extreme of age extent/loaction of burn inhalation injury comordibities obese etoh substance abuse major causes of death are multiple system organ failure and infection

3 factors of Severity of injury:

etiology of burn TBSA % depth of burn

Epidermis only

first degree

Epidermis + upper dermis

superficial second degree

Pain, blister formation

superficial second degree

Pain absent due to destruction of nerve endings

third degree

Tissue necrosis centally due to destruction of tissue by injury, non viable tissue

zone of coagulation

Surrounds zone of necrosis and can progress and lead to increase in the skin area of necrosis or depth of injury

zone of stasis

Surround zone of ischemia nd manifestly by increased vascular permeability with extravastion of fluid from intrvascular to interstitial space leading to edema

zone of hyperemia

Tissue still viable and can respond to treatment

zone of stasis

Although not directly injured it responds to injuries of other 2 zones

zone of stasis

Susceptible to vascular compromise with excessive edema

zone of stasis

With adequate resuscitation then this zone is preserved

zone of stasis

Fluid resuscitation formula

3ml/kg. X. TBSA%

Considered a major burn:

25% TBSA 20% in elderly, pets 3rd degree involving > 10% any ELECTRICAL burn any burn with INHALATION injury (doubles mortality) age + % > 115 = mortality 80%

Type of burn that double mortality:

inhalation

Burn Shock: 3 factors that influence magnititude and duration of shock:

TBSA 20% pre-existing illness inhalation injury

Burn Shock Patho:

disruption of transmembrane Na++ leading to increase INTRAcellular sodium > hypovolemia > cell edema heat injury: activated endothelial cells > inflammmatory cascade, local vasoconstriction, increase capillary permeability, systemic vasodilation

heat injury: activated endothelial cells > 4 results:

inflammmatory cascade, local vasoconstriction, increase capillary permeability, systemic vasodilation

Inflammatory mediators of burn shock:

complement proteins kinins histamine serotonin prostaglandins oxygen derived free radicals

Burn shock: Fluid shifts between ________ and __________ spaces lead to > _____________

intravascular interstitial hypovolemia

Burn shock: goal is to: Rather than:

PREVENT rather than treat

Burn Shock Pulmonary: Directly damaged: Indirectly damaged:

direct: exposure of upper airway to smoke, fire, heat > edema, obstruction exposure of lower airway to steam, smoke, toxins > surfactant malfunction > atelectasis, shunt indirect: inflammatory cascade activation

Burn Shock Pulmonary: considerations Parenchymal injury due to _______ Increased permeability > ___________ Hypoxemia starts __________ Circumferential chest burn> _____________ Inhalation injury as a result of exposure to > ________________

Increased permeability > pulmonary edema, ARDS Hypoxemia starts 24-36 hours post burn Circumferential chest burn> consctiron and increased peak inspiratory pressures Inhalation injury as a result of exposure to >. toxic chemicals of combustion

Inhalation injury: cotton synthetic fibers combust and >>

aldehydes damage respiratory mucosa and impair ciliary function

CO2 shifts oxyhem curve to the

left

CoHB in smokers

over 10%

CO2 affinity for hgb is _____ times greater than O2 Use of 100% O2 will shorten the half like of CoHB from 4 hours on RA to _____

200 less than 1 hour

Hydrogen cyanide: Released from ____________ ________ causes poor extremity perfusion and hypoxia Shifts curve to the ________ Normal cyanide level: _________ may be useful

Hydrogen cyanide: Released from toxic synthetic combustible materials (plastic) mitochondrial cytochrome oxidase causes poor extremity perfusion and hypoxia Shifts curve to the LEFT Normal cyanide level: <2UG/ML HYPERBARIC CHAMBER may be useful

CO2 poinsoning s/s Treatment

headache confusion N fatigue AMS hallucinate combative cardiac instability death late signs: mental deterioration, ataxia, incontinence tx 100% oxygen hyperbaric hemodynamic support intubation/ ventilation

CO2 vs Cyanide poinsoning

CO2 formed as a product of combustion > binds to hgb over oxygen, impairs oxygen delivery to tissues cyanide formed secondary to combustion of synthetics > intracellular anoxic poinsoning and prevent oxidative phosphorylation

Cyanide poisoning s/s Treatment

respiratory depression, convulsions, metabolic acidosis 100% mechanical ventilation anticonvulsants hemodynamic support THIOSULFATE 12.5MG SODIUM NITRATE 300MG hyperbaric may be useful

BURN: Airway considerations: X Intubate all with:

100% for all patients intubate all with: facial burns, singed nasal hair, carbonaceous sputum, tachypnea, unexplained hypoxemia INTUBATE EARLY- may be impossible one upper airway edema develops progressive hoarseness: impending airway obstruction

Burn: intubate all patients with: 6

facial burns singed nasal hair carbonaceous sputum tachypnea unexplained hypoxemia hoarseness > airway obstruction

Why intubate early for burns:

might be impossible if upper airway edema develops

Initial burn hemodynamic state: Acute_________ Decreased: ______ _________ ________ RBC: ________ with ______ Hct due to __________ CO decreased due to: Impaired contractility due to FLUID RESUSCITATION VITAL Decrease of: (clotting)

ACUTE HYPOVOLEMIA decrease plasma, interstitial, blood volume 1/2 life RBC shortened with increase Hct due to contraction of intravascular volume and myocardial depression CO decreased due to myocardial depression circulating mediators and impaired intracellular calcium EDEMA protein c, S, anthithrombin III > DVT prophylaxis

Initial burn: GFR, RBF, UO

decreased

48 hours after burn: GFR RBF UO

INCREASED

INITAL BURN POST 48 HRS CO, SV, HR, SVR, BLOOD VOLUME

1ST HIGH: HR, SVR LOW: CO, SV, BLOOD VOLUME 2ND HIGH: CO, SV, HR LOW: SVR, MAYBE BLOOD VOLUME

AFTER 24-48 HRS BURN: TYPE OF METABOLIC STATE: HR BP CO SVR CIRCUALTING CATS BREATHING TEMPERATURE CO2 VS O2

hypermetabolic state increase HR, BP, CO doubles, decrease SVR increase circulating cats tachypnes, hyperthermia PRODUCTION of CO2 and consumption of O2 interstitial fluid reabsorrpiton capillary integrity returns and colloid solutions will remain intravascular

Burns; renal: Initial: ______ UO due to ___________ and poor renal function Electrical burn can damage: Muscle damage > Altered drug clearance Insufficiency due to - - -

decrease UO due to decrease vascular volume and poor renal function electrical > renal tubules myoglobinuria -hypovolemia activation of RAAS myoglobin

Burns will _________ extra cellular volume

increase

Burns will _____________ volume of distribution

increase

Burns and albumin

hypoablumin alter protein binding of drugs unpredictable amount of free drugs

Due to protein binding with burns: Increase or decrease NDNMB dose

increase

Burns Benzos, phenytoin, salicylic acid: Larger/smaller VOD

larger due to decrease albumin

Burns Lidocaine, meperidine, propranolol have larger/smaller VOD

smaller

Sedatives and analgesics Dose change Why

higher dose higher cat levels

Ketamine Does what to heart Advantage Disadvantage

direct myocardial depression effect - if critically ill and cat depleted- not good advantage: maintain control of airway, BP dis: repeat = tolerance, critically ill drop BP, emergence delirium without benzo

Emergence delirium with ketamine risk factors

young female vivid dreamer

Fluid loss and wound edema with Increase/decrease Plasma concentration of drugs

decrease unpredictable

Hypermetabolic state will increase liver and renal blood flow- increase drug clearance Variable on: - -

volume status phase of recovery

Electrical injury- entry and exit wounds- Significant hidden damage - - -

hyperkalemia arrhythmias hemogloinuria, myoglobinuria goal: maintain urine output 1.5 ml/kg/hr

Goal of fluid resuscitation

avoid ischemia injury (zone of stasis) > maintain tissue perfusion to end organ patient specific difficult due to cardiac compromise and capillary permeability

Brooke formula

colloids in 1st 24 hrs don’t change outcome limit sodium fluid creep- compartment syndrome

Results of under resuscitation

poor tissue perfusion end organ damage distributive shock

Results of over resus

compartment syndrome: orbital, extremity, abdominal pulm edema

Abdominal compartment syndrome Decreased: _______ dysfunction Malperfusion to :

most dramatic decrease pulm compliance cardiac dysfunction malperfusion to bowel, liver, kidney

Peds resus Uses ________ formula for thermal burns Use ______ containing solutions due to depletion of _________ UO goal Track on _______ and don’t exceed by x% of current rate

parkland dextrose, glycogen 1ml/kg/hr flow sheet

Best impact on resus for a new provider

follow guidelines and compliance to flow sheet

Adjective therapy for burn resus: Albumin

as early as 12 hours post burn decreased cystalloid requirement decreased risk of fluid creep: abdominal compartment syndrome

what is fluid creep

compartment syndrome due to fluid shifts of over resus

Adjective therapy for burn resus: FFP

decreased ACS

Adjective therapy for burn resus: Vitamin C absorbing acid

660mg/kg/hr helps liver

Adjective therapy for burn resus: Plasmpharesis

removes mediators

Adjective therapy for burn resus: Hemofilration

for renal failure decrease pressor requirement

Anesthesia for Burn: Preop evaluate: Assess Premed

*****TIME OF BURN***** % TBSA burn source assess: fluid resus labs airway premed: versed ketamine- peds glyco

Most important anesthesia consideration with burns:

communicate with surgeon - how much is going to be grafted what are our limits at what point to transfuse

Anesthesia and burns considerations:

communicate with surgeon warm the room check blood availability blood loss usually miscalculated large bore IV, rapid infuser labs frequent, including clotting factors lines not near surgical sites fluid RESUS early

EBL of TBSA burn grafted

200-400ml/ % grafted or 4-15% blood volume every 1% skin debrieded

Vasoconstrict use: Not epi/phenylephrine because: Preferred use:

cause hemodynamic change if hypermetabolic use thrombin

Monitors for burns anesthesia

standard esophageal stethoscope ekg stapled Aline if 20% CVP if 40% foley

Induction- awake intubation if: X X

facial burn inhaled injury

Induction with ketamine pro/con

pro sypathomiemtic increae HR, BP preserve ventilators drive decrease airway resistance non opioid with alangesia con myocardial depress with critically ill emergence delirium

Succs and burns

hyperkalemia bad worst day 10-50 avoid after 24 hours

NDNMB and burns

higher dose needed due to up regulation of sites proliferation of extrajunctional nicotinic r prolong muscle depolarization due to above

Anesthesia maintenance Hypercatabolic= Soaked swabs of: and dose: Exposure causes__________ loss Prevent hypothermia by:

consume O2 produce CO2 epi soaked swabs 10mg/ml evaporative warm OR 28 C warm blank warm fluids humidity gas

Burn anesthesia extubation considerations

timing critical dressing can take a long time don’t reverse until done avoid coughing with position changes give analgesia before reversal- thrashing bad normal reversal doses

P/o pain considerations

partial thickness very painful donor site very painful IV> IM larger dose req

Burn complications

respiratory septicemia multiple organ failure ARF acute pholynephtiits contractures> impact future anesthetics

Electrical burn considerations Less visible damage but more damage to ________ _________ if extensive muscle damage Heart -

more damage to viscera myoglobinemia if extensive muscle damage arrhythmias

Abdominal compartment syndrome Due to: Intra-abdominal pressure > AND _________ Treat:

over resus 20 plus and organ dysfunction - olguria, cardia instability …. neuromuscular block, sedation, diuretics, lap decompression

CO2 poinsoning Shifts curve: Impairs ________ of oxygen to tissue _________ also impaired >> metabolic alk/acidosis ? Blood= ____ color Pulse ox not accurate- can’t distinguish between O2/CO2 Falsely ________ result

left OFFLOADING TO TISSUE OXIDATIVE PHOSPHORYLATION ACIDOSIS CHERRY RED HIGH

First priority to burn patient

100% o2

Gold standard for dx extend of airway injury

fiber optic bronch

Burns and surgical airway

increase risk of pulmonary sepsis and late pulm complications, last resort intubate EARLY

Up regulation of extrajunctional receptors starts:

24 hours after burn

Succs is safe to use when:

first 24 hours

The dose of NDNMB should be: and why:

increase x2-3 more receptors