & arrhythmia) or resp failure typically in 4th or 5th decade.
particular risk postop resp insufficiency & cardiac dysfunction-
pre-assessment incl resp & cardiac function
intra-op cardiac monitoring, blood loss may be increased (smooth muscle & platelet dysfunction), avoid hypovolaemia due to relatively fixed CO state with non-compliant ventricles, invasively monitor volume status if concerns re: intra-op hypovolaemia
Avoid DMRs due to extra-junctional synapse development & risk of hyperkalaemia & rhabdomyolysis.
Female carriers may show elevated CK levels, mild myopathic changes & cardiomyopathy so avoid volatiles & DMRs
Avoid NDMRs (slow onset & offset, may get prolonged block)- if use, monitor TOF
postop vent support considered. cardiac monitoring should continue
How do the dystrophic & non-dystrophic myotonia vary?
dystrophic myotonia demonstrate muscle wasting & weakness
non-dystrophic myotonia (eg. myotonia congenita, familial periodic paralysis) have symptom of prolonged muscle contraction following stimulation
What’s myotonic dystrophy? inheritance? presentation? anaesthetic considerations? preg concsiderations
autosomal dominant, genetically & clinically heterogenous multi-system disorder, in most pts characterised by:
-myotonia & dystrophy
post-junctional neuromuscular disorder.
Abnormal sodium or chloride channels–> muscle in an abnormal hyperexcitable state, repetitive action potentials, sustained contraction
Phenotypes: DM1, DM2 (proximal myotonic myopathy, less severe & normal life expectancy)
multisystem S&S manifest in early adulthood:
-myotonia (slow or delayed muscle relaxation eg. inability to “let go” of a hand grip after a normal muscle contraction)
-muscle wasting (dystrophy)/muscle weakness (skeletal & respiratory)- DM1 may have wasting face/temporal/distal hands & legs
-myalgic pain/pre-op analgesic requirement
-CNS: increased sensitivity to sedatives, hypersomnolence (may be disabling in DM1, may be on modafinil), behavioural/personality/attention/memory disturbance, intellectual impairment (particularly early onset DM1, impacts consent discussion)
-CVS: cardiac abnormalities eg. conduction defects (do they have a pacemaker/ICD?), arrhythmias, cardiomyopathy, heart failure, MVP, may get RHF if restrictive lung disease/pulmonary HTN
-airway: may have features of difficult airway eg. DM1 narrow facies, high-arched palate, limited mouth opening, bulbar dysfunction (incl tongue, pharynx) & impaired GI motility/GORD–> aspiration risk
-Resp: weak respiratory muscles may –> restrictive lung disease (consider PFTs esp sitting vs supine VC- reduced important potential risk postop pulm morbidity), OSA/altered central resp drive (do they use CPAP/BiPAP)?
May have kyphoscoliosis (weak paraspinals)
-Endocrine: INSULIN RESISTANCE/diabetes, thyroid/adrenal/gonadal dysfunction
Other:
-cataracts, ptosis, hearing impairment, polyneuropathy, LFT abnormalities, myalgia, hypogammaglobinaemia
May be on steroid, analgesics, anticonvulsants, quinine/mexilitine/other anticonvulsants
Anaesthetic considerations:
Multi D, optimising, tertiary centre, risk discussion, planning incl HDU
Triggers to myotonias: cold/shivering/stress/suxamethonium (also risks fatal hyperkalaemia), neostigmine, K+, electrical/mechanical stimulus (eg. electrocautery, NMT, surgical stimulation)
If myotonias occur, Mx by:
-reversing cause (stop stimulus, warm)
-deepen volatile
-phenytoin, procainamide, quinine, lignocaine
-muscle relaxants & IV anaesthetics DON’T work
Monitoring: art line (for K+, bgls, pH,O2/CO2), 5-lead, nibp, temp probe, nmt w caution, BIS, consider CVC if sig cardiac issue
Ensure prophylactic ABx 15-60mins pre-incision & meticulous asepsis (risk hypogammaglobinaemia)
employ multimodal opioid-sparing (regional/neuraxial (cognisant that may cause significant shivering/myotonia, carefully titrate mindful of haemodynamics)
have difficult airway trolley in room, plans a/b/c prospectively decided, if concerning dysrhythmia, pads on & ALS trolley/drugs in room
Pre-O2 upright, care w pressure areas/muscle wasting
Induction: highly sensitive to sed/hypnotic, reduced dose, ideally avoid relaxant but if need, roc 30% dose & titrate w NMT
VL & gentle airway instrumentation (risk tmj dislocation)
Maintenance:
volatile or propofol TIVA fine but care re: myocardial depression & sensitivity to sedative:hyponotics, consider MAC sparing (eg. remi)
lung protective vent
fluids: euvolaemia, avoid K+-containing
normothermia (monitor, actively warm) AVOID shivering
Emergence:
fully reversed TOFR >0.9 (w sugammadex)
only extubate when criteria unequivocally met, upright position
Postop:
multi-modal anti-emetics intra- & post-op (aspiration risk)
adequate analgesia (attenuate stress/myotonia) but continue opioid sparing, short-acting sedative-hypnotics reduced dose
continue active warming/avoid shivering
risks of anaesthesia most significant post-op, at minimum all DM pts should have @ least 24hrs continuous SpO2 & 5-lead eg monitoring until pre-op status
consider ICU for resp monitoring +/- support (particularly @ as risk post-op vent impairment). any CPAP or BiPAP the pt usually uses must be used periop
promote early mobility, incentive spirometry, chest physio, cough assist
Pregnancy: risk preterm labour, miscarriage, prolonged labour, PPH due to uterine atony- neuraxial anaglesia/anaesthesia preferred
What’s myotonia congenita? inheritance? incidence? presentation? anaesthetic considerations?
autosomal dominant disease linked to chromosome 17, dysfunctional chloride channel, muscle fibres hyperexcitable–> myotonic contractures
2 per 50,000
symptoms related to widespread muscle hypertrophy- severe state of muscle contraction results, significant stiffness initiating movement
characteristically no muscle weakness but can have palatopharyngeal dysfunction, difficulty swallowing, aspiration risk
may have cardiomyopathy
Anaes considerations:
Avoid DMRs (intractable myotonia)
avoid hyperthermia- pre, intra & postop
limit excess physical manipulation
If myotonia occurs, Na+ channel blockers may be useful, as may be topical LA administration
What’s hyperkalaemic periodic paralysis? inheritance? incidence? presentation? anaesthetic considerations?
Autosomal dominant, 1:100,000, locus on chromosome 17
Underlying abnormality= dysfunctional sodium channel, which following a hyperexcitable period becomes inactive–> weakness
Characterised by episodes of flaccid paralysis associated with increased serum potassium
Precipitated by cold, hunger & stress
Respiratory muscles are usually spared
Dysrhythmias may occur
Anaesthetic considerations:
Preoperative potassium depletion with loop diuretics
Minimise fasting, glucose-containing fluids should be infused during fasting
Avoid any drugs that cause potassium release from cells, including DMRs
Avoid potassium-containing fluids
Continuous ECG monitoring, Ca should be available for the emergency Rx of hyperK-induced weakness
Avoid hypothermia
Volatiles & NDMRs considered safe
What’s hypokalaemic periodic paralysis? inheritance? incidence? presentation? anaesthetic considerations?
Rare autosomal dominant condition
Results in defective Ca channels (usually related to mutations within DHP receptor gene)
Usually presents in 2nd decade of life- severe muscle weakness, asymmetrical muscle paralysis, low serum K+
No definite link between hypokalemic periodic paralysis & MH has been proven
Anaes considerations:
Avoid anxiety (may precipitate weakness)
Cardiac arrhythmias may occur
Definitely avoid sux.
Only use NDMRs with a short duration.
Volatiles may risk a hypermetabolic reaction.
Avoid drugs causing serum potassium shifts (incl salt & glucose loads), keep serum K+ within normal range
Maintain normothermia
Postop ventilation may be required if the pt has a perioperative attack
What are metabolic myopathies & anaesthetic considerations?
A heterogenous group of conditions resulting from an inborn error of metabolism (eg. related to glycogen, lipid, purine or mitochondria), resulting in skeletal muscle dysfunction (since ATP for muscle contraction relies on these factors), eg. acid maltose deficiency
Pts present with muscle cramps, myalgia, myoglobinuria, muscle weakness & atrophy
can involve cardiac & resp systems
Anaes considerations:
Aggressive periop metabolic monitoring required
Adequate hydration with forced diuresis to avoid myoglobinuria
Glucose & amino acid infusions to aid muscle metabolism
Prevent hypothermia to avoid shivering, increased muscle activity
What are mitochondrial myopathies & anaesthetic considerations?
hereditary condition, those related to the mitochondrial DNA are by maternal inheritance while those caused by mutations on nuclear DNA may be AD, AR & X-linked, some aren’t inherited
organs with high energy demands (eg, skeletal muscle) are particularly vulnerable
symptoms range from muscle weakness & exercise intolerance to heart failure, movement disorders, may be fatal
Anaesthetic considerations:
difficult to anaesthetise as most anaesthetic drugs have depressant effects on mitochondria- ketamine & low-dose volatile are recommended.
Avoid or give LA & propofol in reduced concentrations due to their depressant effects on mitochondria
risk post-op respiratory failure; impaired swallow risks aspiration
Access to a temporary pacemaker is required in theatre since total A-V block can occur
stringent glucose control essential
avoid stress (provide adequate analgesia)
avoid prolonged fasting
maintain euvolaemia
What is motor neurone disease? anaesthetic considerations?
acquired pre-junctional disorder that can affect upper (primary lateral sclerosis), lower (progressive spinal atrophy) or both (amyotrophic lateral sclerosis) motor neurones
loss of innervation to muscles–> muscle atrophy & development of extra-junctional ACh receptors
there’s no sensory loss & it never affects cranial nerves
signs include both the upper & lower motor neurone of limbs & bulbar muscles; fasciculations, weakness, atrophy
Considerations:
avoid DMRs
May use NDMRs in reduced doses due to increased sensitivity
Respiratory complications common; risk of post-op ventilation & subsequent weaning difficulties, infection, atelectasis
what distinguishes motor neurone disease from MS & other polyneuropathies?
there’s no sensory loss
it never affects cranial nerves
+What is multiple sclerosis? anaesthetic considerations?
most common demyelinating neuromuscular disorder, acquired, pre-junctional
clinically & pathologically heterogenous CNS disorder which is most commonly relapsing/remitting (90% of cases @ onset) which may become progressive, rarely primary progressive. Symptoms may include optic neuritis, weakness, numbness, ataxia.
characterised by plaques within brain & spinal cause
plaques cause inflammation, demyelination & denervation around axons–> clinical manifestations of weakness, spasticity, sensory dysfunction
Anaesthetic considerations:
multi D planning (esp liaison w neurology +/- HDU), risk stratification & discussion
counsel pts that S&S may worse postoperatively (stress, post-op fever or infection), risk relapse 1-6/12 post-partum with no overall net effect on disease course (pregnancy protective against relapse), however overall risk of relapse is not considered increased because of surgery or anaesthesia, however pts who have had an exacerbation & limited mobility may be more prone to complications, those with severe MS & resp involvement greater risk pulmonary complications- physio useful
CNS:
congitive dysfunction (eg. abnormalities in attention, short term memory, speed of information processing)
depression, fatigue
pain syndromes (eg. may be ass’d w trigeminal neuralgia, lhermitte sign, persistent neuroapthic pain)
seizures may complicate disease progression
Airway:
-aspiration risk (bulbar dysfunction)- consider prophylaxis, RSI
Breathing:
-respiratory insufficiency (combo central hypoventilation & NM weakness)
Circulation:
-if severe progressive disease w significant motor involvement, restrictive lung pathology & pulm HTN, risk RV failure
-ANS dysfunction with possible haemodynamic instability
Disability:
care with positioning particularly if contractures/muscle wasting in very severe disease
Drugs:
-Suxamethonium CONTRAINDICATED: life-threatening hyperkalaemia risk with muscle denervation, proliferation extrajunctional receptors
-generally sensitive to NDNMBDs; can use in normal doses but may consider dose reduction in pts with muscle weakness; overall unpredictable- use NMT to guide dosing
-consider risk post-op vent impairment; avoid paralysis where possible, ensure full NMB reversal, secretion management, multimodal opioid-sparing & titrate short-acting sedative-hypnotics
-multimodal anti-emesis (aspiration risk)
-May be immunosuppressed- steroids, consider stress dosing
interferon, methotrexate- consider immunosuppression
-may be on disease-modifying treaty (eg. natalizumab- monoclonal antibody, risk progressive multifocal leukencephalopathy by reactivation JC virus)
-ensure prophylactic ABx given within appropriate time pre-incision & meticulous asepsis
-Neuraxial is generally considered safe to perform without increasing risk disease progression. Historically, concerns that LA may exacerbate symptoms due to increased sensitivity of demyelinated axons to LA toxicity but prospective studies have shown no increase in rate of relapse after epidural (studies relatively small numbers, risk selection bias). Controversial so I would discuss with patient that evidence suggests safe but limited trials; I’d preference low-dose epidural vs spinal (as lower initial CSF [] LA) in abundance of caution but the limited available evidence doesn’t support this degree of caution. I’d also look @ MRI & see where plaques are.
Peripheral nerve blocks safe (they aren’t involved)
They may be on fluid restriction, antimuscarinic (oxybutynin) if detrusor overactivity
May have botox injection or sacral neuromodulation if refractory
alpha agonists (prazosin, tamsulosin) if detrusor sphincter dyssynergia.
May be on eg. duloxetine (SNRI) if concomitant pain & fatigue w antidepressant
may be on modafinil, dextroamphetamine/amphetamine for fatigue
may be on baclofen for spasticity or BZDs for nocturnal spasticity
Exposure:
-Normothermia important- increased temperature can aggravate symptoms/precipitate relapse as demyelinated axons are more sensitive to heat
Postop:
risk resp complications (bulbar dysfunciton & poor cough, resp m weakness)- some pts may have cough assist, NIV, use these perioperatively, consider postop if significant disease/comorbidities
What’s Eaton-Lambert syndrome?
rare acquired autoimmune disorder of NMJ
antibodies directed against pre-synaptic voltage-gated Ca++ channels
results in reduced ACh release from presynaptic nerve terminals
presents with pros limb weakness without significant atrophy
often associated with underlying malignancy, most commonly small cell lung Ca, associated with other autoimmune processes
treated with guanidine, aminopyridines & anticholinesterases (eg. pyridostigmine)
may receive immunologic therapy with IVIG, oral immunosuppressants or, less commonly, plasma exchange or rituximab.
Anaes considerations:
continue normal meds periop.
may require stress dose steroids
unlike MG, AUTONOMIC DYSFUNCTION IS COMMON (prone to hypotension with induction/vasodilatory agents), while bulbar & respiratory weakness less common
very sensitive to DMRs & NDMRs & they are MORE sensitive to NDMRs than pts with MG- avoid NDMRs unless sugammadex is available.
similar postop concerns to MG.
What are treatments for myasthenia gravis?
-symptomatic Rx with anti cholinesterase agents (eg. pyridostigmine, adverse effects incl N&V, miosis, rhinorrhoea, salivation)- MUST CONTINUE up until & including morning of surgery- can be sensitive to discontinuation of these meds (eg. m. weakness incl bulbar/resp)
-chronic immunomodulation (eg. glucocorticoids)
-rapid immunomodulating Rx (eg. plasmapheresis & IVIG)
-if refractory, may receive monoclonal Abs
what’s the conversion IV:oral pyridostigmine?
30:1
What are the recommendations for perioperative management for long-term immunotherapy (eg, azathioprine, cyclosporine) in pts with MG?
given their long duration of effect, likely can be held morning of surgery & short-term interruption unlikely to have significant symptomatic effect
should take pre-op labs (electrolytes, renal & hepatic function & CBP) for pts on these meds.
What’s a myaesthenic crisis? management?
resp +/- bulbar weakness severe enough to necessitate intubation or delay extubation after surgery.
signs may include increased resp rate/shallower TV (since retain normal respiratory drive), dysphagia, change in phonation, weak cough, obstruction, difficulty handling secretions.
may occur with surg stress or other precipitants (eg. infection, witholding/tapering MG meds, pregnancy, elecrolyte abnormalities, surgical stress, aminoglycosides)
must differentiate from cholinergic crisis (another cause of weakness in MG) as the Rx is very different- formal neurophysiological studies may be necessary to assess cholinergic excess or deficit, tensilon test.
if at end of surgery, keep intubated, send to ICU- Rx cocordinated with neurologist- rapid therapy with plasma exchange or IVIG often occurs along with immunomodulating therapy.
considerations for an obstetric pt with MG?
Pregnancy may –> deterioration (or may be stable/improve, variable), risks myaesthenic crisis
Generally exac in 1st trimester, improve in 2nd & 3rd, relapse postpartum
assess bulbar & resp function, function in general
Ax ability to tolerate a mid-thoracic regional block- pts with significant bulbar or respiratory compromise require GA for LSCS
Consider BiPAP if neuraxial or extubate nto it postop
neuraxial preferred for pts who can tolerate as limits need for systemic opioids- use amide LAs for pts taking anticholinesterases
pts with MG more likely to require instrumental deliveries (2nd state requires use of striated muscle), risks fatigue 2nd stage
Mg++ relatively CI due to muscle weakness
GA: judicious sedative/hypnotics (sensitive, fatigue), sensitive to NDMR but reisstant to DRM, motiror TOFR, risk stratification re: extubation (d/w ICU if Leventhal’s criteria re: postop intubation)
monitor for myaesthetnic/choninergic crisks
care w meds that may exac muscle weakness
cholinseterase inhibitors minimal placental t/f but uterotonic effects; incr risk preterm labour, maternal M&M
risk neonatal myaesthenia (transient) in 16%, maternal transfer IgG antibodies across placenta, self-limiting but maternal support
issues with anti cholinesterase medication for pts with MG or ELS?
may prolong action of sux
may delay onset of NDNMBDs
may make NDNMBD reversal with neostigmine unpredictable
issues with anti cholinesterase medication for pts with MG or ELS?
may prolong action of sux
may delay onset of NDNMBDs
may make NDNMBD reversal with neostigmine unpredictable
What are some of the risks of impaired physical function?
postoperative complications
delirium
SSI
What’s frailty?
decreased physiological reserve, increased vulnerability to poor health outcomes- significantly associated with post-op M&M, preop frailty Ax assists predicting postop outcomes
What are some modifiable risk factors for postop complications which can be optimised?
Smoking cessation- reduces risk resp complications, promotes wound healing. Cease @ least 4/52 pre-op
Fe deficiency with or without anaemia- may incr risk of blood transfusion (M&M), Rx Fe def if EBL >500mL
Churg-Strauss
AKA eosinophilic granulomatosis
Associated with ANCA
Rare- inflammation small-medium vessels
Asthma/eosinophilia & multi-organ vasculitis (skin, PNS, CNS, CVS (need cardiac assessment as risk eosinophilic endomocarditis, coronary dissection, coronary vasculitis), renal & GIT)
Considerations:
Reactive airways
chronic steroid use
cholinesterse deficiency, multi=organ dysfunction
Preference for regional.
Churg-Strauss
Rare- inflammation small-medium vessels
Asthma/eosinophilia & multi-organ vasculitis
Considerations:
Reactive airways
chronic steroid use
cholinesterse deficiency, multi=organ dysfunction
What’s ERAS?
A multimodal approach to improve pre-op status & perioperative homeostasis
Interventions encapsulate:
PREOP: counselling re: expectations, smoking & ETOH cessation, nutritional therapy, thromboprophylaxis, clear liquids up to 2h, solid food up to 6h, carb loading, ABx prophylaxis, antiemetics
INTRAOP: minimally invasive, multimodal analgesia, neuraxial/regional, optimising fluids, actively warm
POSTOP: epidural or TAP block, multimodal analgesia, early enteral nutrition, prevention of ileus (eg. TAP block or epidural), early mobilisation
What did the RELIEF trial (Myles 2018) show? implications?
Major abdo surgery although did exclude pts undergoing urgent or time-critical surgery, liver resection or ESKD requiring dialysis
A restrictive (5mL/kg on induction, 5mL/kg/hr intraop, 0.8mL/kg/hr for at least 24hrs postop but no protocol for fluids >24hr postop) vs liberal (10mL/kg on induction, 8mL/kg/hr intraop, 1.5mL/kg/hr for at least 24hrs) fluid regimen was not associated with higher disability-free survival @ 1yr postop but was ass’d with a higher rate of AKI.
Goldilocks likely appropriate.
:) SS_CS 1.4 discuss the preoperative assessment of filling status
And
My stance on fluid
-what’s fluid responsiveness?
increase in stroke volume of 10-15% when the pt receives 500mL crystalloid over 10-15mins. Can test with straight leg raise (equivalent of infusion of approx 300mL)
Monitoring of intravascular volume status:
STATIC PARAMETERS HAVE LIMITATIONS:
-CVP poor correlation with fluid responsiveness & inaccurate surrogate to determine cardiac preload
-BP & HR responses to IV vol status aren’t predictable (stress response & SNS activation may maintain brain & cardiac perfusion at expense of kidneys, GIT, GA & neuraxial may blunt compensatory vasoconstriction, B-blocked pts may not manifest tachycardia with hypovolaemia)
-UO may be reduced by volatiles or surg stress despite a euvolaemic pt. Intraop oliguria doesn’t predict AKI (but sustained oliguria, esp <0.3mL/kg/hr ass’d with renal injury)
-SvO2 & ScvO2 are proportional to CO, tissue perfusion & tissue O2 delivery BUT they are inversely proportional to tissue O2 consumption so they don’t reflect changes in tissue perfusion when the O2 consumption is variable.
DYNAMIC parameters are superior for assessment of volume responsiveness & guide goal-directed fluid therapy for pts undergoing major invasive surgery, esp with large EBL or fluid shifts (SVV, SPV, PPV or change in IVC diameter)
a) respiratory variations in arterial pressure waveform: normal is <10%. greater variations suggest likely need for fluid administration.
SPV: max SBP - min SBP, reported in mmHg
SVV= (SVmax-SVmin)/SVmean
PPV: [PPmax - PPmin]/PPmean (expressed as a %)
Usually measure these over 3+ breaths to account for variation in resp cycles.
limitations= if the pt is spont ventinng, if the pt has low TVs or high PEEP, if open chest, if the pt has RHF, an arrhythmia or is on a vasoactive infusion, limited sensitivity * specificity (less if spent vent)
Changes in MAP with valsalva may predict volume responsiveness
b) US techniques:
oesophageal doppler- blood flow in desc Tx aorta- to derive estimates of SV useful when indices based on resp variation can’t be used
echo- can quickly estimate LV size & IV volume status with TTE or TOE (trans-gastric mid-papillary short-axis view can easily show hyperdynamic systolic function qualitatively with hyperdynamic systolic function & decreased ED & ES LV cavity dimensions; can quantify with transgastric LV short axis view, taking internal diameter or LV cross-sectional area at end-diastole (arrow immed after p-wave on ecg) & compare with normal/normovolaemic state, TOE has smaller values than TEE). Measure the LV end-diastolic diameter if normal LV size & function, measure at the mitral chordal level. Can measure the LV end-diastolic area (exclude the papillary muscles from the tracing)).
POCUS to look at distensibility index of the IVC during mech vent- IVC size is small if hypovolaemic during forced insp effort (sniff)- utility of IVC size less under GA/PPV
c) noninvasive techniques (eg. pleth variability index, pulse contour analysis, thoracic electrical bioimpedance for CO & fluid responsiveness)- found in a 2017 meta-analysis to have too high % error.
d) lab: lactate or lactic acidosis- useful measure of global tissue perfusion but don’t provide info re contemporaneous clinical IV volume status as measured intermittently, don’t immediately reflect acute changes.
Overall in my practice: use a composite of resp variations in arterial pressure waveform where applicable, urine output, SvO2 & lactate, TOE where possible
Composition of intra-op fluid:
-routinely I choose a balanced electrolyte crystalloid solution for maintenance of intra-op normovolaemia.
-Albumin may be preferred for boluses as minimises the total quantity of fluid and has a long plasma half-life (9hrs!) however evidence for haemodynamic benefit of colloid over crystalloid is scant.
Albumin also costly, anaphylaxis & blood product considerations although pasteurised so doesn’t transmit known infectious diseases.
Avoid glucose-containing solutions unless indicated.
Avoid large vols NS (risk hyperchloraemic acidosis).
Avoid HES- risk kidney failure or RRT, death, bleeding & transufsion (impair plt, reduce VIII & vWF)- less risk renal injury or transfusion with the low molar substitution HES products.
Avoid gelatins- short DOA (2-3hrs), high risk of anaphylaxis, may impact coagulation. Used in some countries as cheap & vol effect of 70-80%.
volume of intra-op fluid:
Goal-directed superior to liberal or fixed-volume approaches HOWEVER GDT doesn’t appear to offer advantages over restrictive approach for pts managed under ERAS, likely because ERAS protocols implement multiple processes reducing risk of periop fluid imbalances
EUVOLAEMIA for adequate tissue perfusion
Must recognise & manage hypovolaemia which may compromise organ perfusion BUT avoid excessive perioperative fluid which risks tissue & organ oedema
Preop bolus considered if hypovolaemic, eg. 8mL/kg on induction (btwn liberal & restrictive), HOWEVER UTD recommends against high-vol preloading prior to neuraxial block or GA induction.
-Intra-op for invasive major surgery with EBL >500mL +/- fluid shifts, employ a goal-directed approach to fluids with invasive dynamic haemodynamic monitoring to a pre-specified goal (eg. the SV value that has resulted after fluid admin with <10% change in SV= the goal, <10% PPV is a goal), ensuring IV status is optimal before adding a vasopressor.
*goal-directed haemodynamic therapy may decr mortality, hospital LoS & infectious postop complications + anastamotic leakage
-Intra-op for major invasive surgery with EBL <500mL, esp if no invasive monitoring, implement zero-balance strategy (unless evidence of hypovol which Rx with slightly > zero fluid balance)- approx 3mL/kg/hr (to replace sensible & insensible losses & support metabolic rate) with boluses of approx 250mL in volume-responsive pts to optimise IV volume (ideally monitoring to do this to PPV <10%, then stop IVT admin to avoid hypervol), replace lost blood with crystalloid on 1.5:1 volume basis OR colloid on a 1:1 basis until a blood transfusion threshold is met.
Don’t replace “3rd space” losses as this may cause morbidity.
Avoid extremely deep anaesthesia which may result in hypotension unnecessarily treated with additional fluids or vasopressors.
-Intra-op for minor/moderately invasive surgery, 1-2L balanced electrolyte crystalloid over 30mins-2hrs, aiming to correct mild dehydration with fasting & risk PONV. Lower end of range if CHF or COPD.
severe vol depletion in adults 1-2L isotonic fluids rapidly to restore tissue perfusion, aiming to improve clinical signs hypovolaemia (BP, UO, mental status). mild-mod hypovol, admin >rate than continued fluid loss (UO + insensible which is 30-50ml/hr) + other GI losses.
What’s the 5-pronged attack to terminate stimulus for bronchoconstriction/secretions?
-terminate stimulus for bronchoconstriction/secretions (stop smoking)
-dilate airways (B agonists, muscarinic antagonists, high-dose steroids eg. 25mg daily, 4/52 to see if can improve baseline spirometry)
-lessen/loosen secretions (hydration, smoking cessation, ABx)
-remove secretions (postural drainage, chest PT, coughing)
-increase pt participation (educate, motivate, cough, IS, exercise, WL)
What’s the difference btwn operability and resectability?
Operability= ability for surgeon to perform the procedure- resect the lesion with clear margins/nodes etc
Resectability= prediction of the ability of the pt to survive long-term with the reduced resp capacity expected after the resection of lung (ie. 6-12 month survival irrespective of Ca prognosis). This isn’t impacted by surgical technique (thoracoscopic vs open) as considering longer-term, but periop nadir worse if poor analgesia & likely less pain with videoscopic.
-Consider postop predicted FEV1 & DLCO (considering that in the past there was more likelihood that a lobectomy would progress to pneumonectomy; now surgeons better at selective lung reduction, adjunctive options have improved)
Does pre-op bronchoscopy generally occur prior to lobectomy/pneumonectomy these days?
not generally, given the quality of CT/PET etc
considerations for NF1?
Neurofibromatoses= autosomal dominant- affect ectodermal & mesodermal tissue. NF1= most common.
multiple cafe au last spots (their presence suggests NF1 but familial cafe-au-lait spots can rarely occur. Neurofibromas, lisch nodules, sphenoid bone dysplasia, freckling of intertriginous area of axilla or groin, are characteristics. 30% have plexiform neurofibromas- affect long portions of nerve involved & may infiltrate nerve, surrounding tissue (disfigure) & may undergo malignant change (malignant peripheral nerve sheath tumours). LIsch nodules (benign hamartomas of iris) in 95%, dysplasia of sphenoid wing common. Phaeochromocytoma more common in NF1, as are intestinal tumours which may be carcinoid (esp duodenum ampulla of vater). Associated with juvenile CML.
CNS:
Cerebral & spinal neurofibromas are common. Learning disabilities in 50%, lower IQ only slightly more frequent than in general population. Epilepsy, headaches & hydrocephalus more common. Deafness common (NF2= a distinct entity, associated with bilateral acoustic neuromas (vestibular schwannomas) but the incidence of vestibular schwannomas is not more common in NF1 cf general population. NF2 autosomal dominant but 50% sporadic (as with NF1). Bilat vestibular schwannoma or unilateral or 2 of meningioma, glioma, schwannoma, cortical cataracts).
vertebral deformities or spinal cord tumours may make spinal/extradural techniques difficult.
AIRWAY: Neurofibromas may occur in tongue, oropharynx & larynx (often aryepiglottic fold or arytenoids), macroglossia/macrocephaly/mandibular abnormalities or C-spine involvement may impact airway Mx- may impact laryngoscopy & tracheal intubation- suspect with Hx dysphagia, dysarthria, stridor or change of voice (CT/MRI imaging warranted if suspicion). May have relative macrocephaly & overall shorter stature.
RESP: may have pulmonary fibrosis, if intrapulm neurofibromas usually good prognosis but should be excised (risk malignancy), intrapulmonary neurofibroma & cystic lung disease. scoliosis/kyphosis may compromise lung function. Pectus excavated or carinatum in up to 30% (should have CXR, consider CT thorax, PFTs). Mediastinal neurofibromas may compress trachea/bronchi.
CV: may have RV failure (ass’d w lung disease). may have HTN, usually essential HTN but consider be ass’n with aortic coarctation, phaeochromyocytoma or RAS. May have hypertrophic cardiomyopathy (idiopathic- no clear evidence of link with congenital heart defects). may develop mediastinal tumors & SVC obstruction.
GIT/GUT: neurofibromas may affect the GIT (may obstruct ureter/urethra, intestines) carcinoid tumours may be found in the duodenum (–> jaundice or carcinoid syndrome)
how frequent is pulmonary aspiration of gastric contents with GA? in-hospital mortality rate?
1 in every 2000-3000 elective GAs (1 in 900 pts undergoing surgery), 20% incidence of in-hospital mortality
what probe & how perform gastric US?
low-frequency (1-5MHz) curved array transducer set with “abdominal settings”, higher freq 5-12MHz for low BW or paeds <40kg
pt supine or R) LD (the latter more sensitive for smaller volumes, in supine the fundus is dependent & gastric contents may gravitate there), probe sagittal plane in the epigastrium, perpendicular to skin, with cephalad to the L) of the screen
to quantify the antral CSA, pt in RLD, freeze image btwn peristaltic contractions (when the antrum is it’s largest), use trace caliber function & trace entire circumference to determine the astral CSA (follow the serosa), calculate the mean of 3 readings. calculate as:
gastric volume (mL) = 27 + (14.6 x RLDCSA) - (1.28 x age (yrs))
what gastric volume is consistent with fasting vs “full stomach”?
<1.5mL/kg clear fluid= fasted. >=1.5mL/kg of clear fluid or solids= “full stomach”
Characteristics of empty antrum on gastric US? how about if clear fluid in stomach? solids in stomach appearance?
“bulls eye” appearance, thick hypo echoic muscularis propriae layer- can only interpret the image as being “empty stomach” when observed in R) LD for a continuous period of time & when ass’d with a Hx of low risk for pulmonary aspiration
antrum distends, becomes thinner walled, invariably swallowing is associated with air consumption so may see “starry night” appearance with hyper-echoic dots. a grade 1 antrum has fluid visible in RLD position only- low aspiration risk. if grade 2 antrum, with fluid in both supine & R) LD, high pulmonary aspiration risk. CSA <1.5mL/kg is consistent with baseline secretions. >1.5mL/kg consistent with >baseline secretions. thick flu9ids are more echoic & homogenous in nature.
distended antrum- “frosted glass” if recently ingested (due to air), later stages hyper echoic, heterogenous consistency
When is point-of-care gastric US useful? how should it be viewed?
uncertain prandial status or suspected delayed gastric emptying
Backed up by a Hx & physical exam, considered an adjunctive tool for planning anaesthetic approach, with a high (1.0) sensitivity, 0.975 specificity, PPV (0.976) & NPV 1.0 if clinical equipoise
when deciding ULN for normal gastric secretion (1.5mL/kg), what BW metric is used?
ACTUAL body weight
Anaesthetic considerations with allergic bronchopulmonary aspergillosis
complex hypersensitivity reaction in response to colonisation airways with aspergillus fumigatus, almost exclusively in pts with asthma or CF
S&S= asthma & recurrent exacerbations
if severe, may get mucus plugs, haemoptysis
may have wheeze or may have asymptomatic pulmonary consolidation
may have concomitant rhino sinusitis with nasal congestion/obstruction
Lab= eosinophilia, elevated total serum IgE, specific IgE to aspergillus, specific IgG antibodies or precipitins to aspergillum
Imaging= bronchiectasis of the central 1/2 to 2/3 of the chest (findings incl “tram-line”, “parallel lines”, “ring shadows”, “toothpaste shadows”, “gloved finger shadows”, “ring shadows”, “toothpaste shadows”, “gloved finger shadows” due to abnormalities the bronchi, evidence of mucus plugging (atelectasis), parenchymal opacities (usually upper lobes)
HRCT shows predominance of central and upper/middle lobe bronchiectasis, nodules, mucus plugs, tree-in-bud, atelectasis, consolidation.
PFTs GENERALLY SHOW REDUCED FEV1 & INCREASED RV, >50% don’t have a positive bronchodilator response
may have a mixed obstructive & restrictive pattern
very few have reduced DLCO (generally that happens with bronchiectasis)
risk recurrent bacterial infections, haemoptysis, chronic resp insufficiency
What’s Ehlers-Danlos syndrome?
rare genetic connective tissue disorder characterised by:
-skin & joint hypermobility
-tissue fragility
“classical EDS”= autosomal dominant mutations within collagen genes. main feature= large & small joint hyper mobility. Fatigue, hernias, cervical insufficiency, uterine prolapse. vascular & valvular heart complications are uncommon. aortic root dilatation in 6%. MV prolapse in 6%. carotid artery tortuosity. Pulmonary complications incl spont PTx.
“hypermobile EDS”= autosomal dominant, large & small-joint & spine hyper mobility, frequent joint dislocations, chronic joint pain. May develop scoliosis & OA.
May have DELAYED GASTRIC EMPTYING & IBS, ANS dysfunction including POTS, syncope, sleep disturbance (incl apnoea), LL swelling/varicosities. May be an association with atlantoaxial hyper mobility & chair I malformation. may have headaches. May have resistance to LA & opioids. 12% may have mild aortic dilatation, 6% MV prolapse.
Main issues:
chronic pain
airway:
potentially difficult (fragile vessels/skin)
potentially jaw & (?atlantoaxial) instability or premature spondylosis
delayed gastric emptying w ANS dysfunction
sleep apnoea
more risk spont CSF leaks
potential scoliosis/joint deformities (ventilation, positioning, pressure areas)
PTx risk, ?risk spontaneous organ rupture
ANS dysfunction- POTs (*pre-op crystalloids +/- vasopressors)
poor wound healing/easy bruising
fragile vessels/skin care ++ w IVC & tourniquet (**discuss with surgeons tourniquet may be catastrophic in pts w vascular fragility- massive compartment bleeding & haemorrhagic shock), care with eyes (may have brittle cornea syndromes)
volatiles, propofol, N2O (care if spont PTx), depolarising (unless immobile) & NDMRs all safe.
avoid art line & CVC wherever possible, at risk ++ of vascular rupture. If must do CVC, jugular pref to subclavian (PTx, bleeding risks if vascular EDS).
neuraxial on case-by-case basis (*pt may have tarlov cysts (CSF-filled perineurial cysts) which are a sign of meningeal involvement & of specific EDS subtypes. Risk vascular/tissue fragility complications vs benefits of neuraxial), may be more complicated if spinal pathology.
If considering neuraxial, should have pre-interventional MRI to Ax spine pathology.
EMLA may be ineffective due to tissue scarring.
peripheral nerve blocks should be avoided in vascular subtypes, nor should neuraxial.
PONV prophylaxis (risk yes rupture w vomiting)
Anaesthetic considerations for posterior spinal instrumentation for adolescent idiopathic scoliosis?
PATIENT:
-scoliosis >30 degrees 5x more common in female adolescents vs males
-may have pre-existing pain & opioid tolerance from their condition
PATHOLOGY:
-confirmed on radiograph if coronal spinal curvature exceeds Cobb angle of 10 degrees.
-severe scoliosis accompanied by psychosocial distress, back pain & cardiorespiratory dysfunction
-AIS >45 degrees requires surgical management as likely impair cardio resp function, produce increasing back pain & may be ass’d w shift of vertebrae
PROCEDURE: most commonly posterior spinal instrumentation with arthrdesis (posterior spinal fusion) under intraoperative skull femoral traction.
POTENTIAL COMPLICATIONS:
Prone case so risk ocular damage which may include temporary/permanent blindness
neurological injury
complicated postop pain management
PRE-OP:
Consult: See paediatric anaesthetist at least 2/52 pre-op
Optimise:
Planning:
Explain/consent:
Patient likely to= be a minor- consent can be provided by parent if they are acting in best interests of child however the child can provide their own consent if assessed as having capacity (understanding, maturity, intelligence) to comprehend the procedure (and consequences of not having the procedure) and risks/benefits/alternatives of anaesthesia. Irrespective of who is giving consent, I would discuss the expected course of events including postoperative pain management plan and material risks of anaesthesia with the child. Given this is major surgery with significant risks, it is good practice to encourage the child to have their parent involved in the consent discussion and to have their involvement in early recovery. If the child does not wish for the parent to be involved, the child is deemed to have capacity and I believe the procedure is in the child’s best interests, for a major procedure such as this with significant risks associated with significant postoperative pain, I would make sure the child is seen in clinic well in advance of the procedure and that a second anaesthetist also assesses and documents their assessment of the child’s capacity to provide their own informed consent.
consent to include discussion of risks/benefits/alternatives of blood products
Disposition:
Surgery planned at a tertiary centre in-hours with postop HDU availability if required, skilled surgeon and neuro-monitoring personnel
Intra-op:
Main issues:
Mod-severe pain & risk chronic post surgical pain with neuropathic component: Apply preventive analgesia & a comprehensive intra- & post-op multimodal analgesia strategy:
-Pre-op gabapentin 600mg (dose ranges 5-15mg/kg reported!) (AND multi-day, reduces postop morphine consumption APSE- not single dose which doesn’t modify pain scores or opioid use & increases sedation) & paracetamol, intrathecal morphine (ITM (5microg/kg analgesia lasts 16hrs- larger doses than adults, >=9microg/kg ass’d w resp complications!) + PCA shown in retrospective study to provide superior analgesia cf PCA alone or PCEA OR, according to APSE, epidural LA infusion & PCA morphine (some would use background infusion 1-2 days postop) better than PCA alone wrt pain scores & pt satisfaction & less PONV & doses 0.125% bupivacaine or 0.2% ropivacaine don’t interfere with neurophysiological assessments, epidural better pain scores cf systemic), ketamine 0.5mg/kg soon after induction (consider ketamine infusion 2-3microg/kg/min during & if uncontrolled pain consider continuing for 48hrs postop. APSE: adding IV Mg+ (50mg/kg bolus & 8mg/kg/hr infusion) to ketamine reduces postop morphine consumption), remifentanil infusion 0.28microg/kg/min (may be ass’d with slightly higher postop morphine requirement than just intra-op IV morphine (?limited as a surrogate of OIH) BUT this is negated if use pre-incisional ITM. Also, remi may be useful for propofol sparing which limits interference with neurophysiological monitoring & minimises haemodynamic consequences of anaesthesia), IV parecoxib intra-op, postop morphine PCA (encourage rapid transition to PO opioids), regular paracetamol & NSAID >16hrs after parecoxib (or could use intra- and postop ketorolac 0.3mg/kg IV to max 30mg 8-hrly for up to 73hrs (transition to PO ibuprofen by D2).
Aggressive PONV prophylaxis & management (may exacerbate pain/impair recovery)
-dexamethasone 0.15mg/kg up to total 8mg, ondansetron 0.1mg/kg up to 8mg during surgery, aprepitant (neurokinin 1 receptor antagonist with 9-13hr half-life, can give 40mg PO 30mins before surgery, 40 & 80mg provide similar antiemetic effects to ondansetron).
Apply anaesthesia techniques that don’t interfere with neurophysiological monitoring
Antibiotic prophylaxis & prevent surgical site infection- relatively common 6% with this surgery- cefazolin 40mg/kg (max 2g) 10-60mins prior to skin incision, repeat 4hrly until skin closure.
Temp 36-38deg from incision until skin closure (reduce SSIs)- PRE-WARM with FAWB, warm the OT prior to pt arrival & actively warm intra-op (warm IVT, FAWB), cognisant of risks of pt exposure & hypothermia with long time from induction to start of surgery- multiple position changes & application of monitoring in prep for procedure
Blood conservation management- EBL 275-907mL. Discuss with surgeons re: TxA
(20-30mg/kg loading then 10mg/kg/hr infusion).
Prevention of neurological injury, ocular/visual injury & pressure areas (prone, prolonged procedure); prone positioning ass’d with posterior ischaemic optic neuropathy, stroke secondary to arterial occlusion in neck, injury from inhibiting venous drainage, peripheral neuropathies).
Monitoring:
SpO2, 3-lead ecg (unless specific CV concerns), NIBP 15-minutely (will have art line due to pt position/access & case duration), EtCO2
Temp probe IDC
2x large IVC & art line (aseptic technique)
BIS
NMT (for initial depth for intubation and ensure TOFR >0.9 prior to extubation, neurophysiologist will monitor SSEPs & MEPs intra-operatively)
Induction:
standard IV induction with small dose of muscle relaxant (eg. roc 0.4mg/kg) for successful intubation (ensure worn off prior to neuromonitoring +/- use of reversal)
reinforced tube useful when in prone head-ring & limited access to patient.
Maintenance: TIVA as less interference with neuromonitorinng, remi infusion propofol sparing
nitrous > volatiles depress amplitude & incr latency of SSEPs & MEPs. ketamine may enhance amplitude of SSEPs & MEPs.
Goal-directed fluid therapy, watching SVV (aim <13%) and monitoring urine output >0.5mL/kg/hr.
Postop:
multimodal analgesia as above (plan for early discontinuation of IV opioid & removal of IDC to promote early mobilisation which reduces ileum & hospital LoS)
keep warm in PACU
aggressive anti-emetic to encourage early mobility and participation in physio
+What are the usual signs & symptoms & investigation findings of hypertrophic cardiomyopathy?
Perioperative considerations?
Many patients with HCM are asymptomatic or have minor symptoms and are diagnosed through family screening, murmur detection or an abnormality on ecg.
Signs & symptoms are variable & not strongly correlated with presence or magnitude of LVOTO or extent of LV hypertrophy.
Symptoms typically are due to:
LVOTO (presyncope & syncope, particularly during or immediately following exertion)
heart failure (dyspnoea, fatigue)
ischaemia (chest pain)- both from increased myocardial O2 demand +/- reduced coronary flow (impaired vasodilation, diastolic & systolic compression of coronaries)
arrhythmia (palpitations, pre-syncope/syncope)
HEART FAILURE, manifesting as dyspnoea on exertion, is the MOST COMMON presentation in HCM (in >90% of symptomatic patients), either due to:
-diastolic dysfunction (myocardial hypertrophy)
-LVOTO, increasing LVEDP & impairing LV emptying
-MR
-systolic dysfunction if extensive myocardial involvement
(PND/orthopnoea are uncommon)
Occasionally pts may develop acute haemodynamic collapse precipitated by events acutely increasing outflow obstruction, incl:
-decreased preload
-decreased afterload
-supraventricular tachyarrhythmia
-acute MR
-demonstrated by echo with hyper dynamic undefiled LV, SAM of the MV (with SAM-septal contact) and MR
Physical exam may be normal or may have:
-S4
-systolic murmur (mostly related to LVOTO (harsh crescendo-decrescendo systolic murmur at apex/LSE, radiating to axilla, louder if upright from squatting or valsalva, softer if hand squeeze or going from standing to sitting or with passive leg raise (attenuation of obstruction)). MR (holosystolic murmur loudest @ apex, radiates to axilla)
-LV lift if significant MR or pulm HTN
-systolic thrill
-may have bifid arterial or carotid pulse, prominent a-wave
Most patients have normal lifespan however they are at risk of sudden death (usually in the absence of symptoms)
ECG is generally abnormal- the most sensitive test for HCM but findings nonspecific.
LV “strain” pattern often seen: high voltages and horizontal or downscoping ST and TWI in I, aVL, V4-6 (anterolateral). May see prominent abnormal Q waves esp in inf and lateral leads. P wave abnormalities (LA or biatrial enlargement). LAD. deeply inverted T waves precordial.
Pts with HCM should have 48hr holter to Ax for ventricular arrhythmias & risk SCD.
Echo to look at cardiac morphology, systolic (often hyper dynamic) & diastolic function & presence/severity of any LVOT gradient and MR. also look for atrial dilatation (ass’d with higher risk of AF & consideration anticoagulation prophylaxis if AF occurs).
Clinical Dx of HCM is confirmed with unexplained incr LV wall thickness >=15mm anywhere in the LV wall (the hypertrophy may be concentric, asymmetrical, mid-ventricular, apical)
Assess the presence & extent of LVH in parasternal short-axis plane, level of MV.
Assess for LVOTO with continuous-wave doppler, apical long-axis imaging window.
Provoking gradients is important for management decisions- can do exercise stress echo using symptom-limited bruce protocol (preferred, treadmill or bike, most mimics reality), or could do pharmacologic and valsalva (but non physiologic). LVOT PG >=50mmHg at rest or exercise= indication for myomectomy & ETOH septal ablation. Pts are at risk of developing angina, ST changes, AF, hypotension or large gradients & risk serious arrhythmia however incidence of sustained VT/VF during exercise testing is very low.
Pts with > mild LVOTO or septal thickness >15mm should have a B blocker: metoprolol (esp in pregnancy) bisoprolol
Those w AF should be considered for anticoagulation
Pre-op:
C: Hx/examination/Ix, with quantification of exercise tolerance (DASI, NYHA), signs HF, cognisant that symptoms/signs don’t always correlate with severity
Management to date (eg. AICD, B blocker)
Recent echo vital (eg. diastolic function, mitral valve function, wall thickness, chamber size), any signs of LVOTO (rest or provocation)), EST may be useful to see if haemodynamically significant LVOT gradient.
O: multi-D, consideration of therapy eg. B blocker, AICD, antiarrhythmics, pre-op fluid status optimisation (limit fasting, consider IVT)
Plan: in-hours, tertiary centre w cardiology, postop HDU, TOE capability
E: high periop risk, d/w pt
D: postop HDU likely
Intra-op:
Monitoring: art line +/- CVC, 5-lead, BIS to titrate depth anaes, standard
Assistant: skilled, consider notify cards anaes in case TOE
Drugs: rapid-acting opioid, B-blocker, vasopressors, fluids, consider regional block for opioid-sparing anaglesia but neuraxial unlikely to be appropriate
Equipment:
Pre-O2 & ensure euvolaemia/slight hypervol
I: GA generally safer unless overwhelming other risk factor; neuraxial risks preload/afterload drop. GA gentle, titrated aiming to defend preload, afterload (SVR) & limit excess contractility (care w inotropes which may worsen LVOTO & MR, risk pulm oedema & CV collapse), avoiding tachycardia (slowly titrated proprofol or volatile with vasopressor & fluid running, adequate dose NMBD, rapid acting opioid & IV lignocaine to blunt SNS response to laryngoscopy) or arrhythmias
M: ongoing vigilance to haemodynamic goals, titrate opioids +/- esmolol to points of SNS stimulation (eg. incision, pneumoperitoneum)
E: limit SNS stimulation (analgesia, limit cough)
Post:
Recovery: ongoing art line monitoring defending haemodynamic goals
Analgesia & anti-emetics: effective, multimodal (incl regional) to limit SNS stimulation & myocardial O2 demand
Warming: continue for pt comfort, limit SNS stimulation & MRO2
Disposition: likely HDU for haemodynamic monitoring & optimisation
follow-up: consider trops/monitoring for postop complications- may require periop/cards input on ward
how does the cresc-decresc murmur of aortic stenosis differ from hypertrophic cardiomyopathy?
doesn’t change or slightly decreases with valsalva (worse in HCM as outflow obstruction may worsen) & it radiates to neck (HCM radiates to axilla)
What peak VO2 adds weight in determining candidacy for transplant?
<14mL/kg/min VO2 (or <=50% per for age)
:) when should temperature monitoring be used?
must be AVAILABLE for every pt undergoing GA. should be used whenever warming devices are used. use for GA lasting >30mins, major surgery with neuraxial (ie. where thermoregulatory control isn’t well-maintained) or when clinically significant changes in temp are suspected.
What is systemic sclerosis (scleroderma)?
in which gender is it more common?
10-year survival from diagnosis?
main causes of death?
what are the particular considerations for pre-anaesthetic review, multi system effects & anaesthetic considerations?
systemic, immune-mediated disease characterised by abnormal cutaneous & organ-based fibrosis
female
66%
pulmonary artery hypertension, interstitial lung disease, myocardial disease
Pre-op evaluation:
Quantify extent & severity of scleroderma manifestations; Disease is limited cutaneous (less severe, confined to skin thickening of extensor surfaces, many have manifestations of CREST syndrome: calcinosis, raynaud phenomenon, oesophageal dysmotility, sclerodactyly, telangiectasia) or diffuse (more severe, internal organ involvement)
determine management, pts may be on:
disease-modifying agents such as:
cyclophosphamide (ILD)- immunosuppression, drug-related cardiomyopathy
mycophenolic acid (ILD)- immunosuppression
azathiaprine (ILD)- may antagonise atracurium, vecuronium, pancuronium
epoprostenol (PAH) may incr risk blood loss for LVAD placement
endothelial receptor antagonists (PAH) may impair vasoconstriction during haemorrhage, negative lusiotropy
glucocorticoids may precipitate scleroderma renal crisis
methotrexate: may be ass’d with thrombocytopenia, interstitial pneumonitis, pneumonia but possible protective effect for MACE
chelating agents (for calcinosis): nephropathy
bislphosphonates (for calcinosis) may incr risk AF
rituximab (for skin fibrosis)- infusion reactions, leukoencephalopathy
Functional capacity
- DASI
-6MWT
- UCSD SOBQ responsiveness to negative changes in patients with ILD & PAH
challenges: rare, multi-system, limited evidence-based guidance for periop care
Neurological:
CNS:
-headaches, epilepsy
PNS:
-neuropathy from nerve entrapment (trigeminal neuropathy, carpal tunnel syndrome)- meticulous positioning/pressure areas
ANS:
-postural hypotension, decreased compensatory HR variation with valsalva)- care with induction (carefully titrated vasopressors, euvolaemia)
psychiatric:
-depression, anxiety
May have chronic pain?
consider neuraxial/regional (may be technically difficult), bearing in mind there may be ANS instability with neuraxial anaesthesia. May have more prolonged block w regional (vascular insufficiency slows clearance)
neurovascular:
-raynaud’s phenomenon
vascular:
-small-vessel vasculopathy, telangiectasis
haematological:
-anaemia (marrow aplasia or malnutrition- pre-op CBC & implement PBM strategies)
-incr risk unprovoked VTE (underlying pro-thrombotic inflammatory state (also higher rate antiphospholipid antibodies), particular risk factors are Dx <12/12, AF, CCF), implement VTE prophylaxis strategies
Resp:
challenging airway management (microstomia, TMJ fibrosis, limited Cx extension (fibrotic changes)): careful airway assessment & difficult airway preparedness- consider fiberoptic bronchoscopy- weigh up aspiration risks with airway risks
incr risk sleep disordered breathing: STOP-BANG, sleep studies: limit sedative-hypnotics, post-op SpO2 monitoring
resp examination and assess for signs of pulmonary HTN (eg. RV failure), CXR considered for pts with dyspnoea on exertion, HRCT may show SSc-related ILD changes; non-specific interstitial pneumonitis. PFTs useful wrt guidance for prep optimisation.
high rates of ILD, pulmonary artery HTN thought related to vasculopathy of small pulmonary arteries
-Pulm HTN main symptom= exertion dyspnoea. initial Rx usually sildefanil to improve exercise tolerance & anticoagulation with warfarin. Avoid incr PVR & give R) heart anaesthetic with art line +/- CVC
-ILD main symptom= reduced functional capacity before radiological evidence. Reduced FVC with normal FEV & FEV1/FVC ratio. DLCO may be reduced. CRP >=5mg/L, ESR >=20mm/r suggestive worsening ILD or PAH. Employ LPV strategies, ideally limit mechanical ventilation given that invasive ventilation may contribute to SSc-related morbidity. USE REGIONAL TECHNIQUES where possible (may be technically challenging). may have incr O2 requirement >24hrs after surgery. low threshold for workup if signs post-op exac ILD or pneumonia (these adverse events high-mortality).
CVS:
-pathological ECM deposition–> progressive CCF, diastolic dysfunction, arrhythmias, 3-fold incr risk of MI. Ask re: cardiac symptoms/Hx/Mx, cardiac exam, pre-op ECG, consider echo prior to mod-high risk surgery. Consider art line, possible CVC +/- TOE (** but risk oesophageal strictures & perforation) depending on surgical & pt risk, pre- & post-op trop. careful intra-op haemodynamic monitoring & management (eg. may require pulmonary vasodilators).
-care re: ANS instability.
GUT:
incr risk oesophageal dysmotility, LOS hypotonia, GORD & dysphagia–> aspiration risk (employ aspiration chemoprophylaxis, consider NGT suction, careful consideration of RSI bearing in mind risk of difficult airway (balance)). May risk pseudo-obstruction, volvulus, intestinal telangiectasia.
malnutrition & sarcopenia (pressure areas, frailty)
Renal involvement- may develop scleroderma renal crisis (ACEIs have improved traditionally poor outcomes)- malignant HTN, encephalopathy, CCF= characteristic presentation of SRC.
Msk:
Proximal limb involvement in diffuse disease
sarcopenia
care w positioning, pressure areas padded/perioperative nutritional support
US as anticipate difficult IV access
Obstetrics: consider high-risk, multi-D planning, neuraxial safe & should be encouraged but may be technically difficult.
SS_NS 1.12: Describe the mechanism and management of disorders of sodium control detected after neurosurgery
What is central diabetes insipidus?
What causes it?
How does it manifest?
Diagnostic criteria?
Management?
Differential diagnoses?
-decreased secretion of ADH
-can result from CNS trauma or tumour, CNS surgery (esp to pituitary or hypothalamus); 10-20% of pts get DI following transsphenoidal removal of an adenoma (incr to 60-80% with large tumours).
It’s due to a defect in one or more sites involving hypothalamic osmoreceptors, supraoptic or paraventricular nuclei or the superior portion of the supraopticohypophyseal tract (above median eminence).
Can be familial/congenital.
-manifests as polyuria, nocturia, signs of dehydration & polydipsia (due to increased serum sodium & osmolality) by diminishing ability to concentrate urine. Usually appears 4-24hrs after surgery (not intraoperatively), moderate to severe hypernatremia can develop when pts (eg. Perioperatively) can’t access free water.
-Dx with high serum sodium (>145mmol/L), high serum osmolality (>290mosmol/kg), incr urine volume (>2mL/kg/hr), low urine osmolality (<200mOsm/kg) or specific gravity, may have low urine sodium depending on access to free water
-manage to correct any free water deficit if hypernatremia (5% dextrose in water, 1.35mL/hr x body wt along with isotonic fluids to correct any volume deficit if chronic (aim correct Na+ by 10mmol/L/24hrs), 3-6mL/kg/hr (max 666mL/hr) if acute, monitoring serum sodium & glucose every 1-3hrs.
If not hypernatremic, manage with 5% dextrose & normal saline maintenance rate + 2/3 previous hour’s UO, monitoring for hyperglycaemia.
Add desmopressin if fluid requirement exceeds 400mL/hr.
Desmopressin has potent antidiuretic but no vasopressor activity.
Desmopression typically initiated at night to limit nocturia & promote adequate sleep.
Care re: hyponatremia- desmopressin dosing is generally given at the minimum dose required to control polyuria, eg. 0.1 or 0.2mg tab or 5-10microg nasal spray (only 5% absorbed from gut) @ bedtime. equivalent IV 0.5-1microg. Desmporessin should be continued for as long as the pt has symptomatic central DI; it may be corrected or worsened following the surgery & removal of their lesion.
also have low-solute (low sodium, low protein) diet, to limit renal solute load, along with consideration of a thiazide diuretic (inhibits Na/Cl channel on DCT, inhibiting reabsorption of Na & water but thought to help by promoting hypovolaemia-induced proximal sodium & water reabsorption)
-differentials= excess intra-op fluid, psychogenic polydipsia, osmotic diuresis, cerebral salt wasting or SIADH (both low serum sodium)
What is central diabetes insipidus?
What causes it?
How does it manifest?
Diagnostic criteria?
Management?
cautions with desmopressin?
Differential diagnoses?
-decreased secretion of ADH
-can result from CNS trauma or tumour, CNS surgery (esp to pituitary or hypothalamus); 10-20% of pts get DI following transsphenoidal removal of an adenoma (incr to 60-80% with large tumours). It’s due to a defect in one or more sites involving hypothalamic osmoreceptors, supraoptic or paraventricular nuclei or the superior portion of the supraopticohypophyseal tract (above median eminence). Can be familial/congenital.
-manifests as polyuria, nocturia, signs of dehydration & polydipsia (due to increased serum sodium & osmolality) by diminishing ability to concentrate urine. Usually appears 4-24hrs after surgery (not intraoperatively), moderate to severe hypernatremia can develop when pts (eg. Perioperatively) can’t access free water.
-Dx with high serum sodium (>145mmol/L), high serum osmolality (>290mosmol/kg), incr urine volume (>2mL/kg/hr), low urine osmolality (<200mOsm/kg) or specific gravity, may have low urine sodium depending on access to free water
-manage to correct any free water deficit if hypernatremia (5% dextrose in water, 1.35mL/hr x body wt along with isotonic fluids to correct any volume deficit if chronic (aim correct Na+ by 10mmol/L/24hrs), 3-6mL/kg/hr (max 666mL/hr) if acute, monitoring serum sodium & glucose every 1-3hrs.
If not hypernatremic, manage with 5% dextrose & normal saline maintenance rate + 2/3 previous hour’s UO, monitoring for hyperglycaemia.
Add desmopressin if fluid requirement exceeds 400mL/hr.
Desmopressin has potent antidiuretic but no vasopressor activity.
Desmopression typically initiated at night to limit nocturia & promote adequate sleep.
Care re: hyponatremia- desmopressin dosing is generally given at the minimum dose required to control polyuria, eg. 0.1 or 0.2mg tab or 5-10microg nasal spray (only 5% absorbed from gut) @ bedtime. equivalent IV 0.5-1microg. Desmporessin should be continued for as long as the pt has symptomatic central DI.
also have low-solute (low sodium, low protein) diet, to limit renal solute load, along with consideration of a thiazide diuretic (inhibits Na/Cl channel on DCT, inhibiting reabsorption of Na & water but thought to help by promoting hypovolaemia-induced proximal sodium & water reabsorption)
-desmopressin= risk hyponatremia that may be life threatening (seizures, coma respiratory arrest, death)- contraindicated if excessive fluid intake. may also cause headache, HTN.
-differentials= excess intra-op fluid, psychogenic polydipsia, osmotic diuresis, cerebral salt wasting or SIADH (both low serum sodium)
by how much does a net +ve free water balance of 3mL electrolyte-free water per kg lean body weight allows serum Na to fall by?
approx 1mEq/L
what’s chronic hypernatremia & how correct it?
(>48hrs) replace with 1.35mL/hr x pts body weight (max 150mL/hr). If hypovolaemic also give isotonic fluids to expand ECV. Can correct orally if stable/level of consciousness allows. Aim to reduce the serum sodium by approx 10mEq/L/24hrs, no >12mEq/L/24hrs (max safe limit infants)
how correct acute hypernatremia?
replace with 5% dextrose in water at 3-6mL/kg/hr (max 666mL/hr). Monitor serum sodium & BGL every 1-3hrs, aim serum Na <145mmol/L, then reduce rate to 1mL/kg/hr until serum Na <140mmol/L. Aim is to reduce the serum sodium by 1-2mmol/L per hour until normal in <24hrs
What’s nephrogenic DI? Causes? Treatment?
What’s nephrogenic DI? Causes? Treatment?
-resistance to ADH action in the kidney–> decr ability to concentrate urine, seen in CKD, lithium toxicity, hypercalcaemia, hypokalemia, tubulointerstitial disease
-managed with NSAIDs (esp indomethacin, incr urine concentrating ability by inhibiting renal synthesis of prostaglandins which are ADH antagonists) & thiazide diuretics
Why can’t just replace IV fluid for free water with fluid sans dextrose?
IV sterile water–> haemolysis
what’s carcinoid syndrome?
a constellation of symptoms mediated by various humoral factors elaborated from some well-differentiated neuroendocrine tumors (NETs) of the digestive tract & lungs which synthesise, store & release a variety of polypeptides (eg. Serotonin, histamine, dopamine), biogenic amines (eg. Bradykinin, somatostatin) & prostaglandins.
manifestations of carcinoid syndrome?
flushing- in 85%, hallmark of carcinoid syndrome- in typical carcinoid, flushing is 30 secs to 30 mins, mainly face/neck/upper chest, when sever can have hypoT & tachycardia. most sport but may be agg’d by eating, ETOH, stress, anaesthesia
venous telangiectasia due to prolonged VD (nose/upper lip/malar region)
HTN or hypoT
carcinoid heart disease- stimulation of fibroblasts–> fibrous plaques, most commonly in R)-sided valves (TCV, PV), chambers, rarely L) side (since lung inactivates humeral substances), aorta & pulmonary arteries
secretory diarrhoea
abdo cramping (mesenteric fibrosis or intestinal blockage by primary tumour)
niacin deficiency (hypoalbuminaemia, muscle wasting, angular stomatitis, glossitis, scaly skin, mental confusion)
what’s a carcinoid crisis?
life-threatening form of carcinoid syndrome, associated with release of an overwhelming amount of biologically active compounds from the tumour that may be triggered by tumour manipulation (biopsy or surgery) or anaesthesia, rarely by other factors such as hepatic artery embolisation or chemotherapy- generally in pts with extensive tumour bulk
how does somatostatin work?
14aa peptide that binds to somatostatin receptors expressed on a broad range on NETs to inhibit release of serotonin & other vasoactive substances
Why may some pts on octreotide be undergoing prophylactic cholecystectomy if undergoing abdo surg for other reasons?
Octreotide can inhibit gallbladder contractility–> gallstones or sludge. Nausea/abdo discomfort common which usually subsides.
What type of therapy is essential for pts undergoing hepatic resection for pts symptomatic from tumour bulk or carcinoid syndrome with hepatic NET mets?
Octreotide pre- and intra-op to prevent carcinoid crises that can arise from anaesthesia &/or tumour manipulation.
What are some benefits of octreotide in pts with carcinoid syndrome?
Symptom control
Also inhibit tumour growth
What may be done for pts with symptomatic carcinoid but unresectable liver-dominant mets?
Hepatic transarterial embolisations.
What may be used for refractory carcinoid bowel symptoms? And some other less common treatments for refractory symptoms?
Telotristat, an oral tryptophan hydroxylase inhibitor
Interferon which may have debilitating toxicity eg. Fatigue
What proportion of pts with carcinoid syndrome get carcinoid heart disease? What’s a near universal finding?
<50%
Tricuspid regurg
What’s the predominant symptom in carcinoid crisis? How long last?
Wide blood pressure fluctuations with a predominance of profound hypotension & tachycardia
Typically the crises are short (minutes)
may have associated flushing, bronchospasm, hypertension
Is the modern recommendation to give prophylactic octreotide prior to any surgery, particularly resection of hepatic mets?
No- this has been called into question (was 300-500microg subcut), as intraop complications can still occur despite preop prophylactic octreotide, not considered necessary particularly if pts are already receiving a long-acting somatostatin analogue.
What should always have in the room for a pt with carcinoid?
octreotide
How to manage carcinoid crisis?
IV fluid, vasopressors
Should have octreotide available intraoperatively for “as needed” IV use for pts with carcinoid syndrome who develop haemodynamic instability during surgery. Can use 500microg IV, may follow by IV infusion of 50-200mcirog/hr.
which pts should be screened for carcinoid heart disease?
all pts w carcinoid syndrome screened every 6-12/12
particularly important for those undergoing hepatic resection or other abdominal surgery due to the risk of bleeding if carcinoid syndrome & elevated R) atrial pressures- need urgent echo if signs of valvular heart disease or heart failure or NT-proBNP >260ng/mL
what’s the sense & spec of urine 5-HIAA for carcinoid tumour?
73 & 100%
what are some adverse effects of octreotide?
QT prolongation
bradycardia
conduction defects
abdo cramps, N&V
what is inhibited by somatostatin?
growth hormone (octreotide is a more potent inhibitor of GH)
glucagon
insulin
splanchnic blood flow
serotonin
gastrin
VIP
AT_PO 2.6: Assess the severity of, and provide perioperative care for patients with thyroid disease, consulting and managing collaboratively when appropriate:
What’s subclinical or overt hyperthyroidism?
How does the degree of hyperthyroidism impact clinical presentation & anaesthetic care?
How is hyperthyroidism managed & practicalities with some of the medications?
What are absolute or relative contraindications to B blockers (depending on disease severity)?
How is hypothyroidism classified?
Specific anaesthetic implications of hypothyroidism?
All pts having thyroid surgery should have serum TSH checked to determine thyroid status- which pts don’t need thyroid function tested periop?
What other blood tests should be undertaken?
What other conditions may be associated with medullary thyroid cancer?
How is MEN2B & MEN1 different?
What are the top 10 considerations for patients undergoing thyroid surgery or those with thyroid disease?
Is antibiotic prophylaxis required for thyroid surgery?
What is the form of local/regional anaesthesia that could be used for thyroid/parathyroid surgery?
What does it mean to be CLINICALLY euthyroid in a patient with known hyperthyroidism?
How do T4 and T3 vary?
How does being hyperthyroid impact induction?
What are the signs & symptoms of hyperthyroidism? Hypothyroidism? Thyrotoxicosis?
Subclinical= low TSH w normal FT4 or T3, overt is low TSH, elevated FT4/3
As the degree of hyperthyroidism increases, clinical manifestations more prominent & greater impact on anaesthetic care- if overt hyperthyroidism more risk of thyroid storm.
3 angles:
1. Stop T4 production (PTU or carbimazole; carbimazole (converted to methimazole) is preferred for it’s more rapid achievement of euthyroid state, once-daily dosing, longer DOA, less likely than PTU to be associated with failure of radioiodine therapy, less toxicity (PTU concerns re: hepatotoxicity) but PTU recommended during 1st trimester of preg or for initial management of thyroid storm)
2. Stop peripheral conversion of T4 to T3 (PTU or steroids (which also block release of thyroxine from thyroid gland) or propranolol)
3. Treat tachycardia with B blockade (propranolol 60-80mg every 4-6hrs, use cardio-selective eg metoprolol or atenolol if reactive airways disease, if B-block CI, use CCB eg. diltiazem)
Preoperatively in pts w hyperthyroidism, oral Lugol’s solution (potassium iodide) may also be given to block iodine uptake & secretion of thyroid hormone, may also decrease vascularity of the thyroid gland & reduce intraop bleeding (doesn’t tend to be given if toxic MND or adenoma as less vascular & may worsen hyperthyroidism)
Preop vit D & Ca++ supplementation may reduce risk of symptomatic hypoCa postop.
asthma, COPD
DM associated with hypoglycaemia where early warning symptoms of hypo may be masked
severe PVD
Raynaud phenomena
bradycardia, 2nd or 3rd-degree HB
mild: subclinical, elevated TSH with normal FT4
moderate: elevated TSH, low FT4, no clinical features of severe
severe: severe clinical features such as altered mentation, pericardial effusion/heart failure, myxedema coma, very low T4 levels
Exaggerated responses to anaesthetic agents/sedatives/opioids (incl resp depression), vasopressor-resistant hypotension, slow emergence, incr risk periop complications.
Pts who are on a stable dose of thyroid med with documented euthyroid state in the past 3-6 months doesn’t need testing prior to OT
Serum Ca++ level should be taken to identify parathyroid disorders
Hyperparathyroidism, pheochromocytoma (may be part of MEN2A syndrome)
MEN2B = mucosal neuromas & marfanoid body habitus instead of hyperparathyroidism. Also ass’d w phaeochromocytoma.
MEN1= pituitary adenoma, parathyroid hyperplasia, pancreatic tumors
- Hx & Ax focused on establishing thyroid function; are they euthyroid? (by labs or clinically- bearing in mind that TSH results can lag behind FT4 in response to anti-thyroid therapy) & if not, what are their manifestations/severity? If they have a thyroid-secreting tumour, should be euthyroid preop
- Elective surgery should be delayed in pts w thyroid disease who are hyperthyroid or severely hypothyroid until euthyroid; if urgent, Rx of the disease prior to surgery as time allows to minimise complications. If unable to achieve euthyroid, endocrine consult, invasive monitoring (eg. IAL) & consider postop ICU.
- Risk of intra-op thyrotoxic crisis
-hyperthyroidism- delay OT for thyrotoxic pts where possible, surgery should be performed when pt euthyroid. Urgent endocrine referral/advice necessary if pt not euthyroid. - Disease management & level of control (which impacts symptomatology & risks): thionamides (antithyroid drugs PTU/carbimazole, steroids, B-blockers) or thyroid replacement, radioiodine, prev surgery?
If malignant, have they had adjuvant external beam radiotherapy? If they’ve had recurrent/metastatic disease have they had chemotherapy (implications eg. Difficult IV access), are they malnourished/cachectic? - Ax for potential difficult airway/haemodynamics; evidence of large goitre/mass effects?:
a. signs of mass effect on trachea or SVC obstruction, signs retrosternal extension (ability to lie flat? OSA, voice change eg. Hoarseness (FNE useful)? dysphagia/stridor? Cough? Dyspnoea? Wheeze? Pemberton’s?.. flow-vol loops
b. assess with CT/MRI neck & chest to Ax position of lesion if symptoms or substernal goitre suspected to Ax for retrosternal extension, whether ant or post mediastinum (substernal mediastinal goitres can cause airway or cardiovascular structure obstruction on induction), tracheal size & deviation, other mass effects
c. is it malignant (4 M’s; metastases can be to lungs)
d. no consensus on primary management plan for large retrosternal goitre; discuss w surgeons re: nature of the mass.
-in general, large benign goitre without symptoms of obstruction seldom changes management. Meta-analysis of airway management in thyroid surgery showed that tracheal deviation was the only thyroid-specific factor ass’d w difficult intubation. Other risk factors are the usual predictive factors (eg. High MP, short TMD, low IID, obesity, male). Cancerous goitre higher risk (tissue infiltration/fibrosis reduce mobility of laryngeal structures, impede glottic view on laryngoscopy)
-May need AFOI w intubation behind the stenosis as plan A or spont vent induction if the pt has stridor or other signs tracheal compression, plan B should involve a rigid bronchoscope. May need a smaller tube? Surgeons should be ready for FONA if difficult airway but consider that if large goitre FONA may be challenging (may be deviated trachea or large mass obscuring- consider US). If the lesion extends beyond AA or carina, may need sternotomy (do @ cardiothoracic centre). Difficult airway equipment readily available intra-op & in PACU.
-consider access if SVC obstruction (IJ difficult/unreliable access before mass removed)
-if concerned re: CV collapse, invasive monitoring, tertiary centre, even consider VV ECMO prior to induction if large thyroid mass
-thyroid can be performed with ETT generally (SGA has been done if not neuromonitoring & no other pt risks; benefit of less coughing on emergence but may need adjustment after neck extension for surgical positioning or gland manipulation during surgery) - CVS features/risks:
-hyper= tachycardia, arrhythmias (sinus tachy, AF), incr contractility, incr myocardial O2 consumption (since hyperthyroidism causes epinephrine surge, incr SNS activity, risk demand>supply mismatch), systolic HTN & reduced SVR (SBP incr, DBP decr), higher circulating blood volume, more prone to coronary spasm & ischaemia, may develop cardiomyopathy over time.
-hypo= bradycardia, decreased myocardial contractility, diastolic dysfunction & impaired VR, diminished response to adrenergic agents, reduced CO, decr blood volume, incr SVR, SBP decr or normal, DBP incr or normal, may induce or worsen vent arrhythmias, incr risk IHD - Respiratory risks:
Risk post-extubation stridor if large nodular goitre/solid mass/malignancy/longstanding. Pre-OT compression symptoms may be positional (implications for induction).
Hyperthyroidism: respiratory muscle weakness, reduced FEV1 & VC which improve with Rx of hyperthyroidism (risk issues with extubation), pulm HTN is a known complication of neonatal thyrotoxicosis & in adults w hyperthyroidism esp FEMALES (pulm pressures drop w Rx of hyperTh), more likely to desaturate as have higher BMR. Also have incr resp drive & risk dyspnoea on exertion
Hypothyroidism: resp muscle weakness (reduced FEF& FVC, reduced DLCO (reasons unclear); skeletal myopathy, neuropathy, VC improves w Rx), reduced pulm function, exercise intolerance (worse maximal O2 consumption & MV), reduced resp drive (Rx improves, severe hypothyroidism= marked depression hypoxic & hypercapnic ventilatory drives, in extreme cases of myxedema coma there may be marked hypercapnia), risk OSA (depressed vent drive & enlarged tongue/pharynx/larynx due to myxedema), risk pleural effusion (& pericardial & peritoneal- exudates, indicating incr capillary permeability). Subclinical hypothyroidism is common among pts w idiopathic pulm HTN & autoimmune thyroid disease is incr in pts w pulm HTN. Hypothyroidism is ass’d w pulmonary, liver & cardiac fibrosis. - BGL state
-hyperthyroidism higher rates of gluconeogenesis, risk hyperglycaemia
-hypo risk hypoglycaemia - Thermoregulation
-hyperthyroidism high metabolic rate, more likely higher temperature- monitor temp, risk over-warming
-hypothyroidism risk hypothermia - Positioning/general
-hyperthyroidism tremor- challenge w invasive lines, SpO2 probe placement
-thyroid surgery limited access to tube/head once draped, positioned supine head elevated arms tucked (limited access to ULs), neck extended & roll under shoulders (ability to extend neck assessed pre-op), head support. Risk postop neck pain/injury; if known C-spine disease, assess preop by ortho surgeon or neurosurgeon.
Antibiotics given at my centre however according to literature they’re generally not required unless pt has high risk for infection (poorly controlled diabetes, immunocompromise; cefazolin)]
Superficial cervical plexus block & local infiltration (excision of a single parathyroid gland can be done with LIA alone) +/- sedation, inappropriate if sternotomy or lateral neck dissection or if Cx lymphadenopathy, locally invasive cancer, LA allergy, pt refusal or pt unable to cooperate/communicate or lie flat (eg. Severe OSA) or if predicted difficult airway (conversion to GA 2-12%). Superficial Cx plexus block may also be useful for postop pain.
HR <80, no tremor & FT4 normal (TSH may lag, may take 6-8/52 given large colloid stores of thyroid hormone)
T4 is thyroxine, comprises 90% while T3 (triiodothyronine) comprises 10% of thyroid follicular cell secretion. 99% of T4 is bound, it’s converted to T3 & shows changes before T3 is so it’s more important to measure.
Induction may be slower & require incr [] anaes agents due to incr CO
Hyperthyroidism: anxiety, insomnia, tremor, if Grave’s, exophthalmos, tachycardia/systolic HTN/palpitations/arrhythmias eg. AF, sinus tachy, sweating, heat intolerance, hyperglycaemia, dyspnoea with exercise, weight loss (raised BMR)
Hypothyroidism: depression/lethargy/apathy, OSA, pleural/pericardial effusion, bradycardia, systolic hypotension, dry skin, cold intolerance/hypothermia, exercise intolerance, myxoedema, weight gain, anaemia, hyponatremia (decr free water Cl), hypoglycaemia, reversible incr serum Cr
Thyrotoxicosis= hyperthyroidism + organ failure, fever >40degC, diaphoresis, tachycardia >140bpm, n/v/d, coma
AT_PO 2.6
What are the perioperative considerations with WPW?
Identify the condition
Assess if symptoms, Mx
Main risks are perioperative AVRT if goes through antegrade through AVN then retrograde through accessory pathway, narrow complex 140-150bpm may occur with p waves following the QRS, the delta waves can’t be seen. If antidromic, antegrade conduction through accessory pathway & broad/bizzare QRS.
If AF & WPW, may get antegrade conduction via accessory pathway, broad/bizarre qrs mixed with normal QRS if antegrade via AVN. Very rapid ventricular rates >300bpm may occur which can deteriorate to VF.
Consider having defib pads on, ALS cart in OT, art line, emergency drugs (procainamide, amiodarone) ready.
Minimise SNS stimulation (anxiolysis, adequately analgese, avoid hypovolaemia, avoid ketamine)
Avoid drugs that could enhance antegrade conduction through the accessory pathway (ie. Avoid AVN blocking drugs- adenosine, digoxin, verapamil, B blockers).
If orthodromic, same approach as SVT (vagal, adenosine; 2nd line procainamide, amiodarione).
If antidormic, must cardiovert if unstable. Procainamide infusion (20-50microg/min) until arrhythmia suppressed, hypoT ensues, QRS prolonged by 50% or total 17mg/kg has been given.
If AF + WPW, cardiovert if unstable. If stable, procainamide or amiodarone (150mg over 10min then 1mg/min for 6 hrs, 0.5mg/min for 18hrs. or ibutilide.
+ Describe the adverse effects of antimicrobial agents
-what’s antimicrobial stewardship?
-what’s antibiotic prophylaxis?
Adverse effects of gentamicin?
Coordinated program to promote appropriate use of antimicrobials, improving patient outcomes, reducing microbial resistance and decreasing the spread of infections caused by multi-resistant organisms.
use of ABx to prevent SSI. rationally used to balance risk of SSI w risks of antibiotics (resistance, ADR)
the agent should which targets likely pathogens based on site & type of surgery (eg. clean generally doesn’t need unless prosthesis)
use for the shortest duration possible
applied at a suitable time prior to incision so MIC achieved @ surg site & interval so MIC maintained for surgical duration
wide therapeutic index
cost-effective
consider pt factors (allergies, intolerances, multi-resistant organisms)
Cefazolin- 1st gen cephalosporin, bactericidal, inhibit bacterial wall synthesis, low spectrum, GP & some GN, more effective vs many beta lactamases vs penicillins. Half life 2hrs, re-dose 4hrs. dose adjust renal impairment. 3g if >120kg.
main adverse effects: pain on injection, diarrhoea, vomit, abdo pain, rash.
true cross-reactivity w penicillins 1%. if true allergy, clindamycin/lincomycin or vancomycin.
ototoxicity: vestibular, auditory dysfunction or both, parallels accumulation in inner ear, dose-dependent destruction of vestibular & cochlear sensory hairs.
Nephrotoxicity: accumulate in renal cortex, ATN
Skeletal muscle weakness (inhibits prejunctional ACh release), effects exagg in pts w MG. potentiates NMBDs, Ca++ overcomes NMJ effects.
clearance 20-40x longer in renal failure.
vancomycin: for serious GP infections (effective for C-diff, staph enterocolitis, endocarditis (enterococ, staph strep), MRSA while cefzol for MSSA). glycopeptide, bactericidal, inhibit cell wall synthesis.
nephrotoxicity, mast cell degranulation (hypotension), redman (rapid infusion)- flush, pruritis, erythema face/neck/torso.
BT_PO 1.5: Describe the implications for anaesthetic management and perioperative risk of a range of medical conditions, including but not limited to: CARDIOMYOPATHY
What’s cardiomyopathy?
What’s DCM, it’s pathophys/hallmarks?
Assessment & periop considerations?
What’s restrictive CM, it’s pathophys/hallmarks?
What’s arrhythmogenic RV cardiomyopathy?
Symptoms/signs?
Particular risks?
ECG features? What technique may help diagnose?
Management?
What type of cardiomyopathy is peripartum cardiomyopathy? rate? when does it usually manifest? Dx? risk factors? What determines prognosis? mortality? Management? main peripartum/periop concerns?
What are some other conditions may be associated with cardiomyopathy?
Disease of the heart muscle that can be inherited or acquired, affects shape, function & electrical system of the heart. Although some cardiomyopathies (eg. The DCM of takotsubo, tachycardia-mediated, peripartum) can resolve completely, generally CM not considered curable but S&S can usually be successfully managed w good life expectancy.
Dilated- disease of the myocardium characterised by impaired systolic function & dilatation of the L) +/- R) ventricles. Progressive enlargement of ventricles inefficient actin/myosin interaction, reduced SV, systolic impairment. Wall thickness to chamber diameter reduces, incr ++ wall stress & O2 demand, further systolic impairment.
A major cause of HF & arrhythmia in young adults, leading cause of heart transplantation in chn & young adults.
2/3 are idiopathic, can be familial, post-viral or ass’d w many underlying diseases sharing the common end-stage phenotype of LV +/- RV dilatation & systolic impairment: eg. IHD, HTN (*some classifications would exclude cardiomyopathy due to primary IHD or abnormal loading conditions (HTN, valvular heart disease) from the Dx of DCM), DM, inborn errors of metabolism, cardiotoxic (chemotherapy, illicit drugs (cocaine, amphetamines, MDMA), ETOH, Fe overload), takotsubo, arrhythmogenic, LV noncompaction, sarcoidosis, tachycardia CM, myocarditis (HIV, lyme), malnutrition (eg. Thiamine, copper), hypo or hyperthyroidism, cushing/Addison, pheochromocytoma, acromegaly, immune-mediated (SLE, Kawasaki, churg-strauss), neuromuscular disorders (Duchenne/becker), mitochondrial disorders, peripartum.
PRE:
CONSULT:
Medical & FHx.
Manifestations depend on degree of systolic dysfunction: early= asymptomatic, as progresses S&S of HF (dyspnoea, fatigue, ascites, peripheral oedema, arrhythmias). Late stage: embolic events, sudden death.
Management: to control symptoms & prevent further disease progression & complications (eg. LV thrombus)
-medical Mx includes: ACE-Is (limit RAAS, improve dyspnoea & ET, slow disease progression & improve mortality)
-ARB if can’t tolerate ACE-I
-B blockers & aldosterone inhibitors reduce mortality in HF
-anticoagulation if EF <30%
-advanced HF may have ICDs, pacing, LVAD or heart transplant
Examination: cardiac (S&S HF), resp
Ix:
Bloods
CXR
ECG
Exercise or pharmacological stress test may unmask ischaemia
ECHO: key role in Dx & identification of high-risk.
Features:
Fractional shortening <25%, EF <45% (initially cardiac output may be preserved & symptoms minimal despite impairment in EF (SV/LVEDV), since dilatation may be an adaptation to preserve stroke volume. Incr HR may also occur to maintain overall CO). Later signs of CCF are more related to elevated LV filling pressures.
MAPSE <10mm
LVEDD >117% predicted (corrected for age & BSA)
LV shape changes from elongated to globular (reduction of sphericity index (LV length to width ratio, normal is >1.6))
Diastolic dysfunction ass’d w poor prognosis & S&S
TAPSE <14mm suggests RV dysfunction & poor prognosis
MR often seen, may be the cause or consequence of DCM
Doppler echo: using continuity flow equation, SV = LVOT CSA x LVOT VTI; this is reduced in advanced DCM.
Optimise: Multi-D optimisation & planning, eg. Medications or devices for rate/rhythm control.
Planning: Continue regular medications, centre (cardiology/HDU), senior operators, daylight hours. Consider cardiac anaes on standby in case need TOE. Consider biventricular pacing or IABP if severe systolic dysfunction.
Explain: High risk postop mortality, CCF, arrhythmias, embolic events
Disposition: HDU for all but most minor procedures, advanced monitoring & haemodynamic Ax/monitoring.
INTRA:
Throughout, defend haemodynamic goals, cognisant that LV +/- RV dilated, usually dysfunctional
Rhythm/rate: avoid tachycardia/arrhythmias (rapid rate inadequate diastolic filling in high wall tension state, inadequate emptying. Brady excessive fill)
Preload: maintain
Afterload: avoid increases- this may exac incr wall tension, O2 demand>supply, chamber dilatation
Contractility: VERY important- avoid myocardial depression
Cor PP: prevent sudden hypotension, defend DBP @ least 60mmHg (may have high LVEDP, risk ischaemia)
R) heart considerations (MAP at least 60, avoid incr PVR) esp if RV dilatation
Peripheral nerve blocks ideal as minimal haemodynamic change
Central neuraxial blocks reduce afterload & improve cardiac output but need to avoid excessive preload reduction & low DBP (risk myocardial hypoperfusion)
M: art line, 5-lead ecg, low threshold for CVC if concerned re: ventricular contractility or diastolic impairment. BIS to titrate depth
A: skilled anaes nurse, consider having cardiac anaesthetist on standby for TOE if need dynamic Ax myocardial function
Drugs: limit myocardial depression/-ve inotropy, titrate volume & pressors to maintain preload but avoid excessive afterload. Blunt SNS response & spare GA w multimodal, opioids. Inotropes (dobutamine), can use NAdr for hypoT but care re: excess afterload.
Induction: art line pre, ensure euvolaemic, effective pre-O2, circulation time impaired so gentle/titrated induction. Opioids have minimal cardiovascular effect & reduce GA requirement, blunt response to laryngoscopy. ETT to control ventilation/PaO2/PaCO2. Consider avoiding ketamine as SNS potentiation (risk incr SVR). Propofol useful in reducing SVR although -ve inotrope.
Maintenance: avoid high MAC (-ve inotrope, preload reduction), titrate including BIS
Adhere to haemodynamic goals (maintain contractility, avoid tachyarrhythmias & brady, euvolaemia, adequate preload, avoid excess incr SVR (afterload), DBP >60mmHg for corPP, limit SNS stimulation (titrate opioids), normothermia (avoid incr MRO2, PVR))
Emergence: limit SNS stimulation/response to extubation
Postop:
Recovery: ongoing art line & 5-lead ecg monitoring for DBP, HR/rhythm, supplemental O2
Analgesia: continue multimodal/opioid sparing- regional beneficial ++, anti-emesis
Disposition HDU for haemodynamic monitoring & management
Follow-up postop changes (consider trops, clear communication re: haemodynamic plan on ward)
Restrictive CM= the impairment of ventricular diastolic function due to fibrotic or infiltrative changes in the myocardium +/- subendocardium. These changes reduce diastolic ventricular compliance & elevate ventricular E-D pressure.
The systolic function can be normal or near-normal in the early stages of the disease. It can be primary (idiopathic) or secondary to amyloidosis, sarcoidosis, haemochromatosis, IHD, HTN or valvular heart disease.
Perioperative considerations for restrictive CM?
Pre:
CONSULT:
Hx: usually S&S of biventricular failure: dyspnoea, fatigue, palpitation, orthopnoea, oedema, chest pain
Mx: aiming to reduce & control HF symptoms by lowering ventricular filling pressure without affecting CO.
B-blockers or CCBs to prolong ventricular filling time & improve ventricular relaxation
Diuretics for symptom relief of HF
Maintain sinus essential (arrhythmias can compromise diastolic function & ventricular filling): amiodarone, digoxin, B-blockers
PPMs & ICDs indicated if advanced conducting system dysfunction
Exam: audible S3, systolic murmur, raised JVP, ascites, peripheral oedema
Ix: echo, endomyocardial biopsy, CT or cardiac MRI (to diagnose & distinguish between RCM & constrictive pericarditis)
Key echo findings:
-biatrial enlargement, relatively little IV septal movement during respiration, occasional ventricular septal movement during diastole
OPTIMISE:
Multi-D (cardiology, GP, anaesthetics), optimisation of underlying pathology particularly optimising rate & ensuring sinus, diuretics to control volume status & HF signs/symptoms
Plan:
Tertiary, cards & HDU on-site + TOE capability intra-op
Explain:
High risk M&M, informed consent
Disposition:
HDU with haemodynamic monitoring/optimisation
INTRA-OP:
Main considerations: Cardiac output is both preload & HR dependent; significant reduction in blood volume or filling pressures (eg. If decr preload from VD with anaes agents & positive pressure ventilation), myocardial depression (eg. w GA agents), brady or tachycardia & atrial arrhythmias aren’t well-tolerated.
Monitoring: art line, very low threshold for CVC +/- intra-op TOE.
Rate: avoid brady or tachy
Rhythm: sinus
Preload: defend
Afterload: maintain SVR & DBP but avoid excess (may precipitate HF)
Use anaesthetic with minimal CV effects (ketamine or etomidate), attenuate SNS effects with opioids +/- rapid-acting B-blocker (eg. Esmolol)
Postop: HDU, comprehensive effective analgesia & anti-emesis (limit SNS stimulation)
Structural abnormalities & dysfunction of the RV, can also involve LV. Adipose & fibrous tissue replace myocardial cells, can form re-entry electrical circuits triggering arrhythmias. Starts localised with RWMA’s, progresses to RV thinning, dilation & loss of contractile tissue. Can develop R) BBB, RV failure. It’s seen in up to 20% of cases of sudden death in young people. Genetic condition with genetic variation. Likely involves ryanodine receptor gene (association between exercise, arrhythmia & sudden death).
Arrhythmia, syncope, cardiac arrest or sudden death
Drug-resistant arrhythmias, sudden cardiac death.
VT with L) BBB morphology, PVCs with L) BBB morphology, spont non-sustained VT, TWI V1-3
Cardiac MRI with gadolinium enhancement
Prevent/reduce risk arrhythmias: sotalol, verapamil, amiodarone
Catheter ablation palliative vs curative
ICD insertion may be lifesaving
dilated
huge global variation (1:100 Nigeria, 1:20,000 Japan). Higher in subsequent pregnancies.
manifests during the last few months of pregnancy (T3) or the first 6/12 postpartum
DEFINED AS DEVELOPMENT OF SYSTOLIC HF TOWARD END OF PREGNANCY OR IN THE MONTHS FOLLOWING, W LVEF GENERALLY <45% IN ABSENCE OF ANOTHER IDENTIFIABLE CAUSE OF HF
Diagnose after excluding other causes of acute HF
Risks= pre-eclampsia, tocolytic therapy, obesity, advanced age, viral infection, multiple pregnancies
Prognosis depends on the recovery of LV contractility & resolution of symptoms within the first 6/12 after disease onset
mortality as high as 30-60% due to pulm oedema & systemic embolization
Management is similar to Rx other types of HF, additional therapeutic issues incl arrhythmia Mx, anticoag therapy, mechanical support. Delivery timing joint multi-D decision (cards, obs, anaes, neonatology) generally prompt delivery indicated if advanced HF.
-Acute (O2, diuresis, vasodilators, inotropes): supplemental O2 & ventn as needed, optimise preload (esp if pulm oedema, w diuretics- loop preferred, frusemide cat C (standard risks met alk, hypoK, hypoNa, vol contraction & reduced plac perfusion. If refractory, can add thiazide cat C but more risk bleeding diathesis & hypoNa in neonates. No data on loops in breastfeeding, thiazides acceptable), vasodilators of choice hydralazine cat C & ISDN © (since ACEI (cat D) & ARB (cat C trim 1, Cat D thereafter) contraindicated in preg but ACEI can be used in breastfeeding (evidence lacking but hydrazaline ok, isdn not enough data), haemodynamic support inotropes (dobutamine (preg cat B)- B agonist with inotrope & VD properties, dopamine (cat C)= inotropic w variable vasculature effect depending on dose. Milrinone ©- inotropic & vasodilatory properties), vasopressors as needed (generally avoided in acute HF since usually high SVR & incr afterload may impair CO, also in preg may impair uterine blood flow. Dopamine may be preferrable for uterine blood flow). If elevated BP IV nitroglycerine © (care ++ re FHR & maternal BP, continuous foetal monitoring from age of viability. If need pronounced afterload reduction consider nitroprusside (eg. Acute acute aortic regurg or mitral regurg)- only if necessary despite cat C due to risk cyanide poisoning. Avoid SNP or nitroglycerine in breastfeeding, VTE proph (VTE in 1:500-1:2000 preg, more common postpartum)- consider if evidence of systemic embolization or mechanical prosthetic HV- some may anticoagulated if severe LVEF <=30%, international guidelines don’t recommend routine anticoag for PPCM. Heparins generally considered safer (LMWH cat B vs UFH cat C for all but final weeks of preg or if CrCl<=30), foetal monitoring & haemodynamic monitoring. Avoid B block in acute decomp HF, if on chronic B block often w/h or dose reduce if acute decomp.
-arrhythmia Mx (if AF, rhythm vs rate control (flecainide (cat C ok for BF) or sotalol (risk newborn brady if use near delivery, no ass’n w FGR, not teratogenic, cat B. monitor bub if BF), if need rate, could use B-selective blockers (avoid atenolol as FGR if prolon duration T2 or T3, reduced placental weight if only used in T3. Risk foetal brady, hypogl if taken near delivery so monitor 72-96hrs. metoprolol best cat C. avoid atenolol if BF but other B blockers ok just monitor bub. verapamil (cat C, ok preg or BF) or digoxin (cat C, ok BF))
-device therapy (generally await 3-6/12 from Dx to see if optimal medical therapy effective, ideally place prior to or after preg to avoid radiation)
-relief of symptoms
-chronic therapies that improve long-term outcomes when possible (but ACE-Is, A2RBs, angiotensin receptor-neprilysin inhibitors & mineralocorticoids avoided in pregnancy as teratogenic, risk foetal renal failure or death. Can be used postpartum if not breastfeeding (little data on ARB or ANRI in bf so avoid, some ACEIs have been studied (enalapril) & not exp to cause adverse effects). HFrEF symptom control w diuretics, B blockers (some risk FGR. B-1 selective (metoprolol) preferred as less likely to interfere w B2 mediated uterine relaxation of peripheral VD. Avoid atenolol (ass’d w FGR). If chronic B blocker, monitor foetal growth, occ neonatal apnoea, hypoT, brady, hypoglycaemia have been reported- monitor bubs w mum on B-blocker for 72-96hrs postpartum. Metoprolol ER if breastfeeding- is excreted into breast milk but low serum levels in bub. In contrast, avoid bisoprolol as relatively low PB & moderately high renal excretion, higher risk accumulation. Atenolol also low PB & extensive renal excretion- avoid), digoxin (there is transplacental passage but considered safe. Low levels in breastmilk, avoid bf for 2 hrs after IV to lessen ingested dose). Diuretics, B blockers, ACEIs, ARBs, ARNIs, hydralazine, nitrate, aldosterone antags improve survival. If HFpEF, Rx empiric (less data)- same antihypertensives & diuretics, HR control, CCB may be useful esp if tachycardia for HFpEF but generally avoided in HFrEF. Digoxin not indicated for HFpEF.
-consider genetic testing (15-20% of pts w PPCM have mutations known to induce CM)
Physiological changes of preg & labour or anaesthesia may be detrimental (early labour epidural recommended). Can safely have GA or neuraxial if defend haemodynamic goals (CSE may be preferred for LSCS);
avoid tachycardias/arrhythmias
defend preload: optimise fluid administration
excess afterload may decompensate
avoid myocardial depression (VERY important)
defend diastolic perfusion
avoid raised PVR esp if RV dilatation
Drugs (eg. Disease-modifying agents)
Myotonic dystrophy, myotonia congenita, duchenne muscular dystrophy (50% have DCM by age 15), NF1 (hypertrophic), hyperthyroidism (over time)
BT_PO 1.5: Describe the implications for anaesthetic management and perioperative risk of a range of medical conditions, including but not limited to:
Right heart failure:
What is right heart failure?
How may RV dysfunction occur & how does RV structure make it vulnerable to this?
Perioperative management RV failure & anaes considerations?
A clinical syndrome due to alteration in the structure/function of the R) heart circulatory system leading to suboptimal delivery of blood flow to the pulmonary circulation and/or elevated venous pressures @ rest or with exercise
Pressure overload (increased afterload), volume overload (increased preload), impaired contractility (eg. Myocardial ischaemia, arrhythmias).
Thin-walled, low pressure, relatively high compliance so can better tolerate increases in preload than sudden increases in afterload, eg. Acute LV failure, APO, pulmonary embolus, hypoxia.
In response to chronic afterload it progressively hypertrophies & increases contractility to maintain CO then when compensation exhausted, decompensation occurs eg. RV dilates, contractility & output reduce, end-organ failure, also may get arrhythmias which further reduce CO, more susceptible to ischaemia if higher RV pressures (CorPP= ADP – RVEDP), particularly if systemic hypotension. Raised RVEDP also raises RAP which impairs systemic venous return. More vulnerable to acute afterload increases (eg. PE) where the thin-walled, compliant RV may not be able to maintain sufficient ejection (inadequate contractility to generate adequate pressure, RVEDP>LVEDP may cause septal bowing, tricuspid annular dilatation & regurgitation reduce forward flow). May occur if an otherwise health RV suddenly has to generate mean pressures >40mmHg.
CONSULT:
History: medical history to assist diagnosing aetiology (eg. Idiopathic pulm HTN, pulm HTN due to LV failure, pulm HTN due to pulmonary disease, pulm HTN due to chronic thromboembolism, pulm HTN due to misc causes eg. HIV, sarcoidosis, pulmonary infection, pulmonary embolus, myocardial ischaemia/infarction, congenital heart disease, valvulopathies (TCR), haematological disorders (eg. Sickle cell), sepsis, pericardial disease
Management to date
Symptoms/level of control, functional status (DASI, NYHA)
Examination:
Signs of low CO state:
Observe walking into waiting room- exercise tolerance/dyspnoea/fatigue?
Vital signs (particularly if hypotension, tachycardia, desaturation)
Cool peripheries, oliguria
signs systemic venous congestion:
S3
TCR murmur: holosystolic, LSE radiates to RSE
Elevated JVP
Hepatojugular reflux (JVP >3cm sustained >15 secs)
Pulsatile liver
Peripheral oedema
Investigations:
Incr lactate
Deranged liver biochem (liver congestion +/- organ hypoperfusion from inadequate CO)
Renal impairment
Cardiac biomarkers: BNP, cardiac trop T non-specific but elevations may correlate w reduced RV function after PE
ECG: normal or show RAD, R) BBB, RVH, S1Q3T3 triad of RV strain in up to 10%
TTE: may be more useful (it may also be useful for LVOT velocity since alignment easier), since anterior location of the R) heart. TOE limited by distance of probe from important structures & poor doppler alignment.
If pulm HTN, key consideration is how RV holding up; if heterometric (dilated but performing well) or dilated with severe TR/dysfunction
Measures of RV function:
TAPSE normal >16mm
Fractional area change 4-chamber view, % change in area btwn systole & diastole, FAC <35% indicates RV systolic dysfunction
Tei index: dimensionless myocardial performance index, sum of isovolumetric contraction time & isovolumetric relaxation time / ejection time. Relies on constant R-R so not useful in AF. Normal <0.4 by pulsed doppler, <0.55 by tissue doppler.
Which of these pre-op TTE assessment parameters have been shown to predict periop cardiac complications in non-cardiac surgery?
Lower TAPSE & increased Tei index.
How is the TR jet useful?
If present, permits estimation of RVSP.
RVSP = 4v2 + RAP (or CVP), equivalent to PASP in absence of pulmonary stenosis
Most accurate non-invasive technique to assess the RV?
Cardiac MRI: mass, volume, EF, perfusion
What’s normal RV ejection fraction?
47-75%
What’s the utility of PA catheter?
Due to risks (PA rupture, arrhythmia), reserved for situations where having additional info (eg. Ax RV failure where Rx resistance or aetiology unclear) outweighs rusks involved. No evidence.
OPTIMISE:
Multi-D (cardiology, anaesthetics +/- respiratory)
Continue regular meds
Electrolytes (esp. K+ & Mg++ to limit risk new arrhythmias), Hb optimised
Consider surgical factors that put the RV @ risk (eg. Venous air, CO2, fat or cement embolism (ortho or liver transplants), rapid large volume infusions, pneumoperitoneum, patient positioning (eg. Head up)
Optimise RV function prior to OT & plan to avoid conditions that may precipitate deterioration of RV function
Manage severe COPD, ischaemic heart disease, valvulopathies, congenital heart disease (pt groups @ particular periop risk of developing R) heart failure)
Plan: tertiary centre, daylight hours, consider cardiac anaesthesia/intra-op TTE/TOE, postop ICU, consider availability of mechanical supports (IABP, ECMO, VADs)
Explain: incr periop risk, discuss modifiable risk factors, informed consent
Disposition: HDU
Intra-op:
Main goals: Avoid conditions that may precipitate deterioration of RV function (acute incr afterload, preload or reduced contractility)
Rate: preferably faster- 80-100bpm to limit excessive RV distension, but avoid tacchycardia (while RV perfuses in systole & diastole, high RV pressures more dependent on diastole)
Rhythm: SINUS; arrhythmias impair RV filling
Preload: euvolaemia (not excessive volume although RV handles preload relatively well)
Afterload: AVOID incr PVR
-avoid hypoxaemia, hypercapnia, acidosis, hypothermia
-drugs that increase PVR (N2O, ketamine (increases PVR in adults in large doses but generally OK, lack of -ve inotropy & can use for RSI in pulm HTN), desflurane, VERY judicious use of metaraminol (ideally avoid alpha 1 agonists- pulm vasc alpha 1++), ephedrine OK, ensure adequate anaesthetic depth & analgesia (+/- pre-op anxiolysis with midaz) to limit SNS response, avoid high PEEP & lung hyperinflation
-Consider pulmonary vasodilators (NO, prostacyclin), preferred vasopressor= vasopressin
Contractility: avoid myocardial depression, low threshold for inotropic/inodilator support for failing RV
Coronary perfusion: optimise myocardial DO2 (DBP >60mmHg, optimise Hb)
Monitoring: art line (early identification & aggressive Mx of systemic hypoT), large IV access, consider CVC if prolonged OT/anticipate large fluid shifts or severe disease to measure CVP & deliver inotropes (HOWEVER meta-analyses have found a limited relation in CVP or delta-CVP in predicting haemodynamic responses to fluid challenge & CVP has little relationship with intravasc volume status), BIS along with other parameters for depth of anaesthesia titration, TOFR, temperature (aim limit hypothermia which incr PVR, shivering incr MRO2)
Assistant: skilled +/- cardiac anaes
Drugs: in line with goals of avoiding raised PVR (see above)
Equipment: consider availability of TOE/TTE, consider pads on & crash cart nearby; DCCV= Rx of choice for haemodynamic instability, anti-arrhythmic of choice= amiodarone (B-blockers & CCBs may reduce inotropy & further impair RV function)
Pre-O2 meticulous to FiO2 >=0.8, in adequate position for successful airway
Resus: ensure adequate preload/euvolaemia pre-induction, manage any arrhythmias
Induction: gentle, titrated aiming to limit preload reduction and avoid incr RV afterload, maintain RV contractility & ensure no excess O2 demand (eg. SNS stimulation), if bradycardic consider glycol to prevent excessive RV distension with brady but balance against risk O2 demand if tachy. Etomidate would be induction agent of choice, propofol may be safe (reduce RV contractility & SVR) with very cautious dosing & fentanyl for propofol sparing, my choice= propofol sparing, eg. Midaz 3mg, fent 250microg, sevo on, large dose roc once lost verbal response (if RV function not decomp & still awake w fent midaz, they’ve earned some props). Other option is spont vent induction, benefit= separate induction from PPV (potential times of haemodynamic risk).
A time of risk is transition from spont vent to PPV; aim to make transitions smooth “R) heart doesn’t know it’s getting an anaesthetic”, gentle BMV with guedel to avoid hypercapnia & hypoxia but limit Pit). Comprehensively blunt SNS stimulus with laryngoscopy (rapid-acting analgesia eg. Fentanyl IV, adequate depth of anaesthesia and complete NMB with TOFC<4 to limit cough/strain & PVR). Gentle laryngoscopy eg. With VL, limit instrumentation (if bougie gentle++), tube, cuff up & GENTLE APL (eg. 12cmH2O)
Likely have +ve inotrope running if significant RV impairment +/- vasopressors to attenuate post-induction hypoT:
-vasopressin 1-4 units/min preferred; at low doses may be ass’d w DECREASED PVR
-NEpi improves coronary perfusion by incr aortic root pressure but >0.5microg/kg/min can incr PVR, generally limit to <0.2microg/kg/min
Maintenance:
Attention to detail: immediate ABG once settled to see A-a gradient.
Mechanical ventilation: avoid hypox/hyperc/acidosis, avoid atelectasis & high lung volumes. TVs 6mL/kg with PEEP of 5, plateau pressures <30cmH2O, titrate rate to EtCO2 30-35mmHg, confirm on ABG PaCO2 35-40mmHg. Adequate dept NMBD to optimise resp mechanics. Challenge if pt obese/has obstructive lung disease.
CLEAR reciprocal communication with surgeon re: times of risk to anticipate (eg. Incision, pneumoperitoneum, head down, blood loss) with adequate analgesia/preload & afterload manipulation.
Cautions IVT maintaining euvolaemia but avoiding RV overdistension.
Judicious opioid: large doses blunt SNS tone but may precipitate systemic hypT & reduce RV contractility, OIH may hypercarbia & incr PVR. Use opioid-sparing adjuncts & regional pre/intra/post. If neuraxial, carefully-titrated epidural.
If come “unstuck”, revisit haemodynamic goals (euvolaemic? Rate & rhythm? RV afterload?) bedside TTE could help identify/exclude causes of acute RV deterioration or unexplained haemodynamic instability & to guide management, eg:
-acute PE (50-75% of pulm vasculature needs to be occluded by emboli for RV failure to ensue in normal circumstances)
-cardiac tamponade
-RV MI (acute inferior MI, 30-50% of pts with RCA occlusion develop RV impairment); if prox RCA occlusion, avoid nitrates & diuretics which may compromise RV preload
-acute RV or LV dysfunction
-acute valvulopathies
Inotrope of choice= dobutamine, B1 agonist with B2 (VD) properties. 2-5microg/kg/min incr CO & decr PVR, may decr SVR so may require co-administration of vasopressor. 2.5microg/kg/min is the rate if RV coping, 5microg/kg/in if not. If >7.5microg/kg/min, likely get incr rate without further inotropy.
Milrinone promotes myocardial contractility while reducing RV afterload (inodilator), 0.25-0.5microg/kg/min reduce PA pressures & augment RV function; co-admin of a vasopressor generally required. Nebulised milrinone useful in pulm hypertensive crisis (pulmonary selectivity, less systemic hypoT)
Dopamine <5microg/kg/min may improve RV function but limited by tachyarrhythmias
Levosimenden is costly, need to administer via IV infusion over 24hrs, actions last several days (active metabolite), calcium sensitiser which improves diastolic function & myocardial contractility sans incr CMRO2, Ca++ dependent so manage hypocalcaemia.
Digoxin may improve CO by 10% acutely, doesn’t affect HR (1mg)
DCCV= Rx of choice for haemodynamic instability. Anti-arrhythmic of choice= amiodarone.
If RV dilated, Diuresis may be indicated to offload ventricle & reduce RV filling pressures.
Pulmonary vasodilators reduce PVR & improve RV SV but risk systemic hypoT & may risk hypoxaemia through V/Q mismatch; optimise RV perfusion prior to administration
-IV epoprostenol, neb iloprost: incr pulm prostacyclin I2 pulm VD & reduce PVR
-Bosentan= endothelin-1 antagonist, pulm VD by inhibiting endothelium-derived pulm VC
-PDE5 inhibitor: sildefanil (PO), milrinone is PDE3 inhibitor
-PVR can also be reduced by CCBs, Mg++, GTN, adenosine
Consideration of mechanical support for the RV (aim to prevent multi-organ dysfunction while RV recovers) if RV failure due to a reversible cause (eg. PE, ischaemia)
-IABP augment coronary flow
-ECMO (lim’d to days or weeks)
-paracorporeal RVADs only approved for 1/52
Emergence: fully reverse to TOFR >0.9, upright, competing interests of want pt awake & spont breathing to limit hypoxia/hypercarbia but want to limit cough (incr PVR, de-recruits, remove FRC). Suction deep, lignocaine 1mg/kg approx. 1 min before extubate, once adequate TVs & awake, extubate onto HFNO to blow off CO2.
Recovery:
Postop= greatest risk deterioration, ICU generally appropriate immediate postop period (depending on pt factors, surgery duration & complexity, anticipation of ongoing fluid shifts & haemodynamic challenge, postop pain, vasopressor/inotropic requirements). Postop goals (as in OT):
Maintain preload, avoid incr PVR, support contractility, avoid atelectasis (chest physio), prevent hypoxia & hypercarbia, normothermia, optimise analgesia & anti-emesis.
THROMBOPROPHYLAXIS once haemostasis assured
*for other cardiac: excellent communication w surgeons re: times of risk, thromboprophylaxis, consider pads
BT_PO 1.5: Describe the implications for anaesthetic management and perioperative risk of a range of medical conditions, including but not limited to:
Restrictive lung disease:
What are restrictive respiratory diseases?
Perioperative & anaesthetic management considerations?
A heterogenous group of conditions characterised by a restrictive pattern on pulmonary function testing (ie. reduced TLC & VC), reduced resp system compliance & preservation of expiratory flow.
The cause of the restrictive changes may be intrinsic (eg. idiopathic pulmonary fibrosis, granulomatous disorders (sarcoidosis), rheumatoid lung, scleroderma, occupational/environmental/drug/radiation exposures (eg. silica, asbestos, coal dust, aluminium, Fe, thermophilic fungi (farmer’s lung), aspergillum, animal proteins (bird fancier’s lung), amiodarone/nitrofurantoin/azathioprine/IL-1 blockers/methotrexate/NSAIDs/rituximab/TNF alfa blockers/cyclophosphamide/bleomycin/paclitaxel/hydralazine or procainamide or isoniazid (if drug-induced SLE), cocaine/heroin/methadone, bromocriptine/oxygen/statins, irradiation of thorax for mediastinal lymphoma)) or extrinsic (eg. abdominal (pregnancy, ascites, obesity), chest wall (kyphoscsliosis, ankylosing spondylitis, pectus carinartum, thoracoplasty, space-occupying lesions), pleural (mesothelioma, effusion), neuromuscular) to the lung parenchyma.
PRE:
Consult:
Hx: Diagnosis, medical management (letters from pulm specialist), disease SEVERITY/LEVEL OF CONTROL (exac/hospitalisations, episodes of resp failure/endotracheal intubation/ICU?)
Continue regular medications (?need stress steroids, are they on immunosuppressive agents, are they on home O2 prescription)?
Other comorbidities (eg. PH & RHF?)
symptoms with disease association eg. musculoskeletal pain/joint swelling, dry eyes
if orthopnoea, peripheral oedema, skeletal muscle weakness, pleuritic or fever, consider myocardial or pericardial disease
smoking/THC: teachable moment
other exposures; eg. chest radiation, antineoplastic agents, occupation
Symptoms:
dyspnoea, cough, wheeze, haemoptysis, particular activities or positions exac? morning headaches (suggests hypoxaemia), muscle twitch/lethargy/confusion/headache suggest hypercapnia
functional capacity (DASI)
Idiopathic pulmonary fibrosis (the most common type of idiopathic interstitial pneumonia (others incl cryptogenic organising pneumonia, IPF has fibrotic predominance, the other IIPs predominant inflammation (more responsive to glucocorticoids), pts with respiratory bronchiolitis-interstitial lung disease may respond to smoking cessation):
Typically older adults, may have comorbid conditions that further increase periop risk (PH, OSA, COPD, lung Ca, IHD, GORD).
Interstitial lung disease may be associated with underlying connective tissue disorders (eg. RA, polymyositis/dermatomyositis, Sjogren, SLE, systemic sclerosis, common feature of sarcoidosis); typically while these pts have similar clinical/histologic manifestations to IPF, disease progression is often limited & may not require Rx, generally better response to immunosuppressive Rx & better prognosis vs IPF.
symptoms IPF= nonproductive cough, dyspnoea on exertion, risk acute exec (worsening dyspnoea not fully explained by HF or fluid overload)
Ix: restrictive pattern on PFTs with impaired gas transfer. HRCT: bibasilar peripheral reticular opacities, traction bronchiectasis, lower lobe volume loss, sub pleural honeycomb cysts (in acute exac HRCT may show new bilateral ground glass opacification/consolidation)
Exam:
observe walking into office; work of breathing, wheeze
BMI
SpO2 AT REST & ON EXERTION (ILD may have normal SpO2 @ rest but desat on exertion)
chest wall deformities
lung ausc/percussion for baseline creps/wheeze
cardiac exam esp signs of RHF
systemic manifestations eg. muscle weakness/joint deformity
Ix:
ABG: baseline PaO2, PaCO2 (indicated if resting SpO2 <93% or if high serum bicarb)
PFTs:
to clarify type & severity of resp impairment which may help guide ventilation during surgery, A likelihood for prolonged ventilatory dependence, identify pts w such severe resp impairment that elective surgery may be reconsidered or GA avoided where possible
Consider comprehensive pre-op pulmonary evaluation including spirometry if:
-hypoxaemia on RA (or home O2) if cause uncertain
-serum bicarb >33 or PaCO2 >50mmHg if pulm status hasn’t been evaluated prev
-Hx resp failure from a persisting problem
-severe dyspnoea esp if suspect resp cause
-difficult assessing pulm function by clinical examination
-suspected pulmonary HTN
-the need to determine response to bronchodilators
-the need to predict lung function after planned resection
-examine previous PFTs, consider repeating before major surgery if dyspnoea at rest or minimal exertion or if imaging studies show new abnormalities
Hallmark of restrictive physiology on spirometry= matched decreases FVC & FEV1, absence of airflow obstruction (ie. FEV1/FVC ratio preserved)
Following spirometry, also need to measure lung volumes to CONFIRM RESTRICTION, quantify severity & exclude air trapping (which causes similar changes in spirometry); use TLC: mild restriction= TLC 65-80% pred. mod TLC= 50-65% pred. severe TLC <50% predicted.
Gas transfer:
ie:
1. spirometry- obstruction?
2. volumes- restriction?
3. gas transfer- low in disease of pulmonary parenchyma eg. ILD or PH, normal/high if chest wall issue or neuromuscular (maximal insp/exp pressures low in neuromuscular)
early ILD: normal volumes, mildly reduced DLCO
late: restrictive with significant DLCO reduction
In extrinsic conditions causing restriction (low TLC, VC), gas transfer typically normal
Exercise capacity:
6MWT or CPET
6MWT Ax distance walked in 6mins & SpO2 during test compare w age & sex-based norms. Useful in ILD & PH were exertional desat typical.
CPET may provide useful prognostic info for periop risk stratification for high-risk intra-abdo surgery
Imaging:
repeat imaging may be ordered by pulmonary specialist if >1yr old or symptom change
OPTIMISE:
modifiable factors prior to elective surgery:
-DELAY OT if acute exac/active resp infection: exclude pulm infection (consider if recent COVID-19 or other acute viral illness), malignancy, thromboembolic disease. Consider bronchoscopy w BAL to Ix for infection. Broad-spectrum Abx & empiric systemic glucocorticoids
-optimal use of meds incl home O2 in liaison w pulmonary specialist
-secretion clearance (chest physio)
-smoking cessation- optimal benefits from 8/52 pre-op but even 2 days benefit (decr HbCO, elimination nicotine effects, improved mucociliary Cl)
-pulmonary rehabilitation may improve dyspnoea, exercise capacity, QoL
-weight loss for obese- improve resp mechanics, sleep apnoea risk
-HF optimisation
-optimise all preexisting co-morbid conditions (eg. diuretics/drainage of tense ascites)
-education & emotional support
RISK STRATIFY:
Clarify the type & severity of respiratory impairment which may help guide ventilation during surgery, assess likelihood for prolonged ventilatory dependence, identify pts who have such severe resp system impairment that elective surgery should be reconsidered
PLAN:
MULTI-D, discuss with surgeon times of risk (eg. positioning head down/pneumoperitoneum), discuss w surgeons risk attenuation (eg. low insufflation pressures or consider open))
Discuss with pt’s respiratory physician +/- cardiologist +/- GP & other relevant disciplines (eg. physiotherapy if pulmonary rehab) re: pre-op optimisation
Tertiary centre in-hours, senior operator, postop HDU available & ideally pt’s respiratory team to consult
Explain:
High risk periop M&M
consent
D: book postop HDU
INTRA:
Goals:
Strategy (sedation/neuraxial/peripheral block/GA) on individual basis weighing up severity of restrictive lung disease & other co-morbidities with surgical factors.
Benefits of sedation: faster recovery time, less pulmonary complications, risks= unintentional over sedation reduces responsiveness to hypercapnia & hypoxia & reduces TVs (use short-acting agents, minimal or rapidly reversible resp depressant effects); dexmedetomidine useful as spont resp, airway potency & vent response to hypercapnia maintained
Neuraxial benefits= minimal impairment of pulmonary gas exchange, risks high block & reduced IC/ERV
Peripheral nerve block benefits= minimal impairment of pulmonary gas exchange but AVOID inter scalene block (100% incidence phrenic nerve block resulting in hemi-diaphragmatic paralysis, 25-30% reduction in FEV1 & FVC. Risk of PTx ( enlargement/rupture of the cyst & tension PTx.
Use regional/neuraxial where possible for opioid sparing
Equipment:
Pre-oxygenation: meticulous, effective to FiO2 >=80%
Position in reverse trendelenburg/semi-recumbent position to optimise FRC.
Resus: euvolaemic
Induction: aim to LIMIT APNOEA TIME (poorly tolerated due to low FRC), secure airway immediately after induction (use video laryngoscope to optimise first attempt success). lignocaine 1mg/kg 1 min before tracheal intubation may decr airway irritability during laryngoscopy/ETT/LMA. can use inhalation induction if no risk factors for pulm aspiration. consider awake technique if severe restrictive disease & need to avoid apnoea, esp if anticipate difficult BMV.
Maintenance:
Consider impact of mech vent & positioning on ventilation, perfusion, Pit. Limit risk of VALI (pts w restrictive vent defect particularly vulnerable).
Vt 6mL/kg with I:E 1:1 to 1:2 to minimise Pit (which decr VR & CO, risk baro & volutrauma & risk ALI/ARDS), PEEP initially 5, avoid >10 (risk hypoT, may worsen V/Q by redistributing Q from aerated lung to atelectatic areas, FiO2 titrated to maintain PaO2 >60mmHg & peripheral SpO2 >90%, RR titrated to maintain PaCO2 resulting in Ph 7.35-7.45 (or close to baseline PaCO2 if the pt has chronic resp acidosis); resp acidosis is a complication of low vol ventilation but incr RR without inducing auto-peep & reduce deadspace (eg. shorten ventilator tubing) may help. Humidification or low insp gas flows to prevent desiccation of resp secretions & limit atelectasis.
Adequate NMBD (titrate with NMT) facilitates coordination with ventilator-delivered breaths & minimises airway pressures, inhaled BDs in pts w reversible bronchoconstriction may further improve oxygenation & ventilation.
normothermia
normovolaemia (excess fluid accumulate in dependent lung, incr Paw & impair vent).
Positioning:
Supine reduced FRC esp with GA, reduced lung compliance, atelectasis, V/Q mismatch.
Lat decubitus: V/Q mismatch: perfusion incr but vent decr in dependent lung, FRC & compliance reduced. FiO2 may need to be incr. PEEP may help improve non-dep lung ventilation but avoid high PEEP. Also avoid high volumes of fluid which accumulate in dependent lung, incr Paw & impairs ventilation.
Prone, if abdo/lower ribs not free, may reduce pulm compliance & incr Paw, if abdomen compressed venous return to heart is decr & systemic & pulm vasc resistance increased. BUT if well-positioned, prone incr FRC, improves V/Q & oxygenation. Prone benefits of reducing the difference between the ventral & dorsal transpulmonary pressure, ventilation more homogenous, less dorsal alveolar collapse & ventral alveolar overinflation (as occurs with supine). Effects exagg in ARDS.
Sitting: lowest Pit, improved FRC and lung compliance as abdo contents fall away from diaphragm. Ultimate effect on oxygenation dependent on CO (tends to fall in sitting position).
Trendelenburg: incr VR, central blood volume, MAP. Cephalic movement of abdo viscera against diaphragm decr FRC & pulm compliance. can—> atelectasis, V/Q mismatch, shunt.
Reverse trendelenburg: pooling of blood in LLs, reduced central blood vol & VR decr SV & CO but relieves pressure of abdo contents on diaphragm/chest wall (incr FRC & pulm compliance)
Lithotomy: minor transient incr VR, cephalic displacement of diaphragm may result in decr FRC & pulm compliance.
Pressure areas if connective tissue disease (eg. systemic sclerosis, RA)
INTRAOP complications to anticipate which require rapid identification & treatment:
-clear & constant communication with surgeons re: times of risk (eg. insufflating pneumoperitoneum)
-hypoxaemia (eg. V/Q mismatch (atelectasis- Mx with incr PEEP to max 10; mucus plugging, ETT migration), diffusion impairment (eg. incr HR decr perfusion time), decreased mixed venous O2 content (anaemia, decr CO, incr O2 consumption (sepsis)), PTx/PE (consider if ass’d w hypoT), arrhythmias (these pts vulnerable due to hypox/hypercap/acid-base disturbances, SNS activation, frequent comorbidities eg IHD), exac PH (avoid factors that may incr PVR))
Emergence:
Position pt reverse trendelenburg, TOFR >0.9, adequate analgesia to limit splinting/atelectasis but avoid long-acting opioids or BZD.
Consider extubation when the pt is alert & cooperative and:
-PaO2 >60mmHg w FiO2 <0.5, not hypercapnia
-normal arterial pH (7.35-7.45)
-normothermia
-RR <20/min, not tachycardia or hypotensive
-VC >15mL/kg (unless the pt has a lower baseline)
-negative insp pressure >-20cmH2O
Consider extubating onto CPAP/NHF
POSTOP:
Recovery:
maintain close respiratory monitoring; sit upright to optimise FRC, consider weaning onto NHF or NIV to decrease WOB, reduce RR & decrease risk re-intubation
Analgesia/anti-emesis: opioid-sparing particularly avoiding long-acting sedative agents; regional blocks ideal, paracetamol & NSAID, opioid as rescue must be immediate-acting PRN with instructions to begin at the lower end of dose range titrated to optimise functional recovery & limit risk post-op complications eg. pulmonary/VTE (ie. need to facilitate deep breathing, coughing, incentive spirometry, limit atelectasis, facilitate early upright posture & mobility) & keep SS<2
anti-emesis multi-modal (eg. ondansetron +/- D2 blocker) & minimally sedating to facilitate early mobilisation & enteral intake
Warm: normothermic to limit MRO2
Disposition:
HDU, ongoing pulmonary monitoring, consideration of NIV, aiming to attenuate risk of requiring reintubation (rarely pts may require postop mech vent)
Follow-up: chest physio, resp physician, APS to ensure analgesia adequate with limited side effects
Consider chemical thromboprophylaxis once haemostats assured
Newies:
add in “SEVERITY/DISEASE CONTROL in Hx & risk stratify & under optimise, “if acute exac, delay” in pre-op
under maintenance, include intra-op complications to anticipate which require rapid identification & treatment
Under analgesia/anti-emesis, “if opioid it is immediate-acting PRN with instructions to begin at the lower end of dose range titrated to optimise functional recovery & mobility limit risk post-op complications eg. pulmonary/VTE. Anti-emesis multi-modal (eg. 5HT, D2 blocker) & minimally sedating to facilitate early mobilisation & enteral intake”
BT_PO 1.5: Describe the implications for anaesthetic management and perioperative risk of a range of medical conditions, including but not limited to:
EPILEPSY
What’s epilepsy? periop/anaes considerations?
A common (0.4-1%) disorder characterised by recurrent seizures (a predisposition to generate abnormal synchronous neuronal activity, disrupting normal brain function)
Dx is based on 2 unprovoked seizures @ least 24hrs apart. If pt has been seizure-free for 10 yrs off anti epileptics, no longer considered to have epilepsy. Several subtypes.
Preoperative:
Consult:
Hx:
Severity of epilepsy/disease control
-when was the last seizure
-type of seizure
-triggers (eg. infection/stress)
-seizure action plan
-management to date: medications, any recent changes, other treatments (eg. vagal nerve stimulator, surgery such as anterior temporal lobectomy or corpus callosotomy)
-associated conditions eg. TBI, intracranial mass, CNS infection, congenital conditions, CVA, metabolic disorder, NF-1, systemic sclerosis, down syndrome (epilepsy in 10%)
-Are there associated cognitive deficits that may impact on discussion of periop risks & informed consent?
Exam:
Neuro assessment to see if any focal deficits
Consider end-organ effects of medication regimen (eg. cardiovascular assessment- valproate ass’d w the metabolic syndrome)
Ix: electrolytes optimised, Hb optimised
Optimise:
Multi-D in liaison with Neurology
Medication compliance, consider drug levels & neurology consult if poor control (or if major GIT surgery, to establish baseline)
Electrolytes (esp Na), glucose, Hb, other medical conditions (eg. sepsis, dehydration, pain management/N&V) which may trigger seizure
Risk stratify:
Predict risk of periop seizure based on pt/surgical factors
ASA for well-controlled epilepsy? II
Plan:
action plan to be pre-emptively established in liaison with neurologist, in case intra-operative seizure occurs
book pt early on list, minimise fasting time, surgery daylight hours, ideally pts neurology team (or ability to consult) on-site, postop adult ICU in case required (with capacity for continuous EEG monitoring)
Continue all anti-epileptic medication throughout periop period; plan for medication to be administered intra-op on-time if prolonged surgery & understand requirements (eg. phenytoin requires separate line & filter). If potential interruption to resuming normal oral AED, consult neurologist for plan.
Explain:
discuss periop risks & minimisation w pt so shared mental model
verbal informed consent (if condition ass’d with cognitive impairment, may require 3rd party consent
Intra-op:
Goals= avoid risk periop seizure (airway & musculoskeletal risks, implications for pt eg. potential loss of license); maintain normal medication regimen & avoid potential triggers
Consider end-organ effects & drug interactions or complications of anti-epileptic regimen
-hepatic enzyme induction (carbamazepine & phenytoin CYP450 induction- increase metabolism & reduce drug levels (eg. antimicrobials, paracetamol, fentanyl) & inhibition (valproate—> CYP450 inhibition, reduce metabolism & increase drug levels). Some drugs incl antimicrobials may incr serum [] AEDs by inhibiting their metabolism, risking AED toxicity (metronidazole, ciprofloxacin)
-Carbamazepine 70% PB, reduces effectiveness of hormonal contraception, risks hypoNa (serum sodium should be monitored), N&V, diarrhoea, rash, fluid retention, SJS/TEN, BM suppression.
-Phenytoin 90% PB. Renal failure may incr free phenytoin [], pts with low Alb or use of highly PB drugs risk high free phenytoin levels. phenytoin risk hypoT on induction, needs separate line & filter. POBA 70%. Rapid admin brady/hypoT occ systole (rate <50mg/min, <25mg/min elderly), avoid extravasation (tissue necrosis), may cause hyperglycaemia in diabetics, risk rash, hypoCa, gingival hypertrophy.
-Levetiracetam has more reliable Pk, no hypoT on administration & doesn’t require serum monitoring, 100% POBA. Reduce dose in renal impairment. metabolism independent of CYP system (limited Pk interactions with other seizure meds, hormonal contraception). Fatigue, somnolence, dizziness, URTI, sedation, mood disturbance, SJS/TEN.
-Lamotrigine: 55% PB, clearance reduced in elderly so more adverse effects. hormonal contraception & HRT & pregnancy increase lamotrigine clearance. dose adjust in renal or hepatic impairment. non-CYP metabolism. adverse effects rash & nausea, SJS/TEN. pro-arrhythmic so avoid if cardiac conduction disorders or cardiac disease, pro-arrhythmic effect exac by use of other Na+ channel blockers.
-Topiramate minor liver metabolism, mostly elim in urine. serum levels decline in preg, reduces effectiveness of hormonal contraception. cognitive impairment, weight loss, paraesthesia, sedation, fatigue, mood problems, metabolic acidosis (esp in chn), renal stones.
-valproate: 100% POBA, tightly PB (90%), metabolised in liver, inhibit CYP system, adj dose if hepatic insufficiency, incr free [] in hypoalbuminaemia, OCP incr valproate Cl. if give IV, give over 60mins (<=20mg/min). nausea, vomit, hair loss, easy bruising, tremor, weight gain, obesity, insulin resistance, metabolic syndrome, thrombocytopenia & other coagulation disturbances, subclinical hypothyroidism, reversible parkinsonism. most teratogenic (cat D).
seizure management plan prospectively determined & communicated to team with drugs available
Monitoring: BGL, temperature, consider art line if want serial glucose/Na+ checks), NMT (esp as inducers of hepatic enzymes may cause resistance to amino steroid NMBDs)
Assistant:
Drugs:
Have pt’s anti-epileptic ready for administration if timing occurs intra-op (phenytoin, valproate, levetiracetam can be given IV, carbamazepine can be given PR)
premed BZD may be useful (anticonvulsant, attenuate surgical stress/anxiolysis).
Plan for comprehensive multi-modal analgesia (consider incorporating regional) as poorly controlled pain may trigger seizure
Medications to avoid in epilepsy:
alfentanil potently enhances EEG activity, tramadol, meperidine (lower seizure threshold); other opioids may lower seizure threshold but long Hx safe use in epilepsy.
some drugs are pro-convulsant @ low doses but anticonvulsant @ high dose (avoid etomidate or low-dose ketamine (anticonvulsant @ high doses))
avoid N2O (seizures in animals)
avoid enflurane
varenicline (partial nicotine agonist), ergometrine, cocaine
Equipment: good well-running IV access (& separate line if phenytoin)
Seizure rare under GA, may occur in high-risk pts with neurosurgery
Also difficult to diagnose under GA (esp. if muscle relaxants used). Signs: mydriasis, tachycardia, HTN, incr EtCO2, incr m tone, incr O2 consumption
Induction:
Pre-warm in anaesthetic bay
Pre-oxygenate to FiO2 >=80%
Induction & maintenance agent that raises seizure threshold (eg propofol- excitatory movements can be distinguished from seizure), volatiles raise seizure threshold (not enflurane)
All muscle relaxants safe (laudanisine issue with atracurium is theoretical), avoid suxamethonium after status epilepticus (risk hyperK)
LA is safe provided in safe dose range to limit toxicity
maintenance:
ventilate to maintain normoxia & avoid hypercapnia
normothermia
normal glucose & electrolytes & Hb
anti-emetic prophylaxis
multimodal analgesia
Emergence:
fully reversed, normoxia/capnia/tension/thermia
comfortable, anti-emetics
Periop-op complications to anticipate:
seizure- declare & inform surgeons so stop manipulation
100% O2, deepen anaesthesia, correct precipitating factors (hypoglycaemia, hypoxaemia, hypercapnia, hyponatraemia), consult w neurology & consider anti-seizure meds, EEG may help
Postop:
Recovery: ongoing goals to avoid seizures (warm, normoglycemia, normoxia & normocapnia, comprehensive analgesia & anti-emesis (promote PO intake & early return to enteral route for AEDs- conscious that dopamine antagonist may cause EPSE which may be mistaken as seizure activity- avoid metoclopramide, droperidol).
If seizure:
Airway support & patency
B: pulse ox & supplemental O2
C: NIBP, large bore IV x2
D: protect pt from harm, ideally recovery position
If not self terminate in 5mins, BZD in one line (midaz 0.1mg/kg (or 5mg/nostril nasal or 10mg buccal), diazepam 0.15mg/kg IV or max 10mg @ 5mg/min, lorazepam 0.1mg/kg or 4mg fixed dose
consider AED in other line if persistent seizures: phenytoin 15-20mg/kg, propofol 2.5mg/kg or thio (4mg/kg boluses), infusion if refractory
cardioresp Ax, emergency Ix (ABG/venous glucose, Ca++, Mg++, Na+, renal & liver functions, FBC, clotting screen, AED assay, toxicology. advanced investigations incl brain imaging depend on presentation)
Continuous EEG if seizure continues
Neurology consult
ICU for refractory cases (complications= CNS injury, hyperthermia, pulm oedema, arrhythmias, CV collapse, metabolic derangement, AKI, liver injury, rhabdo, fractures). RSI & mech vent if seizure persists beyond 30mins.
Convulsive status epileptics is a medical emergency, >30min continuous seizure activity or sequential seizures sans full recovery of consciousness. Start Rx after 5mins as spont recovery unlikely.
Pt informed & letter (impact on lifestyle eg. driving, work w heavy machinery), neurology follow-up.
Surgery for pts w epilepsy:
-implantation of intracranial electrodes (GA, avoid BZD to prevent abolition of epileptiform activity- intraop seizure activity is induced to identify seizure focus but this may precipitate generalised seizures; manage w cold saline to the exposed brain, 10-30mg propofol +/- anticonvulsant. Pt may then undergo telemetry monitoring postop to localise the focus before craniotomy & resection.
-resection of epileptic focus: multiple pre-op Ix to locate the focus, may have electrodes in situ. either GA or LA/“awake craniotomy” (if epileptogenic focus close to eloquent areas of the brain to allow cognitive testing & identification of critical functional brain regions).
BT_PO 1.5: Describe the implications for anaesthetic management and perioperative risk of a range of medical conditions, including but not limited to:
PARKINSON’S DISEASE
Parkinson’s disease= a progressive neurodegenerative disease due to central dopamine deficiency encompassing motor, neuropsychiatric & ANS features.
Pts are managed with a regimen of medications which may include MAO-B inhibitors (eg. selegiline), amantidine, dopamine agonists & levodopa (precursor to dopamine), given with carbidopa (a dopa decarboxylase inhibitor, to limit peripheral conversion of levodopa, allowing it to be maximally effective in the CNS)
Pre-op:
CONSULT:
History:
-severity/disease control & management regimen- severe disease may have become resistant to medications, may have DBS, may have continuous levodopa/carbidopa intestinal gel infusion through perc gastrojejunostomy tube
-need to know timing of doses as MUST be continued periop
-previous anaesthetics, airway alerts
-cognitive features if severe/advanced disease (dementia, psychosis/hallucinations, depression/anxiety)
-symptoms of ANS instability (postural hypotension-even in early disease. gastroparaesis (constipation), voiding difficulty, dysphagia)
-hypersalivation?
-pain & use of analgesics pre-op?
-other comorbidities (typically older adult)
Exam:
-high risk difficult airway
-may have TMJ & C-spine rigidity
-bulbar dysfunction (may have swallowing impairment/impaired airway reflexes making them vulnerable to airway obstruction or aspiration, compounded by risk oesophageal dysfunction &
gastroparaesis)
-hypersalivation
-may have thoracic kyphosis & chest wall rigidity (may have restrictive ventilatory defect)
-resting tremor?
-flexed posture?
-vital signs (particularly baseline BP, postural drop?)
Ix:
-general Ix specific to surgery
-PFTs may be useful to assess for restrictive airway disease & risk stratification for regional vs GA & to see if resp function requires optimisation pre-op
OPTIMISE:
-Multi-D, in liaison w neurologist particularly wrt disease control/med regimen
RISK STRATIFY:
PLAN:
-tertiary centre, in-hours, neurology available for consult/advice
-early am to limit fasting time
EXPLAIN:
-consider if the pt has cognitive dysfunction (may occur w severe disease) which may impair capacity to give informed consent
-allow time to discuss risks/plan carefully & give pt opportunity to ask questions/have them answered (if severe PD may have difficulty verbalising related to bradykinesia/slowness of speech vs cognitive impairment; writing may be micrographic. must be seen in clinic if procedure elective to allow time for appropriate assessment & discussion
-discuss risk of POCD
Intra-op:
main concerns:
NOT missing anti-parkinson medication (otherwise at risk of significant muscle rigidity/worsening of symptoms such as ANS dysregulation); time surgery so pt has them pre/post-op or insert NGT to give them intra-op, must be at their regular time.
risk difficult airway: carefully assess, make airway plans A/B/C prospectively & have equipment ready in room & plan clearly communicated with assistant.
Patient mobility/staff safety with transfers if pt has significant rigidity; consider manual handling & ensure adequate numbers of staff, slide sheets & padding for pressure areas when position patient with joints supported neutral
GA vs regional depends on pt/disease severity/fasting status/other co-morbidities (eg. severe restrictive resp pattern, airway difficulty, ANS stability) along with surgical factors eg. laparoscopic, urgency
Carefully titrated epidural with vasopressor useful if significant ANS instability but neuraxial may be difficult due to posture/tremor
Particular concern for opioid-sparing strategy (incorporating regional, paracetamol) if Hx chronic pain or significant restrictive lung disease
Monitoring: SpO2 probe may need to be earlobe or adhesive as tremor may impair readings, ecg readings may have interference. NIBP cuff may be unreliable w rigidity/tremors; may consider art line if particularly concerned re: ANS instability or comorbidities for reliable measure of haemodynamic status (access may be difficult). BIS to assist ensuring depth of anaesthesia not excessively deep.
Assistant: skilled, briefed on airway plan
Drugs: consider anti-sialagogue, opioid sparing/multi-modal incl regional, vasopressors to attenuate ANS instability, RSI plan
Potential drug interactions w PD meds: -MAO-Is: caution as increase catecholamine availability (side-effects HTN, tachy, serotonin syndrome; avoid serotonin potentiators (pethidine, tramadol, tapentadol (fentanyl & methadone to a lesser extent), indirect sympathomimetics (*selegiline less NAdr impact than non-selective MAO-Is so less ADRs) -Avoid dopamine antagonists (droperidol, metoclopramide, chlorpromazine) -risk muscle rigidity or dystonia w high-dose fentanyl or remifentanil
Equipment: IV access may be a challenge with tremor, consider US to facilitate, 2x secure IVs. Difficult airway equipment in the room.
If the pt has DBS, bipolar diathermy should be used where possible. if monopolar, lowest possible voltage & power settings. The ground plate should be as far from the neurostimulator & leads as possible. Otherwise no other modifications are required for GA or regional if DBS in situ.
Pre-oxygenation if GA: care w positioning w Tx kyphosis, optimise lung mechanics (upright to optimise FRC), consider anti-sialagogue
Induction: low threshold for RSI & videolaryngoscope given aspiration risk, bulbar dysfunction, sialorrhoea, gastroparaesis
Lung-protective ventilation
pressure areas, normothermia
Postop:
effective multi-modal analgesia (esp if Hx chronic pain)
multi-modal anti-emesis (5-HT, dexamethasone, 3rd line cyclizine) so can continue PO PD meds & aspiration risk
ensure PD meds are charted to be given on-time postop, via NGT until pt adequate PO intake
if pt has a DBS, check that it’s functioning as intended postop (may require neurologist or trained nurse specialist, dependent on local policy)
More prone to postop delirium; have plan for non-pharmacologic strategies to limit (quiet side room, promote normal sleep-wake cycles, adequate analgesia, reorientation strategies (eg. clock))
-consider HDU if procedure prolonged or significant comorbidit
+What are aetiologies of AS & the natural history of aortic stenosis? What are the key echocardiographic features in haemodynamically significant AS?
Aortic valve stenosis= the most common cause of LVOTO in adults & children. Less common causes= subvalvular & supravalvular disease.
Aortic valve sclerosis= aortic valve thickening w calcification without a significant pressure gradient; AS is present if the anteograde velocity across abnormal valve is @ least 2m/s.
3 primary causes of valvular AS:
1. congenitally abnormal valve (unicuspid or bicuspid, prone to calcification & narrowing, symptom onset 40-60yrs)
2. calcific disease of a trileaflet valve (age-related, symptom onset generally >65yo)
3. Rheumatic valve disease (fusion of commissures btwn leaflets, small central orifice, thickened leaflets. rheumatic process typically also involves MV so pt may have MS +/- MR)
Rare causes: radiation, metabolic diseases, SLE, Paget disease, ESRD.
Natural Hx:
Latent phase: typically long symptom latency period with significant, though initially clinically silent, progression of reduction in AV area (average reduction 0.1cm2/yr, peak jet velocity 0.3m/s per yr, avg increase mean systolic PG 3-7mmHg/yr)
Normal aortic valve CSA 3-4cm2 in adults; antegrade velocity remains normal & there’s minimal valve gradient until orifice area < half normal.
Accelerating factors= valve area & jet velocity, calcification, older age, male sex, dyslipidaemia, renal insufficiency, hypercalcaemia, smoking, metabolic syndrome, DM, cause (uni>bicuspid>tricuspid)
Compensation phase: The stenotic process is gradual in onset & progression; LV adapts through initially concentric hypertrophy to maintain normal wall stress (=delta P x r / 2w) & O2 demand in response to increased systolic pressure. When compensated, EF, CO & LVEDV remain normal; diastolic dysfunction may develop (ventricle becomes preload & rate dependent)
Decompensation phase: With progressive stenosis, LV faces progressively increased afterload; continues to hypertrophy but becomes less compliant, LVEDP increase, LV may dilate which increases wall tension & O2 demand.
Abnormal diastolic function contributes to symptom onset (exertional angina from myocardial demand (incr wall tension)>supply (reduced radius intra-mural coronaries, reduced aortic diastolic pressure), dyspnoea a combination of pulmonary congestion with LV failure & reduced output (ejection fraction) from in-coordinate contraction which may result from regional wall motion abnormalities, fibrosis or subenocardial ischaemia, pre-syncope/syncope related to reduced aortic diastolic pressure)
Survival excellent during prolonged asymptomatic phase. Once symptoms develop, mortality exceeds 90% within a few years (AVR prevents this rapid downhill course)
When patient’s develop heart failure, mean survival 0.5-2.8yrs, syncope 0.8-3.8yrs, angina 2-4.7yrs. Angina, 5 year survival. dyspnoea 1-2 year survival, syncope 3 year survival.
Compared to general population, mortality not significantly increased in asymptomaatic AS or for those who received and AVR.
-Stages of AS are defined according to whether or not the patient has cardiac symptoms, valve haemodynamics on echo and haemodynamic consequences.
Generally, symptoms in patients with AS & normal LVEF rarely occur until the stenosis is haemodynamically significant (ie. “severe”), some pts may develop symptoms with milder degree of AS esp if AR. Most pts develop symptoms prior to reduction in LVEF:
Stage A:
“at risk” is bicuspid or sclerotic valve with Vmax <2m/s & no haemodynamic consequences or symptoms
Stage B:
“progressive” is calcification of valve with some reduction in systolic motion or if rheumatic, commisural fusion. features of mild or moderate AS on echo (Vmax 2-29.m/s, mean PG <20mmHg) for mild. There may be early diastolic dysfunction but normal LVEF.
Stage C1: asymptomatic severe: severe calcification/leaflet opening, severe valve haemodynamics, haemodynamic consequences of LV hypertrophy & diastolic dysfunction but normal LVEF. while asymptomatic, exercise testing is reasonable to confirm symptoms. C2 is asymptomatic severe with LV dysfunction (LVEF <50%)
Symptomatic severe will have symptoms including:
D1: symptomatic severe high-gradient: Decreased exercise tolerance or exertional dyspnoea, exertional angina, exertional syncope or pre-syncope; LV diastolic dysfunction & hypertrophy +/- pulm HTN (there may be mixed AS/AR with AVA >1.0cm2), LVEF maintained
D2: symptomatic severe low-flow low-gradient with reduced LVEF (LVEF <50%): AVA severe grading but PG <40mmHg, Vmax <4m/s. These pts have HF symptoms, angina & syncope/pre-syncope
D3: symptomatic severe low-gradient AS but normal LVEF: incr LV wall thickness, restrictive diastolic filling, small LV chamber & low SV but LVEF may be >=50%. HF, angina, pre-syncope or syncope.
Severity of valve haemodynamics on echo:
AS becomes haemodynamically significant when there’s an increased impedance to LV ejection. The haemodynamic consequences relate to presence of diastolic dysfunction (E/A reversal; E (peak velocity of blood flow from LV relaxation in early diastole) < A (peak velocity flow in late diastole caused by atrial contraction)
*mild AS is AVA >1.5cm2, mean gradient <20mmHg, peak velocity 2-2.9m/s
moderate AS: AVA 1-1.5cm2, MG 20-39mmHg, peak velocity 3-4m/s
(may have early diastolic dysfunction but LVEF preserved)
severe AS: AVA <1cm2, MG >40mmHg, peak velocity >4m/s
Once AS severe on echo, there’s hypertrophy & LV diastolic dysfunction +/- reduced (<50%) LVEF
very severe Vmax >5m/s, MG >=60mmHg
critical AS: AVA <0.5cm2
Aortic valve area can also be indexed to BSA (mild >0.85, mod 0.6-0.85, <0.6)
Peak aortic jet velocity is the strongest predictor of clinical outcome (ass’d w death or valve replacement)
If a patient has severe AS but low gradient due to reduced LVEF, the DPI may be useful; ratio of LVOT:aortic root velocity, <0.25 corresponds to AVA <0.75cm= severe AS.
Other haemodynamically significant features include:
-qualitative assessment of valve morphology/leaflet excursion
-L) atrial dilatation (significant as predisposes to atrial arrhythmias, poorly tolerated by a poorly compliant, hypertrophied preload-dependent ventricle)
-Pulmonary hypertension may develop, particularly if associated aortic or mitral regurgitation; estimate by calculating RVSP using tricuspid regurgitant jet velocity, significant as puts the R) ventricle at risk of dilation and dysfunction.
-regional wall abnormalities
-post-stenotic aortic root dilatation.
What’s platypnea-orthodeoxia syndrome?
dyspnoea/deoxygenation when going from supine to upright.
Due to R)—> L) shunt (ASD or PFO) accompanied by a rarer condition eg:
cardiac: pericardial effusion/ constrictive pericarditis/TR
pulmonary: hepatopulmonary syndrome, multiple pulm emboli, pulmonary emphysema, amiodarone toxicity, fat embolisation syndrome, radiation-induced bronchial stenosis
autonomic: parkinson’s
abdo: hepatic cirrhosis, ileus
There is failure of the correction of hypoxia with 100% oxygen. upright has dioxia on PaO2, bubble study on TOE (bubbles in LA within 2-3 cycles of initial appearance in RA)
Mx by closing ASD or PFO, treating any associated condition
What’s postop delirium & how to manage it?
periop neurocognitive disorders encompasses a variety of diagnoses incl:
-persistent or recurrent delirium persisting beyond transient “emergence” from GA
-delayed neurocognitive recovery (cognitive decline not due to delirium Dx up to 30 days after a procedure, ass’d w major procedures or medically complicated postop recovery)
-major or minor neurocognitive decline persisting or diagnosed up to 12 months postop.
For POSTOP DELIRIUM, there are 2 distinct categories:
-emergence delirium: transient (agitation or excessive somnolence, rapidly resolves after emergence).
-persistent or recurrent: acute change that persists or reoccurs after emergence. characterised by impaired attention & altered level of consciousness (agitation/hyperexcitability/disinhibition/crying/restlessness, confusion or hypoactive type: excessive somnolence w impaired mental status.
pre-op cognitive impairment & postop delirium are ass’d w development of dementia within 5 yrs of surgery.
Risk factors:
Pt:
older age
pre-existing cognitive impairment
other sensory impairment
immobilisation
dehydration
hyponatremia, hypoglycaemia
sleep deprivation
ICU admission
critical illness + elderly
preop sleep disruption
excess ETOH
polypharmacy or psychtropic drugs
severe vascular disease, DM or prev CVA/TBI
Frailty
lower educational level (higher education level cognitive reserve)
Procedure:
major (cardiac, major ortho, major head & neck, colorectal)
prolonged surg/anaesthesia
Anaesthetic:
research conflicting re: whether anaesthesia-related factors are clinically significant & there are multiple confounders (stress response, hypox, hypotension, hospitalisation)
HOWEVER:
-avoid excessive depth (no causal relationship established, anaes depth age-adjusted (age decr MAC); monitor MAC age-adjusted or BIS; avoid low PEEG numbers or burst suppression on raw trace
-Avoid excessive sedation during RA (however in hip # pts w spinal + IV propofol had similar incidence delirium if light vs heavy sedation)
*interestingly, GA vs neuraxial vs regionalal anaes w light, deep or no sedation doesn’t consistently decr incidence of delirium or other PND, demonstrated w large RCTs over a range of surgeries (hip fracture, lumbar spine, ESWL)
-TIVA vs volatile based doesn’t impact risk delirium HOWEVER in PAEDIATRICS, emergence delirium IS less likely to occur after TIVA vs inhalation-based anaesthetic techniques.
-minimise IV agents ass’d w incr risk delirium in high-risk pts (BZD, gabapentinoids, opioids (age-adj doses based on ideal body wt & use opioid-sparing techniques HOWEVER uncontrolled pain also a risk for delirium SO individualise, titrate & supplement w other agents to effect). care w ketamine dosing; the psychomimmetic side effects may present as emergence delirium (hallucinations, nightmares, vivid dreams) but it is useful for it’s analgesic, opioid sparing properties; dose carefully).
avoid other agents which may risk postop delirium (anticholinergics, metoclopramide, agents causing hypoglycemia, baclofen, corticosteroids, dopamine agonists); worth knowing that clonidine, B blockers or drugs that may uase serotonin syndrome (eg. tramadol) may risk delirium in vulnerable pts.
-Avoid excessive swings in BP- avoid hypotension or hypertension, keep within 20% baseline, MAP>=65mmHg & SBP >=100mmHg for most pts
-if using cerebral oximetry, avoid rSO2<65% (ass’d w delayed post-op neurocognitive recovery & delirium
-IV paracetamol may be ass’d w reduced delirium
-dexmed infusion may reduce risk agitated emergence delirium
Approach:
PRE-OP:
identify @ risk pts (MiniCog: 3 words, clock drawing with all numbers & set hands to 10 past 11 must do within 3 mins, 3 word recall)
cutoff <3 points (1 point for each word RECALLED, normal clock 2 points)
Dx of dementia (eg. on donepezil or memantine), PHx cognitive impairment postop
Some centres offer cognitive prehabilitation (cognitive exercises, avoiding high risk IV agents, avoid excessive anaesthetic depth, hypotension or cerebral desat, planned postop strategies eg. identifying & avoiding problematic med interactions) however evidence re: reducing POCD or delirium risk is scant
If cognitive impairment identified or concern re: pts understanding of consent process, involve 3rd party. warn re: risk exac cognitife function & planned preventive strategies.
INTRA-OP:
principles above, eg:
optimise medically (electrolytes, analgesia, anaemia), limit fasting time
intra-op multimodal opioid-sparing, limit depth, avoid BP outside 20% baseline
avoid meds incr risk (eg. BZD, gabapentinoids)
postop:
adequate analgesia (if opioids, rapid-acting titratable)
normalise physiology incl normoxia, glucose & temp, hydration, electrolytes
encourage normal sleep:wake cycles
non-pharmacological: clock, familiar people/items, frequent re-orientation, avoid excess light/noise, out of bed during day as able, optimise sensory status (eg. glasses, hearing aids), early mobilisation, remove lines/drains/restraints
If ICU, particular effort to sleep:wake cycle
multi-D imput bundled care may reduce incidence
identify: screening for delirium eg. 3-minute diagnostic assessment (3D-CAM)
Manage any reversible causes (eg. ETOH withdrawal)
if persistent or severe delirium, neuro consult (although acute intracranial event is rare). Delayed recovery consider geriatric neurologis or memory clinic referral.
Delirium @ time of PACU D/C predicts persistent delirium later in postop course, worse outcomes (eg. LoS, D/C to nursing home, mortality, greater decline in functional status, ongoing cognitive decline or dementia esp if elderly), hospitalisation itself can accelerate trajectory of preexisting cognitive decline or dementia.
IT_PO 1.1: Outline the ASA physical status classification system and the implications for anaesthesia
Grading system developed >70yrs ago
predict periop risk
based on Anaesthetist’s subjective assessment of severity of comorbidities & impact on function
performs well as predictor of complications, mortality & LoS but highly subjective, only moderate inter-rater reliability
incidence death ass’d w anaes is 1:100,000 for ASA 1-2, 5-10x higher for ASA3-4 &/or emerg OT
adding E= emergency
ASA1= normal healthy pt. Non-smoker, little or no ETOH
ASA2= mild systemic disease with NO substantive functional impairment
BMI >30<40, preg, well-controlled HTN or DM, social ETOH, smoker, mild lung disease
ASA3= severe systemic disease & substantive functional impairment
BMI >-40 prem infant <60/40pca
poorly controlled HTN or DM
COPD
MI/stents/CAD/CVA/TIA >3/12 ago
ICD/PM
moderately reduced EF
active hepatitis
ETOH abuse/dependence
ESRD controlled w haemoialysis
CF
Hx organ transplant
autism w severe limitations
difficult airway
PET w severe features
GDM w high insulin or complications
thrombophilic disease requiring anticoagulant in pregnancy
ASA4= severe systemic disease, constant threat to life
ongoing myocardial ischaemia, severe valve dysfunction
MI/TIA/CVA/stents <3/12 ago
CKD no dialysis
sepsis, DIC, severely reduced EF
V= moribund, not expected to survive 24hrs sans OT eg. ruptured aneurysm, intracranial bleed w mass effect, maj trauma, bowel ischaemia w severe cardiac pathology
MODS
VI= DBD, OT for organ donation
IT_PO 1.2: Outline the functional assessment of patients based on exercise capacity and performance of activities of daily living& IT_PO 1.3: Outline the functional assessment of patients based on exercise capacity and performance of activities of daily living
Functional capacity= the ability to increase & sustain tissue O2 delivery
important to determine functional capacity as major surgery can increase O2 demand by up to 40% (ie. w major open cavity surgery, O2 consumption can be 5mLO2/kg body wt/min, if reduced functional capacity & global O2 delivery, prone to adverse periop outcomes w surgical stress (need to sustain incr O2 requirement several days postop after major O2)
Functional assessment helps predict suitability for surgery- risk stratification, may prompt prehabilitation/other prep optimisation. Pts w good functional capacity generally have good perio outcomes irrespective of presence of stable CAD or risk factors. unlikely that additional periop testing will be of benefit to pts w good functional capacity.
Subjective assessment, “METs” based on ADLs widely used but poor agreement w validated questionnaires & inconsistent ass’n w post complications (METs study showed it’s got poor prognostic association w 30-day mortality & MI in pts undergoing major non-cardiac surgery, poor correlation w peak O2 consumption on CPET). pts may overestimate their exercise capacity. low NPV (incorrectly classifies many pts as having low functional capacity).
one MET is equivalent to resting O2 consumption of a 40yo 70kg male (3.5mLO2/kg/min). >=4 METs thought to be ass’d w less adverse outcomes after high-risk surgery.
1-4METs: eating, dressing, dishwashing, walking around house
4-10= climbing 1 flight stairs (4METs), walking flat 6kph, brief running, golf, heavy housework
>10 strenuous sport, swimming, footy
METs form part of ACC/AHA guidelines; if elevated risk MACE & <4METs or unknown METS & if Rx thought to change outcome, could do pharmacologic stress testing
DASI 12 measures functional capacity, prognostic info re surgery risk: Has construct validity (measures what it’s supposed to) as a measure of functional capacity
METs study main findings (lower DASI ass’d w the primary outcome, death or MI within 30 days of major non-cardiac surgery)
DASI >=34 cutoff
6MWT= simple measure of aerobic exercise capacity, from ATS. just need a stopwatch & 30m unimpeded walkway. >563m suggests anaerobic threshold 11mL/kg/min. distance walked correlates well w peak VO2 max & max work capacity; cheap & easy. Poor NPV, effort-dependent, some pts can’t do.
CPET= an objective, NON-INVASIVE test of O2 uptake, cardiopulmonary & circulatory function @ rest, during incremental exercise & during recovery.
Considered the gold standard, most reliable & objective measure of functional capacity.
AT is a useful measure as it’s effort independent. varies <10% on repeated testing. doesn’t vary w age but reduces in proportion w degree of organ impairment.<11mL/kg/min & ischaemia on ecg ass’d w 43% periop mortality (only 5.5% if no ecg changes).
peak O2 consumption 14mL/kg/min equivalent to 4METs.
useful for:
1) risk stratification (predicting periop mortality & morbidity (in METs study, lower peak O2 consumption predicted readmission rates, SSI, unplanned ICU admission, postop pulm complications; survival & postoperative cardiopulmonary events correlate w peak O2 consumption), 2) informed decision making re: periop management incl risk reduction, 3) planning disposition incl HDU 4) Dx resp & cardiac diseases (incl occult); parameters eg. VO2max can increase w training so CPET can be used as Ax/re-Ax in prehab
more cost/labour intensive, need treadmill or static bike, 2. computer controlled ramped incr workload, 3. pneumotachograph for gas flow & composition 4. continuous 12-lead ecg & pulse ox 5. trained operators (one w pt, one for monitoring/running the test), resuscitations facilities.
some absolute CIs: severe symptomatic AS, SBP >200, sig pulmonary HTN, decamp CCF
NT-pro BNP predicts 30 day myocardial injury or death & 1 year mortality (METs study)
NYHA functional classification commonly used as fundamental descriptor of heart failure however class II vs class III unreliable predictor of adverse outcomes in HF, poorly discriminates functional impairment, however in periop cardiac assessment, decompensated heart failure classed as an indicator for diagnostic evaluation & Rx.
ACC/AHA hypertension classifications
normal is SBP <120 & <80mmHg
elevated is 120-129 & <80
stage 1 130-139 & 80-90
stage 2 >=140 & >=90
hypertensive crisis SBP >=180, CBP >=120mmHg
pulmonary embolus
obstruction of pulm artery or one of its branches by thrombus, air, fat, tumour that originated elsewhere.
Pathogenesis is similar to DVT; most emboli arise from LE proximal veins (iliac, femoral, popliteal) but they may originate in R) heart, IVC or pelvic veins or renal/UL veins.
presentation= wide variety of presenting features; from no symptoms to shock/sudden death.
MOST COMMON presenting symptom is dyspnoea. chest pain, cough, VTE symptoms.
Dx approach combines haemodynamic Ax, clinical & pretest probability assessment, D-dimer & definitive Dx imaging (CTPA or V/Q).
haemodynamically unstable PE= SBP <90mmHg or drop SBP >=40mmHg from baseline for >15 minutes; these pts are more likely to die from obstructive shock within 2hrs of presentation so may benefit from more aggressive Rx.
Initial resus:
ABC
O2 targeting SpO2 >=90%, I&V if severe hypoxaemia, haemodynamic collapse or respiratory failure.
IV access with cautious IVT.
TTE: Pts who are haemodynamically unstable w definitive Dx presumptive by bedside echo (eg. CTPA unsafe), systemic thrombolysis followed by anticoagulation
if contraindication to thrombolysis, surgical embolectomy
Haem stable, consider 3-tiered pre-test probability:
1. Calculate Wells score:
<2 low prob
2-6 moderate
>6 high
- PERC (age, HR, SpO2, haemoptysis, oestrogen, prior DVT or PE, unilat leg swelling, surgery/trauma within 4 wks). If fulfil all 8, no further test, otherwise:
- D-dimer: >=500ng/mL, diagnostic imaging (*DDx high D-dimer: thromboembolism (DVT, PE, DIC, MI, CVA, limb ischaemia), inflammation (sepsis, severe infections, COVID), surgery, liver or kidney disease, malignancy, sickle cell vaso-occlusion)
- Imaging; CTPA= preferred Dx, >90% sens & spec, highest (>=96%) S&S when CTPA combined w mod-high probability Ax for PE. 10mSV. caution if eGFR <30, mod-severe iodinated contrast allergy (consult radiology & immunology; approach depends on whether the reaction was mild/mod/severe & allergic-like (urticaria, wheeze, hypoT) vs physiologic (n&V, vasovagal, HTN), consideration of pre-med CS +/- antihistamine, alternative Dx test (incl CT sans contrast)or pesumptimve Rx, counselling pt & proceeding w resus facilities. Those @ risk CIN (eg. eGFR <30), 1ml/kg/hr for 6-12 hrs pre-procedure & 6-12hrs post-procedure. isotonic saline. NAC or Na bicarb not evidence-based.
Haem stable mainstay of Rx= anticoagulation, depending on bleeding risk (eg. age, Ca, renal or liver failure, antiplatelets, frequent falls, ETOH abuse)
Wells=
haemoptysis
HR >100
prev Dx DVT/PE
PE most likely Dx
S&S DVT
immobility 3/7 or OT within 4/52
Malignancy w Rx within 6/12 or palliative
Other clinical tests: ecg, CXR (may show “hampton’s hump wedge opacity, Westermark hyperlucency due to oligaemia distal to a vessel occlusion, BNP & trops (none are sens nor specific for PE, used for prognosis/considering other diagnoses)
if low risk, no risk factors, do anticoagulant epirically IF Dx eval will take >24hrs.
if high risk >=2 risk factors, don’t; if high bleeding risk/CI to anticoagulants, IVC filter.
moderate risk case-by-case basis. other Rx= thrombolysis, IVC filter or embolectomy.
haemodynaically stable pts with moderate clinical suspicion for PE & low bleeding risk, empiric anticoagulation if Dx will take >4hrs)
generally not thrombolysis or catheter therapies if haem stable & submassive PE (sPESI I or II (age >80, Hx Ca, COPD, pulse 110, SBP 100, SpO2 <90)).
CI thrombolysis: absolute: prev ICH, knwon cerebral vascular lesion, malignant intracranial neoplasm, ischaemic stroke 4.5hrs-3/12, aortic dissection, active bleeding/diathesis, significant closed head or facial trauma within 3/12). relative= severe uncontrolled HTN, traumatic/prolonged CPR, recent internal bleeding.
All pts are anti coagulated for minimum 3/12. thrombolytic therapy considered if warranted by clinical therapy), if not improved & warranted, surgical or catheter embolectomy.
For pts w first VTE, if persistent but reversible risk factors, continue for a finite period. for pts with high estimated risk of recurrence but not high bleeding risk, consider indefinite antigcoagulant (reduce lifetime risk of recurrent VTE by 80%+), eg. recurrent VTE without identifiable risk factors, VTE w active Ca & no other major provoking event, pts w VTE & high-risk prothrombotic conditions (APLS, anti-thrombin deficiency)
For most pts, LMWH, rivaroxaban or apixaban.
choice based on pt factors: if Ca, LMWH or factor XA. liver disease, use LMWH (DOACs contraindicated if INR raised due to liver disease, VKA difficult to control). if renal disease w CrCl <30, VKA (DOACs & LMWH contraindicated w severe renal impairment). if thrombolysis, use UFH. if pregnancy, LMWH.
Dabigatran is parenteral for >=5 days then 150mg BD. If CrCl 30-50, age >75 & risk major bleed, 110mgBD.
rivaroxaban 15mg BD for 21 days then 20mg daily
apixaban 10mg BD for 7 days then 5mg BD. prevention 2.5mg BD after >=6/12 Rx.
All pts have adjunctve therapy: early ambulation.
Untreated, PE has overall 30% mortality.
PE may be complicated by recurrent thrombosis, chronic thromboembolic pulmonary HTN, death. RV dysfunction—> clinical shock. also predicts risk of recurrent VTE.
Pregnancy: no validated clinical prediction guidelines or pretest probability tools. Give all pts a CXR. If CXR normal, V/Q. if V/Q indeterminate or CXR abnorm, CTPA. Risks of radiation from V/Q & CTAP &ionidated contrasta are low (however CTPA 7.4 vs 0.9mSv maternal radiation). Foetal exposure 100-200x < the dose thought to risk foetal anomalies. Iodinated contrast does enter foetal circ, concern re: thyroid, in vivo very low risk. Gadolinium has been shown to be teratogenic in animals.. calf US can be used to avoid lung imaging. &confirm DVT if LL signs.
What are the periop risks for pts w OSA?
Mx
Anaes agents & sedatives:
incr pharyngeal collapse by reducing tone
decr vent drive
decr CO2 response
UAO out of proportion to sedation (exagg sensitivity to sedatives)
paeds OSA more related to anatomical abnromalities 0.5mcg/kg opioid incr apnoeas by 50%
Severe OSA higher risk cardiovasc complications postop (incl CVA, TE, MI, CCF, new AF, cardiac death). OSA incr risk pulm complications (pneumonia, unplanned intubation), unplanned ICU admission, sepsis.
May have pulm HTN but generally not severe
PRE:
Hx/exam/Ix
-May be difficult airway (difficult BMV, intubation or combo). 50-60% of pts w difficult airway have severe OSA. HOWEVER just having OSA doesn’t mean difficult to intubate (poor evidence); thorough airway exam, prev charts
able to lie flat
-functional capacity
Intraop: SSM guidelines
diff airway Mx precautions (lack of evidence)
regional where possible (this does not have strong evidence, lack of control for confounders)
Cardiostable anaes w art line, maintain haemodynamic goals postop
opioid sparing, muti=modal
incr risk residual NMBA- TOFR reverse to >0.9
consider postop OSA CO2 monitoring
“overlap syndrome”= pts w both osa & another type of airways disease more prone to aw obstruction/desats
AHI worst 3rd postop night (since the pts don’t sleep as much); REM just returns to preop levels then (ie. it’s not worse than preop nec).
If high risk eg. chronic pain, APS plan/documentation (pre-op)
plan disposition (chart looking at surgical & OSA risk factors); limits cancellations/confusion on the day
HDU only for: severe OSA sig OT, no CPAP or can’t use it (eg. H&N surgery) or if other sig comorbidities.
other pts w mod severe OSA & lesser OT. overnight oximetry & line-of-sight nursing.
Who needs further Ix?
How to Ix further?
Pts w stopbang 4+ (probability incr)
Ix useful for risk stratification, considering that significant false +ve rate of STOP BANG
reasons for Ix: periop risk reduction pre- intra- post- (treating everyone as if they have OSA resource-intensive), long-term health benefits OSA Mx (less MVAs, less CVD)
role of periop CPAP?
Untreated OSA significant risk of any cardiac compns, AMI, reintubation while TREATED OSA the same as those sans OSA!
periop CPAP significantly reduces postop AHI
So.. ASA recommends preop institution of CPAP, esp if OSA severe (cat B1 evidence). if inadequte response, NIPPV.
how to screen in clinic
conditions related to OSA?
STOPBANG (rated as having excellent screening for severe osa, unacceptable FN rate for Dx OSA (misses 1 in 6 pts w severe OSA)
if not urgent/time critical, sleep studies
OVERNIGHT OXIMETRY GENERALLY POSSIBLE within a week @ major tertiary hospital; easier, quicker, cheaper & reasonable correlation w gold standard psmn (Se 76 vs 75, Sp 93/97
Has been validated as a reasonable alternative
disease associations:
First degree relative w OSA 1.5-2x as likely have OSA
smoking/COAD
ETOH
CVD, RHF
Obesity
T90 significant on polysomnography?
> 5%; burden of hypoxia significant
Reducing risk VTE:
Pre-op:
Risk stratify (eg. carpini score, considers pt (eg. age, recent CHF/sepsis/pneumonia/immobilising cast, LL FRACTURE, STROKE, MULTI-TRAUMA, ACUTE SCI W PARALYSIS, CLOTTING DISORDERS & surgery factors (eg. major >45 mins, LL arthroplasty)
Factors as per Virchow’s:
-stasis (eg. dehydration, immobility, venous insufficiency)
-hypercoag (malignancy, OCP, thrombophilias)
-inflammation (smoking, chemo, stroke)
personal or FHx also confers risk as does older age
address modifiable risk factors (smoking, weight loss, consider delay non-essential surgery until 3/12 PN, consider cessation OCP (barrier), anticoagulatnt advice.
minimise fasting time esp fluids, consider IVT.
consider canal filter (no evidence for primary prophylaxis)
ideally no surgery within 3/12 of VTE
emergency surgery, consider bridging anticoagulation
enc mobility
if prol inpt stay, pharm vte prop (anh high risk, carpini >=5 points, >=1.8% VTE risk
mod/low risk risk mechanical/non-pharm measures
postop prophylaxis once haemostats assured:
0.5mg/kg BD LMWH (generally 40mg sublet daily provided CrCl>30mL/min), UFH 5000 BD, subcut
DOACS are superior to enoxaparin for VTE prevention after ortho surgery without incr bleeding complications; prophylaxis dose apixaban 2.5mg BD, rivaroxaban 10mg daily. dabigatran: 150mg BD for knee, hip 220mg daily
Prehabilitation:
may shorten LoS & reduce risk postop complications in pts w HF for intra-abdo & Tx surgery.
Unclear what type of exercise & duration but commence while awaiting elective surgery.
powerpoints:
red= UPS
blue= generator backup (outage until generator kicks in)
white; no power in an outage (eg. “cleaning only”)
Sickle cell
multisystem disease
one of the most common serious inherited single-gene conditions worldwide
A substitution on the beta globin gene (so get HbS, which is alpha2,Bs2). HbS is not as effective @ changing shape when O2 binds to facilitate further O2 carriage. MAIN PATHOPHYS IS THAT HbS TENDS TO FORM POLYMERS WHEN DEOXYGENATED, CAUSING RBCs TO DEFORM INTO SICKLE SHAPE.
Altered red cell membrane–> incr adherence to vascular endothelium–> vaso-occlusion, ischaemia-reperfusion injury & end organ damage.
Haemolysis–> anaemia
vascular endothelial damage–> stroke/pulm HTN/priapsim
vaso-occlusion–> acute & chronic ischaemia, acute pain crises, end-organ damage
Homozygous (sickle cell anaemia, HbSS) or compound heterozygous state with another abnormal Hb, eg. B-thalassaemia)
Heterozygous carrier (HbAS)= mostly benign, only relevant @ extremes of physiology (eg. severe sepsis)
HbSS, HbS-thalassemia & HbSD ass’d w severe sickle cell disease, early onset severe pain crises, severe anaemia (typical Hb 60-90g/L)
Pts w higher HbF levels tend to have milder phenotype; hydroxycarbamide raises the HbF level & is recommended as therapy for most pts.
HbSC typically higher Hb & few symptoms but if require blood transfusion when acutely unwell, often need exchange transfusion (higher Hb)
Screening= sickle solubility test. if +ve, full haemoglobinopathy screen (detects if homo/hetero for HbS or other haemoglobinopathies.
chronic haemolytic anaemiaA
painful vaso-occlusive crises
acute & chronic end-organ damage
susceptible to periop infections
Pts may present for OT for complications of sickle cell disease (cholecystectomy, splenectomy, tonsillectomy, hip replacement, bone or joint infection) or incidental
Main periop issue: pts are @ incr risk of sickle complications (acute chest syndrome, acute pain crisis, acute renal insufficiency, stroke), sepsis & VTE perioperatively, most complications occur postop (low threshold to admit to HDU).
Pre:
-ideally in PAC
-seek advice from sickle cell haematologist who is responsible for deciding the periop transfusion plan; they need to be informed if pt w sickle cell disease is admitted for emergency surgery
-Lab needs to be aware that any samples sent are from a sickle cell pt
-OT @ centre w experience managing these pts. Pregnancy= incr risk so manage w a multi-D team @ a centre able to manage high-risk pregnancies & sickle cell complications
-these pts are @ higher risk of COVID-19 infection but may have relatively mild clinical course
-Schedule pt early on the list (avoid prolonged starvation)
Screen for acute sickle-related complications (chn/adults):
CNS:
-STROKE in up to 10% of chn! regular trans-cranial doppler screening (check results before elective surgery)
“silent” infarction in 40% of adults on MRI, may be ass’d w cognitive impairment.
-ACUTE PAIN CRISES: fingers in infants, long bones/sternum/ribs/back in older chn & adults; on chronic pain meds?
AIRWAY:
-ADENOTONSILLAR HYPERTROPHY: OSA, sleep disordered breathing, nocturnal hypoxia]
RESP:
-ACUTE CHEST SYNDROME: New-onset resp symptoms (chest pain, fever, tachypnoea, cough, wheeze) & new pulmonary infiltrates on CXR- common complication postop
IMMUNE:
-APLASTIC CRISIS: commonly if parvovirus B19 infection (or EBV or strep), aplasia for 5-10 days
-HYPOSPLENISM: in first few years of life due to repeated vaso-occlusion & splenic infarct
-ACUTE SPLENIC SEQUESTRATION CRISIS: may be life threatening in 5/12-2yo, splenomegaly, acute anaemia (10-30), hypovol shock
PRIAPISM
Chronic sickle-related complications in adults:
-RENAL:
hyposthenuria (low urine osmolality)
proteinuria (40% adults)
renal insufficiency (20%)
-CARDIORESP:
OSA; check re: symptoms/STOPBANG
chronic lung disease (restrictive common)
CCF
Pulm HTN (6% adults)
-ORTHO:
AVN femoral head
osteomyelitis
surgical:
cholelithiasis
erectile dysfunction
Ophthal:
retinopathy
dermatological:
leg ulcers
Infection:
-GN sepsis (UTI, biliary)
Transfusion related:
Acquired rbc antibodies
Fe overload
neutropaenia (due to hydroxycarbamide Rx)
hyperhaemolysis
Exam:
baseline SpO2
overnight sleep study if suspicion OSA
echo if symptoms suggest pulm HTN
transcranial doppler results from within 12 moths if HbSS (if abnormal, multi-D discussion re: Mx).
Ix:
FBC, urea, electrolytes, G&H with full red cell antibody screen preop
if pt has had transfusion within 3/12, a repeat FBC & antibody count required <72hrs of the OT.
Make it clear on the form that the pt has sickle cell disease. may need to order in specific blood for that pt (even if bleeding risk low).
Consider any TRANSFUSION IN LIAISON W HAEMATOLOGY:
benefits= incr O2 carrying capacity, suppress haematopoiesis of sickled cells, reduced risk vaso-occlusion as dilute HbS.
Risks= hyperviscosity, incr sickling w over-transfusion, allo-immunisation leading to haemolytic transfusion reactions, other transfusion reactions, hyperhaemolysis, transmission of infection.
Higher risk allo-immunusation in sickle cell; should have full ABO, Rh & Kell compatible blood (& HbS -ve & -ve for additional relevant all-antibodies) to reduce risk.s pecial blood supplies may be needed (sickle cell pts should have a card w info about ABx & phenotype or genotype).
Transfusion should occur pre-op for pts having low-med risk surgery; arranged by haematology team (depends on pt age, genotype, transfusion Hx, baseline Hb; target approx 100g/L to avoid hyperviscosity, don’t increase >40g/L in a single transfusion episode.
high risk surgery consider exchange transfusion.
high risk pts (eg. primary or secondary stroke prevention) optimise sickle cell percentage to <30% preop.
If emergency surgery & low risk but Hb >=90g/L, consider proceeding to OT & transfuse pt intra or postop (consult haematologist).
They should have <10 day old blood.
Intra-op:
multimodal analgesia; consider regional/neuraxial depending on pt/surg factors (there may be less complications w neuraxial; both analgesia & improved peripheral flow w sympatholysis but care re: hypotension/hypoperfusion).
consider NIRS.
avoid dehydration (impaired urinary concentrating ability), limit fasting & monitor periop fluid balance. UO, CVP & CO monitoring considered for maj surgery.
pre-O2, maintain SpO2 @ pt baseline or 96% whichever higher
AVOID factors that may precipitate sickling:
-dehydration
-hypoxia
-acidosis
-hypothermia- pre-warm, monitor, maintain normothermia perioperatively w active warming
-pain
-avoid any non-emergent surgery if the pt is febrile or having a pain crisis
VTE proph throughout periop period. if particular risk factors, d/w haematology.
consider may have difficult IV access (US)
ABx prophylaxis, meticulous asepsis
Postop:
consider HDU depending on severity/comorbidities
Consider APS referral esp if pt on chronic pain management; continue baseline analgesia; opioid dependency is rare, opioid sensitivity more common
cont IVT until can tolerate PO fluids, postop fluid balance.
Keep SpO2 >96% or baseline (whichever higher); continuous monitoring if on sedatives.
Encourage early mobilisation (chest infection, VTE risk), incentive spirometry for major surgery.
Chest physio.
inspect cannula sites for infection.
encourage pts to report symptoms of infection; if pyrexial start ABx if temp or signs sepsis.
consider HFNO if needed. If Hx acute chest syndrome, consider bronchodilator.
continue active warming in PACU & ward, monitor temp (spike may indicate sickling).
Daily haematology R/V after mod-major surgery.
High index of suspicion for sickle complications (can be difficult to differentiate from postop pain); ask re: location of any poan.
If acute life-threatening complications (eg. acute chest syndrome, stroke, sepsis)–> ICU, may need emergency exchange transfusion under guidance of haematology.
obs: 1-3% maternal & perinatal mortality!
incr metabolic demand, susceptibility to infection, pro-thrombotic state, aortocaval compressions.
Pre-eclampsia, IUGR, preterm labour, APH & infection more common.
high incidence (60%) of pain crises, caeser & ICU, LBP, preterm labour.
all pts be seen in anaes clinic.
epidural ideal (esp if opioid tolerance).
thromboprophylaxis (care to timing of LMWH w neuraxial).
GA higher risk but if required, care w O2, normothermia, ramping, consider postop ICU.
optimise post-LSCS analgesia.
thromboprophylaxis.
ENT surgery: adenotonsillar hypertrophy.
shared airway, risk oedema postop/obstruction/hypoxia postop esp if OSA. preop transfusion as per guidance, blood available.
transcranial doppler.
severe OSA may need ICU/HDO.
NPA postop to limit hypoxia (same size as age-appropriate ETT & placed under direct vision by ENT). secure carefully, suction regularly.
hydrate, IVT until drinking.
PONV common, treat promptly.
analgesia appropriate timing (sore throat may last 10 days).
Tourniquet theoretical risk; exsanguinate limb carefully before inflate, limit tourniquet & surgical time (senior surgeon), ensure transfused with low HbS%.
Cell salvage can be considered; may have higher rate of sickling from extracorporeal circuit rendering the salvaged cells unsuitable; may be considered if red cell exchange pre-operatively. further evidence required. may be useful in pts difficult to transfuse.
factors confounding HbA1c
abnormal erythropoiesis, incr rbc turnover, haemoglobinopathies
Cerebral palsy
Diverse neurological disorders; varying degrees motor, sensory, intellectual impairment
mainly posture & movement.
severe forms impact neuro, resp, GI, musculoskeletal & urological functions.
many prem bubs may have underlying chronic lung disease (neonatal resp distress syndrome)
Incr risk aspiration pneumonitis, chronic lung scarring (swallowing probs, oes probs, LOS, spinal deformity)
may have bulbar muscle impairment, oromotor dysfunction, hyperactive salivary glands (drooling)
–> difficult airway (also may have poor dental hygiene/loose/awkward teeth, TMJ dislocation secondary to muscle spasticity
Pt may have undergone fundoplication for GORD
impaired cough, resp muscle hypotonia, decr immunity sec malnutrition all make pts more susceptible to recurrent chest infections
Scoliosis may (long-term)–> restrictive lung defects, pulm HTN, cor pulmonale/resp failure
malnutrition–> dehydration, anaemia, electrolyte imbalances
Degree of cognitive impairment can be difficult to determine due to communication issues (expressive language or oro-motor), communication issues may heighten periop anxiety; consider premed (care in pts with sig hypotonia, risk accentuating probs w upper airway m tone)
epilepsy (focal or generalised) in up to 50% of pts
may have visual/auditory impairment, impaired touch & perception
Most have some degree of muscle spasticity- if lower limb, gait
muscle contractures, risk joint deformities & dislocations (potential future problems with joint pain walking & sitting)
risks pressure areas/joint dislocations (flexion deformities, scoliosis, decubitus skin ulcers)–> difficult vascular access/monitoring.
NWB bones prone to fractures
risk blood loss major surgery (CP muscle contracts poorly when surgically incised)
Thin skin, little subcut fat, atrophic muscles–> prone to heat loss; large SA:body wt ratios, can’t conserve heat effectively. Actively warm.
IHD rates in adult CP high; pt unable to exercise, anaesthetist unable to assess cardioresp reserve.
If multiple prev catheterisations, may be @ risk latex allergy.
baclofen anti-spasmodic (may be intrathecal; less of systemic side effects eg. sedation/drowsiness, confusion, m weakness, resp depression, incontinence, lethargy) cf po
T12-L1- care if pt can’t take their regular baclofen, risk withdrawal (anx, disorientation, painful acute m spasms, status dystonicus, seizures, brady, hypoT. can give rectal diaz or IV midaz to counteract, po 100x the IT dose). pts need HDU if risk baclofen withdrawal.
IM botox injections- irreversible binding to ACh receptors on motor endplates. onset 1-3 days, lasts 3-4 months. minimal systemic absorption. resp m weakness if OD or IV injection.
tenotomies, arthrodeses, osteotomies.
often anticonvulsants, antispasticity meds, antacids, analgesics, antisialogogues, antidepressants, laxatives, proph Abx
Sux is NOT contraindicated (while some pts may have extra-junctional AChR).
NDMRs are less potent, shorter DOA as ACh up-regulated; dosing similar as these pts often relatively dehydrated, smaller volume of TBW.
Postop ICU (prone to hypoxia, hypovol, hypothermia, prone to PPCs)
pain Ax & Mx may be challenging; continuous vs “on demand” regimens for postop analgesia may be appropriate for pts where postop pain assessment challenging, however care due to risk of accumulation of systemically or extradural opioids in pts @ risk of over-sedation, resp depression, PPCs.
Consider non-surgical causes postop pain, eg. poorly controlled pain, hypothermia, anxiety may trigger painful m spasms.
consider postop nutritional status; can delay wound healing.
ANKYLOSING SPONDYLITIS:
An inflammatory arthritis of the spine.
Presents with multi-system features incl:
-articular: synovitis, enthesitis, dactylitis
-extra-articular: uveitis, psoriasis, IBD, OSTEOPOROSIS (risk spinal cord injuries, atlantoaxial subluxation), PAIN, risk spondylolisthesis w cord compression, DISABILITY, fatigue, CARDIOVASCULAR DISEASE (HTN, HF, ACS, CVA, VTE, CONDUCTION ABNORMALITIES, AORTIC ROOT & VALVE (EG. AR)), RESTRICTIVE LUNG DISEASE (parenchymal fibrosis + chest wall).
Usually presents as chronic back pain, almost always before age 45. Often HLA-B27.
Sacroiliitis common.
NSAIDs, addition of DMARDS occasionally needed, eg. TNF inhibitor (infection, drug-induced lupus risk, neurologic deficit, heart failure; typically hold pre-op but time OT @ end of cycle, d/w rheum), methotrexate (pulm toxicity, BM suppression, hepatotox, infection). steroids are not generally indicated.
DIFFICULT AIRWAY: often post column; risk C-spine fracture (esp w coexistent osteoporosis), atlanto-ax instability, thoracic kyphosis posture diff; often need MILS, consider AFOI or lighted stylet.
VENTILATION: often kyphosis & restrictive lung deficit
CARDIAC: higher risk CV: IHD, CVA, conduction abnorms, valve (eg. AR), VTE risk, HF
MUSCULOSKELETAL: pressure area risk, posturing, risk spondylolisthesis & neuro signs (pre-op neuro Ax documented)
Difficult regional/neuraxial (axial spine fusion, epidural space obliteration, underlying neuropathies/neuropathic pain)
HIGHER RISK EPIDURAL HAEMATOMA. PARAMEDIAN MAY BE BETTER. CONSIDER US GUIDANCE.
HAEME: ACD
CNS: fatigue, chronic pain
EYES: uveitis
MEDICATIONS: typically NSAIDs, occ DMARDS, axial typically not steroids (occ short-term for flare)
D/W RHEUM
DMARDs adverse effects:
Conventional DMARDs:
MTx: pulm tox, BM suppression, hepatotox, infection
Hydroxychloroquine: renal or cardiotox, blood dyscrasias
Sulfasalazine: CNS tox, granulocytopenia, haemolytic anaemia
Leflunomide: hepatotox, pulm, myelosuppression
Biologic DMARDs eg. infliximab:
HF, neurologic, infection, hep B react, drug-induced lupus
C1 esterase deficiency (hereditary angioedema)
Autosomal dominant lack/deficiency of C1 esterase (release vasoactive mediators, incr vasc permeability & cause oedema)
Presents w angioedema not urticaria; extremities, face, oropharynx, larynx, GI/GU tract, bouts 24-72hrs
May get life-threatening airway oedema & obstruction not responsive to steroids, ephetrine/antihistamines
Triggers= oral/dental manip, laryngoscopy, infection, stress/trauma/light anaes
-gentle ++ airway manipulation, RA if possible
Pre-procedure prophylaxis; C1 esterase inhibitor replacement protein, OR danozol (androgen, 2.5-10mg/day max 600mg/day) 5 days before & 5 days after. TxA not as good as C1NHRP or androgens
Plan for intra-procedure crisis Mx:
-C1 esterase inhibitor concentrate 25U/kg
-FFP 2-4 units (replace deficient enzyme)
-androgens/epinephrine/antihistimines/antifibrinolytics not useful for acute event.
postop monitoring: delay in reaction 60mins-36hrs possible
Contraindications to CPET
Severe symptomatic AS
severe pulmonary HTN
SBP >200mmHg
decompensated CCF
serum osmolality calculation
= (2xNa) + glucose + urea
tonicity is (2xNa) + glucose
Steriod impacts
hyperglycaemia/DM, thinned skin/easy bruising, immunocompromise, HTN, hepatits, PUD, myopathy, dyslipidaeia, adrenal suppression, mood
Cyclosporin: nephrotox, HTN, high K, low Mg, neurol (paraesthesia, seizure), hepatotox
Tacrolimis: similar action to cyclosporine, inhibit T lymphocytes
Nephrotoxicity so avoid with cyclosporin. Also HTN, myocardial hypertrophy, DM, high K & low Mg.
AZT: hepatitis, BM suppression, leukopenia, anaemia, diarrhoea.
Mycophenolate: BM suppression, diarrhoea, incr infection, latent viral activation, malignancy risk.
The metabolic syndrome
Waist circumference >=102cm men >=88cm women
triglycerides >1.7mmol/L or on drug Rx for elevated triglycerides
low HDL (<1mmol/L men, <1.3mmol/L women) or on Rx ofr it
BP >=130SBP or >=85mmHg DBP or on antihypertensives
fasting glucose >=5.6 or on Rx for elevated glucose
