Plastics and burns Flashcards
$What’s resistance as per the hagan-poiseuille equation? and flow?
R = 8nl/r4 Flow= (deltaP x pi x r4) / 8 n l
radius: warm, normovolaemic pt= maximal vasodilation
we can manipulate pressure at both the systemic & venous end (avoidance of oedema important- no lymphatic drainage to the free flap, oedema increases venous pressure altering delta P, limit crystalloid fluid & limit cough/strain on extubation (incr venous pressure))
Changes in viscosity, diameter of the vessels & pressure will affect flow to the flap
$What’s the goal haematocrit for flap surgery?
30-35%
$What are some anaesthetic considerations for flap transfer surgery?
Patient may be comorbid (eg. elderly, cancer- therefore consider metabolic or mass effects, other medications/treatments (eg. radiotherapy, scarring), metastases, MALNUTRITION, previous surgery hence distorted anatomy, heavy smoking & ETOH use, SMOKING CESSATION, BP CONTROL & NORMOGLYCEMIA important goals, also optimising any respiratory conditions given likely prolonged I&V)
VTE risk assessment & prophylaxis plan
Optimise conditions for flap survival:
- Adequate flow to the flap, via adequate perfusion pressure and limiting flow resistance:
- normothermia (monitor temp, minimise heat loss, actively warm)
- haematocrit 30-35% to optimise viscosity
- judicious use of fluids (don’t want to promote flap oedema given that flap has no lymphatics & don’t want to create dilution coagulopathy but want optimal viscosity, target to keep SVV <=13% & UO >1mL/kg/hr
- consider regional techniques (theoretical benefit of vasodilation of the vascular beds supplying the operative area)
- MAP ideally >=70mmHg for anastamosis (higher target if coronary vascular disease)
- aim for hyper-dynamic circulation: high cardiac output, normal MAP, low SVR, wide pulse pressure; if MAP trending to below target, sequence of management:
- optimise preload- titrate fluids, aim SVV <13%
- optimise contractility- measure with art line, titrate inotropes
- judicious use of vasopressors if the above unsuccessful
Potential for primary (related to surgical factors) or secondary ischemia & ischemia-reperfusion injury (due to reactive oxygen species which cause lipid peroxidation, also release of inflammatory mediators & vasoconstrictive substances leading to secondary tissue injury) and risk of flap oedema (no lymphatics)
VTE prophylaxis
Prolonged surgery (pressure areas), limited access to the patient
- meticulous pressure care, q2H movement/repositioning/table tilt
- ensure adequate IV access placed in suitable location in liaison w surgeons & ensure good access to the lines
- pneumatic calf compression (VTE prophylaxis)
- monitor temp/FAWD
- airway well-secured but avoiding pressure areas/accessible as possible
Potential for major occult blood loss over time
- may consider induced hypotension to minimise blood loss & improve surgical conditions during initial dissection, either with prop/volatile, remi, or GTN or SNP (*steal phenomenon may be a problem with systemic vasodilators- steal of blood flow away from the already maximally vasodilated flap. SNP shows marked reduction in flap flow). Best methods for induced hypotension= titratable & rapidly reversible
- have valid G&H
- arterial line & serial ABGs to monitor Hb
- monitor fluid status
Smooth emergence (cough/strain increase venous pressure)
Follow PBM principles; allogenic transfusion associated with complications & worse prognosis
Limit hypothermia, shivering & pain (vasoconstriction)- continue warming, appropriate analgesia, continue strategies to maintain flap perfusion & minimise oedema postoperatively (highest risk flap failure within first 3/7), monitor flap to detect signs of failure
$What doses of propofol are required to get propofol infusion syndrome?
> 4mg/kg/hr for >48hrs
$What proportion of the population suffer burns each year, what proportion require hospitalisation, how about the proportion suffering burns in military conflict?
1%, 10% of these, 15-20%
$What are the 3 major risk factors for mortality in burns?
TBSA >40%
Increasing age (>60yrs)
Inhalation injury
$What proportion of deaths due to burns occur in the first 72/24? etiology? How about the ethology of later deaths?
58%, due to burns shock
Sepsis, multi-organ failure
$what are some factors contributing to improved outcomes following a burn?
Resuscitation protocols hyper metabolic support infection control improved respiratory support early debridement & grafting (excise all burnt tissue within 48hrs of the injury) early enteral nutrition effective perioperative care
$while a minor burn causes release of local mediators (eg. substance P, histamine, bradykinin) producing local inflammation, what is it about the pathophysiology of major burn that makes it so life-threatening if inadequate initial resuscitation?
release of systemic mediators (cytokines, endotoxin, NO) & systemic response of immune suppression, hypermetabolism, proteolysis, reduced cardiac output) that –> sepsis & multi-organ failure
Get swelling in areas other than the burned region
$factors to consider in the initial approach to a pt with a burn?
History:
Factors related to the burn (explosion (more likely other injuries), enclosed space (inhalation of toxic substances/poisoning), substance burning) & patient factors (GCS, ETOH & drugs, knowing why burned gives an idea of comorbiditiesco-morbidities)
Burns are a form of traumatic injury, coexisting injuries may occur
Apply key principles of the EMST, beginning with a primary survey
AIRWAY AND CONTROL C-SPINE= priority
airway obstruction can be rapidly fatal
STRONG CONSIDERATION OF EARLY INTUBATION- record GCS & pupils prior to intubation (may be weeks b4 conscious again)
factors ass’d w airway burn:
pt report, ask pt if their voice different
facial burn
singed nasal hairs/eyebrows
soot in the mouth
stridor
productive cough
carbonaceous sputum
obstructive respiratory pattern
nasendoscopy to Ax cords
HbCO >10%
Consider early intubation if any of these hints or if in doubt (spont breathing technique safest if sign of airway compromise), if there’s a reduced LOC, clear obstruction, if the pt has respiratory distress/failure or is going to OT soon
other factors influencing decision to intubate: circumferential neck burns, decreased conscious state, respiratory distress, partial thickness >30% or full thickness >15% (increased likelihood of resp failure), early surgery or for transfer to a burns centre.
Consider: Is the airway burn & ensuing inflammatory response likely to compromise the airway? (better to secure early if any doubt or concern, pt likely to go to OT anyway if major burn)
B:
Administer 100% O2
observe breathing pattern
assist ventilation if reduced LOC, poor resp effort or evidence of smoke inhalation
If intubated, bronchoscopy should be considered
Inhaled toxic products of combustion may cause chemical burn/injury to the lower airway or SIRS (bronchoconstriction, reduced surfactant, leaky airway capillaries, airway oedema)
Maintain high index of suspicion for CO poisoning (in theory may treat with hyperbaric O2 but no evidence that this improves outcomes & it’ll improve with high FiO2 over 24-48hrs) or cyanide poisoning (Dx of exclusion if acidosis & high BE that can’t explain by other reasons) if a burn in an enclosed space
If circumferential chest burns, severely compromised breathing/ventilation, escharotomy indicated
C:
control obv haemorrhage
Ax for potential blood loss & Ax peripheral perfusion
Identify need for early fasciotomy or escharotomy (can be done in ED if pt already intubated)
two large-bore IVC (pref through intact skin)- will eventually need CVC for inotropes
IMMEDIATE fluid resus (use crystalloid until the volume required is calculated)- should await about the first 8hrs of fluid resus before consider vasopressors?
Hb gives an idea of adequacy of intimal resus
IDC in
D: Ax GCS (considering Ddx for decreased LOC- head injury, CO, ETOH/drugs, epilepsy, hypoxaemia & shock)
E:
fully expose to Ax extent of burn & look for other injuries BUT keep the pt warm (Bair hugger)
Burn DEPTH:
-first degree= superficial (confined to epidermis)
-2nd= partial thickness (epidermis to dermis)
-3rd= full thickness (destruction of dermis)
-4th- muscle, fascia, bone
Size of burn (%TBSA): “rule of 9’s”
head & each arm 9%
anterior, posterior torso & each leg 18%
for infants: larger head 18% if 0-1yr, 11% at 10 yrs, smaller legs 14% @ 0-1yr & 18% at 10yrs
Palm: size of pts palm is 1% TBSA
$pros/cons of different approaches to intubation of a burns patient?
RSI if no airway compromise: Unfasted (aspiration risk), risk of occult airway compromise & obstruction/CICO
Spont breathing safest if signs of airway compromise
AFOI: maintain spont vent, cons= pre-select tube size (eg. nasal would need to be changed for ICU- in ICU they’d be doing repeat bronchoscopy)
$why is sux potentially unsafe for burns pt? should it be used?
with burn, proliferation of extrajunctional nACh receptors (in all tissues, not just those affected by burn)
depolarisation of these receptors by sux can lead to fatal K+ efflux & cardiac arrest
extent of response is proportional to the size of the burn
animal models: 9% burn sufficient to cause fatal hyperK
takes several days to develop- can use sux early in jury injury (only use within the first 24-48hrs following significant burn)
Recovery to a normal response follows healing, wt gain & mobilisation- may take 6/12
If in doubt, avoid sux & instead use roc or AFOI
$why less time to secure the airway w burns fluid resus? why may airway oedema still be an issue even if no airway burn?
oedema from fluid resus
systemic response
$What are the 11 Australian and New Zealand Burns Association criteria for transfer to a major burns unit?
> 10% TBSA adults
5% TBSA children
full-thickness burns >5% TBSA
burns involving face, hands, feet, genitalia, perineum, major joints
circumferential burns limbs or chest (may require fasciotomy)
electrical or chemical burns
burns with an inhalation injury
burns in the very young, very old or pregnant women
burns in ppl with pre-existing medical disorders (ASA >=III
Burns w ass’d trauma
non-accidental burns
$Why is inhalational injury important to recognise? How assess a burns patient for intoxication of inhaled products of combustion?
Independent predictor of M&M
Suspect from the mechanism (eg. enclosed space or if facial burn)
Classified according to site:
- thermal injury to upper airway: from inhalation of superheated air or steam. damage to mucosa. oedema & life-threatening obstruction may occur early (within the first few mins to hrs).
- lower respiratory tract (“smoke inhalation acute lung injury”): due to direct effects of the toxic products of combustion & smoke deposition in lower airways. chemicals dissolve in the mucosa, membrane damage, increased capillary permeability, increased bronchial blood flow, leak in the airways, ulceration, necrosis & oedema formation.
$Why is inhalational injury important to recognise? How assess a burns patient for intoxication of inhaled products of combustion?
Independent predictor of M&M. Increases fluid requirements for resuscitation & incidence of pulmonary complications. Inhalational injury icreases mortality by about 10%.
Suspect from the mechanism (eg. enclosed space or if facial burn)
Classified according to site:
1. thermal injury to upper airway: from inhalation of superheated air or steam. damage to mucosa. oedema & life-threatening obstruction may occur early (within the first few mins to hrs).
2. lower respiratory tract (“smoke inhalation acute lung injury”): due to direct effects of the toxic products of combustion & smoke deposition in lower airways. Chemicals dissolve in the mucosa, membrane damage, increased capillary permeability, increased bronchial blood flow 20x, leak in the airways, ulceration, necrosis & oedema formation. Cellular debris & fibrin deposited in small airways. V/Q mismatch. Reduced hypoxic vasoconstriction (due to NO). worse V/Q.
May get SIRS
$why is carbon monoxide poisoning harmful? how treated?
Has 240x higher affinity for Hb than O2
reduces the O2-carrying capacity of the blood
100% O2 decreases the half-life of HbCO from 240 to 40 mins
While hyperbaric O2 (3atm) reduces the elimination half time of CO to 15-30 mins, no evidence that hyperbaric O2 improves outcome
$What’s the Rx for smoke-inhalation ALI?
Nebulised heparin (help break down local fibrin deposits) nebulised NAC (helps with the cellular debris deposited in lungs) consider Cn toxicity
$what’s “burn shock”?
combination of hypovolaemic (?cardiogenic) & distributive shock:
- decreased IV volume
- incr SVR
- decreased CO (volume losses, incr afterload, decr contractility due to circulating mediators)
circulating mediators disrupt integrity of microcirculation so proteins then fluids move into interstitium
- -> decreased tissue & organ perfusion
- -> haemoconcentration & hypoalbuminaemia
- -> systemic & pulmonary oedema
divided into:
-early hypodynamic phase (24-48hrs after burn):
hypoperfusion due to fluid loss
decreased intravascular volume
increased SVR & PVR (catecholamines, ADH, haemoconcentration)
decr CO even before reduction in plasma volume
decreased SvO2
responsive to fluid challenges, may need stress dose steroids IV hydrocortisone q6h)
-late hyperdynamic, hypermetabolic phase (24hrs +) reduced SVR (impaired VC) high CO (2-3x) tachycardia massive energy expenditure limited response to fluid resus (may need inotropes) increased SvO2 (peripheral AV shunting) can last days to weeks
if left untreated, multi-organ failure= the inevitable result
$what can successful fluid resuscitation achieve? What’s the challenge to balance? how tailor fluid resus to the individual?
Seals capillary leak within 24hrs
challenge= provide sufficient fluid to maintain organ perfusion while limiting oedema formation & avoiding complications of over-resuscitation
base fluid resus on: haemodynamic status, pre-existing comorbidities, extent of the injury, response to fluid challenge (urine output, acidosis etc)
$what are some risks of over-resuscitation with fluid for burns?
abdominal compartment syndrome lung injury increased likelihood of needing tracheostomy organ failure mortality
$what’s the gold standard formula for fluid resus in adults with >15% burn & children with >10% TBSA burn? with what outcomes is it’s use associated?
Parkland formula
reduces the incidence of post burn renal failure and shock
$what’s the Parkland Formula used for? What are the end points?
estimate fluid requirements in the first 24hrs. Half should be administered in the first 8hrs, half in the remaining 16hrs, FROM THE TIME OF INJURY.
End points= UO >0.5mL/kg/hr adults & 1-1.5mL/kg/hr in chn under 30kg.
$what is the Parkland Formula (for adults and kids)
3-4mL crystalloid (eg. Hartmann’s) / kg body weight / %TBSA burned (partial & full-thickness burns only)
For children, same formula but with maintenance with 5% glucose +/- 20mmol KCl in 0.45% saline, the maintenance being 100mL/kg up to 10kg plus 50mL/kg from 10-20kg plus 20mL/kg for each kg over 20kg, give at 4:2:1 per hr rate.
(*important to start the resus early as if jam it all in to catch up rapidly may overload- continually reassess)
$What’s “fluid creep”? how to minimise it & monitor for potential complications?
administering excess fluid in initial resus period
can–> lung injury, incr risk of tracheostomy, abdo compartment syndrome, organ failure, increased mortality
make a plan, attention to detail with what giving, reassess urine output (0.5mL/kg adequate) & reconsider plan.
$What’s “fluid creep”? how to minimise it & monitor for potential complications?
administering excess fluid in initial resus period
can–> lung injury, incr risk of tracheostomy, abdo compartment syndrome, organ failure, increased mortality
make a plan, attention to detail with what giving, reassess urine output (0.5mL/kg adequate) & other clinical endpoints for vol resus (intact sensorium, normothermia, age-appropriate haemodynamics, minimal systemic acidosis) & reconsider plan.
$what solution is best for burns fluid resus?
No evidence that the use of any solution (colloids, HTS, albumin) improves outcome- Cochrane collaboration 2005
BUT colloids do decrease fluid requirements & intra-abdominal pressures
$After the primary survey & initial management, what are some other considerations for burns patients?
- Secondary survey: comprehensively examine pt to identify other injuries
- Immediate analgesia: IV morphine incremental doses
- Early surgery (circumferential burns need urgent fasciotomy & escharotomy)
- Transfer: care in a tertiary burns unit= best outcomes. All major burns should be transferred for specialist care (as per the list from the Australia and New Zealand Burns Association)
$What’s eschar? Why is escharotomy important for full-thickness burns?
Eschar is the leathery inelastic tissue remaining after a full-thickness burn (which destroys the epidermis & dermis + sensory nerves to the dermis)
Important as can develop compartment syndrome with circumferential full-thickness burns
$What information do we want to know about a trauma/burns patient who is coming to theatre?
Extent of injury & proposed surgery? Is the airway secured? Planned airway exchange? Cardio-respiratory status? How much resuscitation have they had? Are they warm (what's their temp)? what access have they got? Blood product availability?
$why is hypothermia problematic for burns pts? what can we do to limit this perioperatively?
Limits the amount of surgery that can be done initially.
Promotes coagulopathy, infection arrhythmia.
Warm the room (to 36 degrees), warm fluids, warm air (can use sterile air hugger) limit exposure.
$why is hypothermia problematic for burns pts? what can we do to limit this perioperatively?
Limits the amount of surgery that can be done initially.
Promotes coagulopathy, infection arrhythmia.
Warm the room, warm fluids, warm air, limit exposure.
$What are the benefits of burns pts coming to OT for excision & grafting early (at a time which, of consequence to us, is when their inflammatory response still evolving)?
decreased rates of sepsis overall less blood loss fewer respiratory complications shorter LoS decreased mortality
$Burns are a hypermetabolic state, metabolic rate increases 2x normal. What’s the plan for enteral feeding while a pt is intubated?
enteral feeds can continue unless airway instrumentation or manipulation is planned
$Across which range of ambient temperature are increases in metabolic rate minimised?
Thermoneutral temperature (28-32 degrees)
$how is tube often secured for long-term intubation in burns patients?
IMF screws in maxilla, wire tube in (wire around the screw, tube & the other screw)
$Blood loss can be massive in burns- where does in come from? how to limit bleeding in OT?
viable dermal layer
TANGENTIAL RESECTION: shaving off areas of burned tissue until healthy tissue layer reached (healthy bleeding tissue, hence large blood loss; plan for 50-100mL per % burn excised). TE removes bacterial load, reduces systemic inflammatory response. Benefits= decreased sepsis, shorter recovery time. Commence as soon as pt stable
Plan w pre-op FBC, coags
centre w ROTEM
avoid hypothermia (manage coagulopathy); hot OT
Active monitoring of blood loss (suction cannisters, watch debridement, weigh swabs, Hb measurement, physiological parameters (eg. HR, BP, CVP, UO)
surgeons use adrenaline soaked packs, tourniquets, limit the area operated on at a time, limit OT duration
dress wounds promptly, pressure as required
hypotensive anaesthesia
haemodilution, blood conservation
$what type of pain is generally associated with burns?
severe, neuropathic
May be chronic pain issues, anxiety & enhanced PTSD related to poorly managed burns pain
$what type of analgesia is employed for burns pts?
Multi-modal, multi-D approach, culture where pain Mx is a priority, input of a pain team.
paracetamol
opioids (care as they induce hyperalgesia)
lignocaine infusions
ketamine- decreases pre-synaptic glutamate release. decreases allodynia, hyperalgesia & opioid tolerance. challenging to use if underlying psych issues.
pregabalin- useful for itch, shooting & throbbing pains
Gabapentin- decreases release of glutamate in the dorsal horn of spinal cord. Useful for secondary hyperalgesia & allodynia. reduced overall pain scores & opioid consumption.
amitryptilline- reduced background burning pain (good for anxiety & sleep).
dressing change: pre-load opioids & pt get their pregabalin, propofol TCI, ketamine infusion, boluses of opioid (oxy or morphine), try alfentanil boluses judiciously.
$What’s the goal for pts to get discharged?
be able to achieve dressing changes without requiring IV sedation/analgesia
$what types of pain do burns pts get/at what time is pain problematic?
background (constant nociceptive) breakthrough pain procedural pain neuropathic pain (neuroplastic adaptation)
$what’s the goal urine output for a major burns pt?
> =0.5mL/kg/hr
$What’s the equation for DO2?
DO2= Q x CaO2
CaO2 = [(Hb x 1.34 x SaO2) + (PaO2 x 0.03)]
$What’s the implication of HbCO for pulse oximetry?
overestimates since resembles HbO in the red range. need co-oximetry.
$What’s the implication of HbCO for pulse oximetry?
overestimates since resembles HbO in the red range. need co-oximetry.
$What’s Ficks law of diffusion?
flux = (diffusion constant x surface area x (C2-C1) / square root thickness
(diffusion constant proportional to solubility / square root MW)
$What are the different types of tissue flaps?
“reconstructive ladder”
- Free flap transfer
- pedicle flap
- random pattern flap
- tissue expansion
- full-thickness skin graft
- split-thickness skin graft
- delayed primary closure
- primary closure
- secondary intention
$What’s free flap surgery?
Transfer of vascularised tissue to a new site, where circulation is restored by microvascular anastomoses to recipient site vessels
$What’s primary & secondary ischemia in free flap surgery?
Primary ischaemia: the period during dissection when vessels are clamped. Influenced by surgical factors.
Secondary ischaemia: occurs after anastamosis due to altered characteristics of flow in the microcirculation (can be affected by anaesthetist
$What factors influence the degree of ischaemia of a free flap?
Duration of ischaemia
O2 consumption of the site (skeletal muscle O2 consumption is 5x that of skin & fat so flaps containing muscle have greater susceptibility to ischaemic injury)
Blood flow to the site (it decreases to less than half during the immediate post-operative period
$do free flaps have intact lymphatic drainage? what are the implications of this?
no, so sensitive to anything that might impair drainage- extravasation of fluids, pressure effects from excessive fluids, occlusion to venous drainage
$do free flaps respond to stimuli?
They are denervated but respond to physical & chemical stimuli
$how to optimise conditions for flap survival?
optimal flow with hyper dynamic circulation, achieved with:
- flow through the microcirculation (thus blood flow & O2 delivery to the flap tissue)
- high CO
- peripheral VD
- wide pulse pressure
- good temp & pain control
- Hct 30-35%
$with regard to optimising the microcirculation, what factors affect arterioles?
They are resistance vessels, susceptible to vasoconstrictive effects:
Constriction: circulating catecholamines, hypothermia, myogenic reflex
Dilation: hyperkalemia, acidosis, hypercapnia/hypoxia, histamines/prostacyclins
$with regard to optimising the microcirculation, what factors affect capillaries?
exchange vessels, susceptible to increase in ECF fluid content (increases diffusing distance for O2, incr permeability may promote interstitial oedema
$with regard to optimising the microcirculation, what factors affect venules?
They’re capacitance vessels, susceptible to obstruction to flow/high venous pressure
$what are some strategies to increase cardiac output, vasodilate/avoid vasoconstriction?
hypervolaemic haemodilution
inodilators (eg. vasopressin, milrinone)
regional anaesthesia
adequate fluid resus (UO >1mL/kg/hr)
$from what haematocrit level is a steep rise in plasma viscosity seen?
> 40%
$what are some measures to limit blood loss during the initial dissection phase for flap surgery?
controlled hypotension
LA w vasoconstrictor
position to reduce venous pressure (ie. head up 30 deg)
monitor for blood loss & IV volume
$when is the highest risk for flap failure?
Within first 3/7
$What are some ways of inducing hypotension to limit blood loss particularly during initial dissection for flap surgery? Problem with systemic vasodilators?
GA (prop, volatiles) remi systemic vasodilators (GTN, SNP)
Methods that are titratable & rapidly reversible are most useful
Steal phenomenon may be an issue- the vasodilator bed is entirely perfusion pressure-dependent. Systemic vasodilators may divert blood away from the already maximally vasodilated flap. SNP has been shown to cause a marked reduction in flap blood flow.
$is there evidence that agents increasing cardiac output (eg. dobutamine) are useful for flap surgery?
no
$What’s burn first aid?
cold running water for 20mins; within 3hrs
$For inhalational injury (exposure to hot gaseous products of combustion), what size particles affect the large airways?
> 5micrometres. Smaller than this can reach smaller airways.
$Where does thermal injury usually occur? why?
upper airway above larynx due to the efficient heat exchange mechanisms there
$What carboxyHb level would make us suspicious for airway burns?
> 10%
$What’s a more conservative formula for burns fluid resus than the Parkland formula?
Brooke formula: 2mL / kg / %TBSA burnt, 20mL/kg bolus indicated if shocked
$What’s the %TBSA for perineum?
1%
$What chart is used for %TBSA burn documentation?
Lund and Browder
$what are the sources & type of injuries seen with electrical injury?
low voltage- domestic (single phase 240V) or industrial 3 phase (415V sources) cause localised tissue destruction
High voltage >1000V:
- deep extensive tissue damage due to the current flow
- arc injury caused by arc of current from source to patient
- Flame injuries: ignition of clothes
- multi-trauma from being thrown/blown away from the source
Generally there’s a small surface area of burn but large amount of damage to deep tissue structures
Fluid losses greater than predicted by parkland (small surface area burn but greater internal burn)
muscle necrosis causes myoglobinuria & renal failure
direct myocardial damage may –> conduction abnormalities or CCF *high current burns pts may benefit from pre-op echo
$What are some considerations & management for chemical burns?
type of agent, concentration, site & duration of contact (eg. may be intentional therefore late presentation)
decontaminate by irrigation +/- buffering or neutralising agent
*spont breathing for chemical burns
$how do superficial (formally 1st degree) burns manifest?
and superficial partial thickness (2nd degree- involves dermis)
deep partial thickness?
full thickness?
erythema, blanching, no blisters- epidermis only
erythema, blister, glistening, painful ++
erythematous OR white, slow/absent cap refill, altered sensation
penetrate into subcut tissue or deeper into structures- insensate, dry as capillaries cauterised
$what are the 3 zones of a cutaneous burn?
zone of coagulation: irreversible tissue loss due to coagulation of proteins
zone of stasis: area of decreased tissue perfusion surrounding the zone of coagulation- can be compromised by oedema, infection & hypotension & become a zone of complete tissue loss
zone of hyperaemia: perfusion decreased & usually recovers unless severe hypoT or infection
$what are some functions of the skin (hence consequences of damage to/loss of these functions through burns)?
barrier
thermoregulation
innate immunity
fluid & electrolyte homeostasis
neurosensory
social & appearance
metabolic
$what are some multi-system effects of burns?
- Resp: may get bronchoconstriction from inflammatory mediators, ARDS with severe burns (leaky capillaries)
- Renal: oliguria from increased ADH, renal failure due to inadequate resus or rhabdomyolysis
-metabolic & endocrine: incr metabolic rate (incr CO & O2 consumption)- hypermetabolic response can result in energy expenditure increasing 100% over BMR, catabolic state can last for months –> immunosuppression, risk infection, impaired wound healing. metabolic consequences of catabolic state= proteolysis, lipolysis, gluconeogenesis, hypermetabolism & insulin resistance
Transcutaneous loss of protein & greater fluid requirements.
- GI: gastric or duodenal stress ulcers common (require H2 antagonist prophylaxis & early enteral feeding)- splanchnic hypoperfusion & incr metabolic rate may threaten gut integrity- early enteral feeding assists this
- Immunological: down-regulation of the immune response- both cell-mediated & humoural, loss of barrier
$How does CO poisoning happen?
released by incomplete combustion carbon-containing products
$how to estimate the amount of blood loss in OT?
50-100mL/per cent burn excised (need to know preop Hb, coagulation & potentially ROTEM)
$What are some reasons for a burns pt to get hypothermia?
loss of skin integrity (insulator effect)
evaporative- fluid loss
large volume infusion of cooler than body temp fluid
vasodilatory effects, abolition of shivering, reduction of BMR & widening of the inter threshold range with sedative-induction agents
$what are some adverse effects of hypothermia?
CNS: disctress/discomfort. reduce CMRO2 7% per deg. impaired judgement/LOC. Incr myocardial O2 demand w incr shivering & arrhythmias may cause myocardial supply:demand issues & ischemia. conduction delay/HB/asystole if severe hypothermia.
CVS: bradycardia/hypotension & reduced CO. below 30 deg risk arrhythmias.
Resp: tachypnoea, bronchoconstriction/broncorrhoea increases DS & V/Q mismatch, L)-shift HbO2 dissociation curve so less O2 available to tissues
decrease metabolism prolongs DOA of many drugs used in anaesthesia, decreased Hoffman elimination
-recovering from heat loss has a metabolic toll- uses energy stores (shivering can double O2 consumption) at a time when needing reserves for burn response, hypothermia ass’d with 3 deg C can take 175cal (3hrs BMR) to recover, increase circulating catecholamines & cause peripheral VC (which impairs peripheral perfusion)
-may get hyperglycaemia from SNS stimulation/catabolism
$what are some measures which could be used to maintain temp of a burns pt intra-op?
measure core & peripheral temps (difference of less than 2 degrees indicates well-perfused)
minimise heat loss- limit exposure
OT temp 24-28deg (higher for children)
warm IV fluids
warming/humidification of gases
underrating matresses
FAWDs
managing metabolic effects periop (burns)
Early nutritional support
enteral feeds within 16hrs reduces stress response. nasojej (gastric stasis). may need oral or TPN nutritional supplementation
minimise fasting times when pts returning to theatre frequently.
monitoring & venous cannulation issues
limited access sites esp large TBSA burn
need prolonged access, may need CVL for inotropes
risk of line sepsis
difficulty fixing lines in proximity to wound areas (may need to suture)
monitoring also limitation with access (invasive likely most faesible if large SA burn
Infection control & prevention
Sepsis= commonest cause of mortality in those who survive initial few days; loss barrier immunity, systemic inflamm response (mediators cause immunosuppression), necrotic tissue/wound exudate ideal culture medium for bacteria.
risk infection w invasive lines.
GP initially, GN from 3-21 days post-injury
isolation, aggressive deridement necrotic tissue, topical anti-microbials (eg. silver sulphadiazine), aseptic technique for invasive devices), mininmise duration indwelling/invasive devices.
methods & materials for temporary & long-term coverage of burns
-Excision burn wound (ideally within 24-48hrs)
-SSGs= gold standard, difficult if large TBSA burn
-allografts (cadaveric); best material for temporary coverage large burns
-xenografts (animal origin)
-skin substitutes/dermal analogue (biocomposites w human/bovine/shark
-permanent cell based coverage using pts own cultured cells are underway
-allografts/xenografts/skin substitutes temp;orary (promote re-epithelialisation, prepare wound bed for autograft)
dressings need to provide protection from contamination & infection, physical protection, gas exchange properties, moisture retention
Discuss the specific pain issues encountered in the burns patient and their management
Can be nociceptive/neuropathic
Itch can also be significant
3 categories:
-procedural (short-lived related to wound cleaning, dressing changes, skin grafting, physiotherapy)
-resting pain: dull, long duration
-breakthrough pain: short duration, similar type to resting pain
Psychological component & risk persistent pain syndromes (18-58%)
poorly controlled/severe acute pain–> greater PTSD
increased early opioids in chn w burns reduces PTSD symptoms in chn
Protocolised pain Mx flowchart may help; limited evidence for pain Mx in burns injury
Initial pain mangement: simple measures such as cooling, covering & immobilising provide analgesia
Cool under running tap water >=20min or apply wet towel, useful for up to 3hrs post initial burn.
temporary burns dressings eg. clinc wrap reduce pain from contact & draft (not circumferential)
IV opioids initially (IM & SC abosrption is unreliable (hypovol, VC)
morphine PCA
switch to oral once GI function returned; gastric emptying or absorption of PO paracetamol generally not affected even by severe burns
MORPHINE Pk IS UNCHANGED IN BURNS PTs
IT infusion of morphine has been used in ICU
dexmed added to IV PCA
PROCEDURAL:
-multi-modal. initially large burns or children need GA for most. post-procedure opioid infusion useful (overcomes issue of infusion wearing off while the pt asleep, overcomes inability of the pt to use the button if hands burnt).
RA useful if site appropriate
dressing changes can take 1-2hrs, debridement of tissue & removal of staples.
intranasal fentanyl paeds
Options: sedation w propofol +/- alf, prop/remi paeds, ketamine +/- midaz in pca, other bzd (eg. lorazepam), bolus opioids +/- benzos, lignocaine infusion, entonox/penthrane
physio: enough analgesia but still alert; ROM & excs to maintain joint mobility
use of biosynthetic dressings reduces pain & time to healing.
multimodal distraction techniques, VR, augmented reality, hypnosis. music interventions.
REST PAIN: best control w low-dose opioids & NSAIDs (avoid in acute initial phase, potential toxicity). regular pre-emptive analgesia & short acting opioids for breakthrough.
RA for donor site pain
Persistent pain: TCAs, anticonvulsants (gabapentinoids, Na valproate), regional, CBT
antihyperalgesia agents useful for burns (area of secondary hyperalgesia around injured site)
also burns damage cutaneous nociceptors & conducting neruons that may–> acute neuropathic pain
For burns pruritis: cetirizine & cimetidine as 1st line & laratadine as 2nd line peripherally acting agents, gabapentin as 1st line centrally acting agent, laser therapy & pressure garments as possible nonpharmacological interventions.
Discuss the risk of a hyperkalaemic crisis in burns patients
sux safe for 24-48hrs
resistance to NDMRs (up-regulation of & altered affinity for, junctional nicotinic receptors)
Describe the anaesthetic issues and the management of patients returning for scar revision following burns, especially for neck and facial scarring
scarring & subsequent contractures may result in difficult airway, intubation
