Crisis management Flashcards
Why is CO2 well-suited to insufflation for pneumoperitoneum?
Chemically inert
highly soluble in blood (rapidly reabsorbed)
less combustible than air
colourless
inexpensive
readily available
Measures for preventing OT fires:
EDUCATION and AWARENESS of OT team- eg. discussion re: at risk pts/strategies during the team huddle, always investigate burning odours, popping noises, promote culture where all disciplines are empowered to proactively speak up if concerned. Simulation & drills can assist. Surgical safety checklist for every case & consideration of formal fire risk assessment tools eg. Silverstein fire assessment tool (anatomical location of procedure, presence of ignition source, open delivery of O2; 1 point if above xiphoid, 1 point if ignition source present, 1 point if FiO2 >30% with cannula or mask. If points add up to 3, high risk & formally assign tasks to OT staff to undertake in event of fire). Ideally if scores 3, reduce the risk by: eliminating ignition source, reduce FiO2 to <30%, use SAD or tracheal tube. Institution should communicate with local fire services & facility engineers to help planning & recommendations for basic fire responses & assistance (in anticipation not reactive to events) with decision-making to evacuate or defend with plans for horizontal/vertical evacuation of anaesthetised patients.
COMMUNICATION: between surgeons, anaesthetists, nurses & others in OT, eg: surgeon communicate to anaesthetist before using potential ignition source, anaesthetict inform surgeon if potential for ignition source to be exposed to O2-enriched environment.
DELIBERATE SEPARATION OF ELEMENTS OF THE FIRE TRIANGLE (ignition source, oxidant, fuel)- ideally avoid open delivery of 100% O2 for surgery above the xiphoid process
Examples from the fire triad?
fuel: alcohol-based skin prep (particular risk- highly flammable, burns with a nearly colourless flame), allow at least 3-5mins drying before draping, use correct-sized applicator to limit ETOH pooling, avoid large-volume preps for head & neck, remove leftover prep before starting surgery), surgical drapes, gauze, tracheal tubes
ignition source: laser, monopolar electrosurgical unit, light sources, defibrillator, faulty electrical wiring, sparks from surgical tools
oxidiser: oxygen, N2O (in concentrations >30% they increase chance of ignition of fuels & cause fires to burn with greater speed & intensity)- particular risk if they accumulate in a closed area eg. under drape. Higher the ambient []O2, lower the time for ignition & fuel to burn completely.
Mechanisms of injury from a flash fire (eg. if ignition source in an O2-enriched environment above T4)?
smoke inhalation (–> thermal injury to mucosa/skin/lung tissue, may–> airway obstruction, inhalational injury from toxins released from burning plastics)
airway burns
delayed onset infection
carbon monoxide
What’s an open O2 delivery device?
face mask or nasal cannula- LMA or ETT seal the airway, effectively eliminating O2 contaminating the surgical field
Which type of electrosurgical instruments are associated with most surgical fires?
monopolar
What procedures in particular pose risk surgical fire?
procedures above T5, use of ignition source in proximity to oxidiser
What procedures in particular pose risk surgical fire? strategies?
procedures above T5, use of ignition source in proximity to oxidiser- strategies as per algorithm (if require FiO2 >30%, should use SGA or ETT vs open O2 source), care with ETOH prep, clear communication eg. prior house of ignition source. If unable to secure the airway, minimise O2 accumulation by insufflating air over face, open draping.
should discuss during team time-out, establish strategy to mitigate fire risk.
if airway procedure, ideally FiO2 <30%, if high concentration ideally cuffed ETT and for laser case, a tube specific to the wavelength, optical density & power of the laser should be used to prevent penetration of the tube by the laser.
considerations for airway laser surgery?
ideally FiO2 <30%, should isolate higher [] by cuffed ETT & use a laser tube specific to the wavelength, optical density & power of the laser to be used. INFLATE THE CUFF WITH WATER OR SALINE and a small amount of METHYLENE BLUE or other dye (if double cuff, methylene blue in prox cuff). moisten any gauze.sponge in the surgical field.
course of action if an airway procedure was occurring with FiO2 >30%?
communicate with surgeon- prior to the time of ignition source reduce FiO2 to <30% (high flows to washout high-[] FeO2 then reduce prior to ignition source)
have water/saline ready
Steps in response to surgical fires
AIRWAY:
1. stop burning: disconnect O2 & remove ETT, pour water or saline into airway & call for help before
2. re-establishing ventilation- facemask air then once certain everything in airway stopped burning, O2 to maintain patient’s sats, re-intubate largest ETT possible (if not possible, temporary JV; pt may require low trache or cricothyroiditomy).
3. maintain anaesthesia IV
4. examine pts airway for fragments of tubes/sponges/instruments (remove). ASAP use laryngoscopy & rigid bronch to examine lower airway for thermal injury; lavage & fibreoptic bronch if indicated by airway injury. Consider ABG & CXR.
5. pt will need ICU intubated after airway fire (maintain gas exchange, risk ARDS/ALI) & transfer pt to burns centre; requires ABG & co-oximetry (assess for CO or cyanide exposure), CXR, corticosteroids
other fires:
RESCUE:
declare emergency, OT stopped, brief attempt to suppress fire (douse with water/saline, cover with towel), if the fire can’t be safely controlled, remove fuel sources from pt & activate code red (which sets off audible & visual alarms, closes doors & calls fire department), safely evacuate pt/staff to designated muster point as per fire warden instructions (pack surg site, transport vent/monitors, TIVA, rescue drugs)
ALARM:
should be activated early & continued while threat remains
CONFINE:
doors closed, ensure oxidising piped gases turned off
EXTINGUISH:
use appropriate extinguisher
What’s negative pressure pulmonary oedema? What are other forms of pulmonary oedema with a similar pathophysiological process?
A form of non-cardiogenic pulmonary oedema involving the generation of high negative intra-thoracic pressure to overcome upper airway obstruction (eg. laryngospasm, biting tube, foreign body airway obstruction)- the pulmonary oedema typically develops within 2 min of obstruction.
The oedema arises due to raised pulmonary capillary pressure, in the absence of LV failure. This hydrostatic pressure along with disruption of alveolar epithelial & pulmonary microvascular membranes–> pulmonary oedema
Neurogenic pulmonary oedema (after a severe neurologic insult eg. SAH, particularly those with posterior circulation aneurysms, poor clinical grade SAH & those <30yo; may also be associated with TBI, epileptic seizures, embolic stroke)
high-altitude pulmonary oedema
pulmonary oedema in a hypertensive crisis
Does NPPE typically resolve?
yes- over 12-48hrs with appropriate care
How to manage neurogenic pulmonary oedema?
Primary determinant for intubation is the pts neurological state
Subsequently, if the level of respiratory support indicates that I&V is required, perform with a technique that limits raises in ICP or SBP yet retains cerebral perfusion
Ventilate with lung protective strategy; 6-7mL/kg TVs, PEEP to aid clearance of oedema & maintain alveolar recruitment ensuring the PEEP doesn’t impair cardiac function
Any pt with raised ICP should be ventilated according to neuro protective parameters which may conflict with optimal ventilation for NPO; AVOID permissive hypercapnia
high-frequency oscillation ventilation may assist refractory hypoxaemia. Proning may assist NPO but C-spine injury a relative CI
Use a combination of inotropic cardiac support & peripheral vasodilation, avoid tachycardia & arrthyhmias, titrate Rx with small changes & observe SpO2 response
Care with maintaining cerebral perfusion
Assess for fluid responsiveness- pts may have relative hypovolaemia, contraindicating diuretic therapy (distinguish from cariogenic pulmonary oedema)- should also avoid diuretics in pts with SAH (deleterious effects on cerebral vasospasm)
How to manage neurogenic pulmonary oedema?
Primary determinant for intubation is the pts neurological state
Subsequently, if the level of respiratory support indicates that I&V is required, perform with a technique that limits raises in ICP or SBP yet retains cerebral perfusion
Ventilate with lung protective strategy; 6-7mL/kg TVs, PEEP to aid clearance of oedema & maintain alveolar recruitment ensuring the PEEP doesn’t impair cardiac function
Any pt with raised ICP should be ventilated according to neuro protective parameters which may conflict with optimal ventilation for NPO; AVOID permissive hypercapnia
high-frequency oscillation ventilation may assist refractory hypoxaemia. Proning may assist NPO but C-spine injury a relative CI
Use a combination of inotropic cardiac support & peripheral vasodilation, avoid tachycardia & arrthyhmias, titrate Rx with small changes & observe SpO2 response
Care with maintaining cerebral perfusion
Assess for fluid responsiveness- pts may have relative hypovolaemia, contraindicating diuretic therapy (distinguish from cariogenic pulmonary oedema)- should also avoid diuretics in pts with SAH (deleterious effects on cerebral vasospasm)
What may be adverse effects of extravasation?
soft tissue necrosis
soft tissue loss
scarring around nerves, joints & tendons–> contractures & deformity
Severe injury may require debridement, tissue grafting, surgical release of contractures or amputation
What are some risk factors for extravasation?
Patient: elderly (fragile skin & veins), neonates (small veins & use of small cannula increases injection pressure), scalp veins= high incidence of extravasation (avoid for induction of anaesthesia). Unconscious/sedated/child may be unable to communicate pain. Thrombosed veins (eg. with multiple IV therapies). Obesity or oedematous tissue may be harder to site & leakage difficult to detect.
Decreased peripheral sensation or impaired circulation may be unaware of discomfort.
Equipment:
syringe drivers- significant amount may be delivered before pressure-limiting mechanism activated.
pressure bags.
multi-lumen catheters that may migrate with proximal lumen outside of central vein.
Substance:
Hyperosmolar substances (anything with osmolarity > plasma 290mmol/L) cause damage by exerting osmotic pressure–> compartment syndrome- eg. CaCl or Ca gluconate, glucose >10%, KCl, sodium bicarb, x-ray contrast
highly acidic or alkaline (pH outside 5.5-8.5) can injure tissues (eg. amiodarone, diazepam, phenytoin, thiopental, vancomycin)
vasoconstrictor drugs cause local ischaemia & tissue death (eg. epinephrine, vasopressin, metaraminol, prostaglandins)
formulations may contain ETOH or PEG that may precipitate–> tissue necrosis
Volume:
localised mechanical compression of tissues may –> ischaemia
What are mechanisms of pathophysiology of tissue damage from extravasation?
-vasoconstriction & ischaemic necrosis
-direct toxicity
-osmotic damage
-extrinsic mechanical compression by large volumes
-superimposed infection
What are some drugs that can cause localised discomfort on injection (related to vessel wall irritation)?
propofol, ondansetron, rocuronium, cyclizine, cefazolin
What are the phases of management of extravasation?
- Stop the injection, stop/disconnect the infusion immediately
- aspirate as much drug as possible out of the cannula
- leave cannula in place until advice sought regarding Rx- once no longer required, remove to prevent further use & injury
- if visible, mark the area of extravasation with a pen or take photos
- elevate the limb (promote venous drainage), consider heat via dry warm compress to promote VD & increase drug reabsorption & distribution
- consider specific Rx for drugs with high risk of tissue damage, eg: saline washout (good evidence for reducing tissue injury: under sterile conditions under LA or GA, 4-6 stab incisions around area of extravasation, insert blunt-ended cannula through one & flush a large volume of saline through the s/c tissues), liposuction (less effective than saline washout), steroids (little evidence), hyaluronidase (no clear evidence; depolymerisation makes tissues more permeable, aiding the flushing out of extravasated material. dissolve 1500 units in 1-2mL saline & inject into area of extravasation). Phentolamine (alpha blocking will relax vascular smooth muscle & produce vasodilation. early use may be beneficial after vasopressor extravasation). Stellate ganglion block may relieve tissue ischaemia from vasopressor or thiopental extravasation.
- Consider referral to plastic surgery for high-risk extravasations, to allow early washout. If conservative management used, pt must have follow-up arrangements in place & counselled to report tissue changes immediately.
- Ensure documentation is complete- debrief/full disclosure with patient, WebAIRS& report to Q&S committee for discussion at Departmental M&M meeting
What is explicit awareness? and implicit awareness?
explicit recall of intraoperative events after complete of general anaesthesia
implicit awareness is development of memory for events during anaesthesia which the patient may not recall but may cause subconscious physiological harm
What is the most important risk factor for AAGA?
use of NMBDs
How to dose induction agents in obese pts as a suitable compromise btwn haemodynamic stability & awareness?
adjusted body weight
What to do if note a pt moving during maintenance?
NAP5 noted that pain was more common during maintenance than induction.
concomitantly give verbal reassurance, increase analgesia & deepen anaesthesia.
Approximately what proportion of cases of AAGA in NAP5 occurred during emergence or extubation?
approx 1/3
How to manage cases of suspected AAGA?
Early identification & supportive intervention at the time & after can optimise long term psychological consequences (pts experiencing AAGA are at risk of adverse psych consequences incl PTSD)
MITIGATION of intra-op distress
If awareness suspected intra-op, the anaesthetist should speak to the patient & provide reassurance that the anaesthetist knows pt may be aware & is addressing it, eg “I realise you are awake & cannot move. This is because of the effect of one of the drugs given to you. Don’t worry; you are quite safe I am helping you with your breathing, though this may feel strange, and I am giving you some anaesthetic drugs so that you will become unconscious very soon”.
MEETING
listen, be sympathetic & promise to investigate the cause of why the experience may have happened to help prevent it happening again to them or another pt
express regret that the event happened (this does not constitute an admission of liability)
consult with clinical psychologist
ANALYSIS
At the meeting it’s important for the pt & anaesthetist to either verify or exclude a diagnosis of AAGA (eg. how plausible is the account)- classify as per NAP 5 categories (eg. probably or unlikely). analyse chart/comments. Grade degree of evidence.
NAP provides standardised & structured grading of: classification (probability), degree of supporting evidence, immediate experience as per Michigan classification & longer-term impact.
Info analysed by a small group with appropriate training, providing an unbiased opinion re: classification, impact & likely causality.
SUPPORT
Seek signs of impact early.
Review within 24hrs, ideally in person. aim to detect the 4 cardinal signs of impact:
(i) flashbacks
(ii) nightmares
(iii) any new anxiety state
(iv) symptoms of depression
early referral to psychologist or psychiatrist is advised if early symptoms are concerning or approach uncertain.
If pt was mistaken (eg. thought that immediate postop events were intra-operative), address gently with care & understanding.
further equivalent follow-up at 2/52, even if true AAGA unlikely, NAP5 showed that pt interpretation is important & impact of unpleasant periop experiences may be severe & they may still need psychological support.
If PTSD-type reactions occur, should be treated either with trauma-focused CBT or eye-movement desensitisation & reprocessing.
If none of the 4 cardinal signs of impact, pt encouraged to make contact later if concerns.
Consideration of open disclosure, M&M/QI processes if unexpected error, WebAIRS to encourage the process of learning from events.
When do most cases of AAGA occur?
induction
actions for suspected MH
declare crisis & call for help + MH box while simultaneously:
-stopping volatile & removing vaporiser
-hyperventilating (flow >10L/min) with 100% O2
-dantrolene IV 2.5mg/kg 10-15 minutely until crisis over (may need to mobilise supplies- 20mg vial mixed with 60mL sterile water)
-don’t waste time changing circuit but change to TIVA, apply activated charcoal filters if available to both limbs of circuit
-actively cool if temp >38.5degC- intra-abdo lavage with saline @ 4degC, cool IV fluids, cool sponging & ice packs, lower OT temp
-insertion of art line+/-CVC
-treat hyperkalemia, acidosis (consider 8.4% NaHCO3 if hyperK), arrhythmias (amiodarone, lignocaine, metoprolol)
-aim UO >2mL/kg/hr (each vial dantrolene contains 3g mannitol)
-monitor ABGs, electrolytes, abc, CK, clotting profile, myoglobin. temp & prepare for ICU
which drug may significantly interact with dantrolene?
CCBs- may cause CV collapse & marked hyperkalemia
AT_RT 1.2: Describe the clinical features and resuscitative management of patients with thyroid storm:
What are some differentials for intra-op hyper metabolic state?
How thyroid storm diagnosed? What are life-threatening complications of thyrotoxic crisis? What proportion of pts with thyrotoxic crisis develop heart failure? What’s the mortality from intra-op thyrotoxic crisis?
What’s the immediate management of thyrotoxic crisis?
Along with stopping surgical manipulation of the gland, 100% O2 (as hyper metabolic), propranolol or esmolol & vasodilators (deepen anaesthesia, hydralazine), what is supportive & specific management for thyrotoxic crisis?
When does thyroid storm occur?
-thyrotoxic crisis, MH, phaeochromocytoma, carcinoid
-thyroid storm characterised by biochemical hyperthyroidism + severe life-threatening signs & symptoms (hyperthermia, cardiac dysfunction, altered mentation)
-cerebral haemorrhage from extreme HTN
-myocardial ischaemia from incr demand > supply
-high-output cardiac failure with high afterload (may need inotropic support); 25%
Intra-op mortality 20-30%
-C (so stop manipulation of thyroid gland) AT (100% O2, propranolol (1mg IV over 1 minute, repeat dose every 2 mins up to 3-6mg, onset 2-5mins peaks @ 10 mins, DOA 3hrs), esmolol (0.5mg/kg IV loading over 60 seconds, onset within 5 mins & duration 10-30mins; then can do IV infusion 50-100microg/kg/min), vasodilators)
-Urgently consult endocrine
supportive: IV hydration & glucose supplementation, cool to normothermia, Rx metabolic abnormalities (esp acidosis)
specific measures to limit free thyroid hormone: thionamide (eg. PTU 1mg over 10 mins, can repeat every few hrs), hydrocortisone, sodium/potassium iodide (should wait at least 1 hr after PTU to prevent the iodine being used as substrate for new thyroid hormone synthesis)
(remember it’s a hypermetabolic state that can put the pt into heart failure); treat arrhythmias but avoid amiodarone
ICU monitoring as high mortality
Thyroid storm can occur during surgery & in the first 18hrs postop in hyperthyroid pts (low incidence in pts who receive preop antithyroid Rx)
Ax/Mx of intraop & other seizures (acute & persistent)
Intra-op seizure rare under GA, may occur in high risk pts for neurosurgery. Difficult to Dx under GA (esp if muscle relaxants used- HTN, tachy, incr EtCO2, dilated pupils). Declare, inform surgeons, 100% O2, deepen anaes (reduce CMRO2), correct precipitating factors (hypoglycaemia, hypoxaemia, hypercapnia, hyponatremia)
Stabilise & support airway & breathing, 100% O2 (RSI w intubation if airway, breathing or oxygenation can’t be maintained or if seizure prolonged).
Continuous cardiorespiratory monitoring & pulse ox
IV or IO access (ideally @ least 2 lines)
Labs for glucose, Ca++, Na+, Mg++, LFTs, CBC, toxicology, anti-seizure medication levels
Manage reversible causes: hypoglycaemia, metabolic/electrolyte abnormalities, fever/infection, incr ICP
If persists >5mins, midaz 5-10mg (0.1mg/kg) over 2-5mins (or 10mg IM or IN); diazepam is 0.15mg/kg IV max 10mg, lorazepam 0.1mg/kg or 4mg fixed dose, max rate 2mg/min.
along with AED- phenytoin 15mg/kg, or keppra 60mg/kg IV or IO over 15 mins
if seizure persists at 10-15mins, further dose benzodiazepine
emergency consult neurologist, portable EEG, ICU
If seizure persists despite appropriate Rx at 15-30mins, could give an additional ASM not given previously (eg. fosphenytoin 20mgPE/kg IV(max cumulative dose 30mgPE/kg), valproate 40mg/kg max 3000mg at 10mg/min, keppra 60mg/kg)
prepare for ICU transfer, prepare for RSI/mech ventilation; refractory if continues beyond 30mins. (requires RSI I&V, CV monitoring, continuous EEG, vasopressors as indicated). Commence continuous infusion for seizure control, either:
midazolam (preferred) 0.2mg/kg bolus loading then 0.1mg/kg/hr up-titrate to seizure freedom to max 3mg/kg/hr, continue for 24hrs before tapering
OR
Props 1-2mg/kg loading over 5mins, repeat 0.5-2mg/kg until seizure stops, then infuse 20mcg/kg/min & titrate to achieve seizure freedom (max rate 200mcg/kg/min). if seizures persist after 45-60mins, change to midaz or pentobarbital. if seizures stop, continue infusion 24hrs before tapering.
Pentobarbital
5mg/kg bolus over 10 mins, max rate 50mg/min. additional 5mg/kg boluses if seizures continue. infusion at 1mg/kg/hr, titrate up until seizure freedom.
max dose 5mg/kg/hr.
if seizures stop, continue inf 24hrs before tapering.
maintain therapeutic anti-seizure medication levels
If resolves,
place L) lat w 100% O2 if seizure terminated & airway patent; continue close monitoring until fully recovered. consult neurology for full neurol Ax, continuous EEG monitoring & neuroimaging if return to responsiveness delayed by >1hr, do any additional diagnostics as needed.
IT_AM 1.16
Describe the clinical features and outline a management plan for a patient with aspiration of gastric contents
NAP4: over 50% of airway related deaths in anaes were a consequence of aspiration
Vital to thoroughly assess, plan to limit risk
gastric contents apparent in oropharynx, tube
high airway pressure
hypercapnia or hypoxaemia
wheeze
Mx depends on timing; if during pre-O2 w FiO2 100%, immediate head down, L) lateral, suction
call for help, delegate (prepare for intubation)
ensure paralysis & intubate w VL (only cric if not actively vomiting)suction as go
once tube placed, suction in tube prior to PPV, then ventilate w 100% O2
if particulate matter, inspect lungs w FoB
If occurs during procedure w SGA, communicate to the room; stop surgical stimulation, call for help, delegate (intubation setup for RSI, diff airway trolley w FoB). If pt maintaining SpO2, suction around, FoB down SGA to look for particulate matter, railroad cuffed ETT into SGA, secure airway for remainder of case (either wake up or proceed depending on urgency).
**ACM: immediately place down L) lat, remove airway & suction pharynx, intubate
*ONLY proceed w OT if emergency
empty stomach before emergence
once extubated, pt doesn’t require ICU after period of obsn 2hrs if no desat <95%, asymptomatic & no evidence consol on CXR
Need ICU if particulate matter or indicator of severe aspiration (eg. desaturation, wheeze)
no role for steriods or ABx preventative; only ABx if pneumonia
IAACQ, FEx
IT_PM 1.14
Outline the management of ‘high spinal’ block (also refer to the Regional and local anaesthesia and Resuscitation, trauma and crisis management clinical fundamentals)
recognition: rapid ascending sympathetic, sensory & motor block w brady, hypoT, dyspnoea & difficulty swallowing/phonation
may progress to unconsciousness (brainstem hypoperfusion or anaesthesia) & resp depression
if large dose intrathecal (vs accidental spread from epidural), first sign may be unconsciousness or rsp depression
generally signs within mins, may be up to 40mins w change of position
ABC
secure airway if needed (LOC= maternal collapse, resus trolley, RSI w cric); sedation & ventilation until block wears off, may take hours. If urgent LSCS required, to OT w paeds in attendance (expecting an anaesthetised baby as induction to delivery longer than expected)
100% O2
IVT, vasopressors (metaraminol, ephedrine)+/- inotropes (glyco 200-600microg, atropine 200-500microg); if no response of circulation, consider Adr w dilution max [] 10microg/mL
sit up
monitor FHR if obs
await regression
open disclosure, full debrief offered to the woman & family during admission & opportunity for follow-up
risk management/Q&S report & consideration of contributing factors/future risk mitigation
opioids after a PCA
dose based on the amount used in the 24hrs prior to ceasing PCA & equianalgesic dosing (unlike for initial oral doses, don’t use age-based dosing since pts opioid requirements are known). As acute pain varies day to day, allow 0.5-1.5x the last 24hrs dose charted as range; divide the 24hr dose by 6 for 4-hourly.
