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.