Burns Flashcards
1
Q
Mortality of burns?
A
↑ Mortality:
- Older age (> 60 yo)
- > 40% TBSA
- Inhalation injury
*(Age of patient) + (% TBSA) = > 115 = > 80% mortality rate **Mortality doubled w/ burn plus inhalation injury*
Death d/t:
- shock secondary to sepsis
- inhalation injury
- extensive malnutrition
Decreased mortality in burns due to:
- increased access emergenyc care
- better airway mgmt
- better infection contorl
- better nutritional support
- early burn excision/grafting
- treatment of hypermetabolic response with EBP
2
Q
Anatomy of integumentary system?
A
- Largest organ
- layers
- epidermis- protective outer surface
- avascular. nourished by dermis
- dermis
- vascular
- heavily innervated
- collagen and elastic fibers
- deep layer dermis- hair follicles, sebaceous gland. afferent nerve endings
- most nerve terminals at dermis and a few penetrate the epidermis
- deep fascia
- deepest layer, dense organized connective tissue layer, seats skin into sq tissue
- subcutaneous
- Function
- protection
- immune function
- fluid/electrolyte homeostasis
- containment
- heat regulationsweating/vasomotor regulation of superficial blood flow
- blood vessels dilate in heat, constrict in cold
- sensation
- vitamin D
- Function
3
Q
Burn categorization?
A
Basis: depth and body surface area
- 1st degree- epidermis
- heals spontaneously
- 2nd degree (2 types)
- superficial partial thickness (basement membrane intact)
- skin will generate and grafting not needed
- deep dermal burn (basement membrane not intact)
- need grafting
- superficial partial thickness (basement membrane intact)
- 3rd degree- full thickness burns
- subcutaneous extension
- will need grafting
- 4th degree
- muscle, fascia, bone
4
Q
What is a first degree burn?
depth? how the wound looks? causes? levelof pain? healing time? scarring?
A
- Depth- epithelium
- How the wound looks- no blisters; dry, pink
- Causes- sunburn, scald, flash flame
- Level of pain- painful, tender and sore
- Healing time- two to five days; peeling
- Scarring- no scarring, may have discoloration
5
Q
What is a second degree burn?
depth? how the wound looks? causes? level of pain? healing time? scarring?
A
Depth- epithelium and top aspect of dermis
How it looks- moist, oozing, blisters,
moist, white, pink to red
Causes
- scalds
- flash burns
- chemicals
Level of pain- very painful
Healing time
- superficial- five to 21 days- no grafting needed
- deep 21-35 days- needs grafting
Scarring:
minimal to no scarring
may have discoloration
6
Q
Characteristics of third degree burn?
depth? how the wound looks? causes? level of pain? healing time? scarring?
A
- aka full thickness
- Depth- epithelium and dermis
- how it looks-
- leathery, dry
- no elasticity
- charred
- Causes
- contact with flame, hot surface
- hot liquids
- chemical
- electrical
- Level fo pain
- very little pain or no pain
- Healing time
- small areas may take months to heal
- large areas to be grafted
- Scarring present
7
Q
What is the rule of nines?
A
- Head and neck 9% (total)
- Ant 4.5%
- Post 4.5%
- RUE 9%
- Ant 4.5%
- Post 4.5%
- LUE 9%
- Ant 4.5%
- Post 4.5%
- RLE 18%
- Ant- 9%
- Post 9%
- LLE 18%
- Ant- 9%
- Post 9%
- Anterior tunk 18%
- Post trunk 18%
- Perineum 1%
8
Q
Criteria of major burn?
A
- 2nd degree burn
- Adults: > 20% TBSA
- Extreme Age: > 10% TBSA
- 3rd degree burn involving:
- Adults: >10% TBSA
- ANY electrical burn
- Burn associated w/ smoke inhalation
- Burns of: (any %)
- Face
- Airway
- Genitalia
9
Q
Pathophysiology of Burns
A
2 distinct phases:
1) burn shock phase
2) hypermetabolic state
SIRS response
Every system affected
- Necrotic area & ischemia area
- Potential viability of ischemic area w/ adequate (fluid) resuscitation
- Minutes to hours – burned tissue releases inflammatory and vasoactive mediatorsAll lead to ↑ capillary permeability:
- Ex: Histamine, prostaglandins, kinins, leukotrienes, thromboxane, nitric oxide
- LATER → reperfusion injury (produces…)
- ROS (reactive O2 species)
- Toxic cell metabolites → causing:
- further cellular membrane dysfunction
- propagation of immune response (worsens immune response)
10
Q
What should we keep in mind in regards to burn zones?
A
- Burn
- zone of coagulation- area dead
- zone of stasis
- zone of hyperemia
- with adequate resuscitation, zone of stasis and zone of hyperemia blood flow can be restored and maintain viabiilty
- without adequate resus, the zone of coagulation will grow and zone of stasis will become infarcted and won’t be able to regenerate
11
Q
Electrical burns?
A
- Devastating injury to bones, BV, muscle, and nerves
- tissue damage based on voltage and duration
- entry and exit are where most energy (damage) are concentrated
- 10-46% with concurrent cardiac arrhythmias; may have damage to the myocardium
- massive muscle damage leads to renal failure secondary to myoglobinemia (from rhabdo)
12
Q
Symptoms Inhalational injury?
A
- hoarseness
- sore throat
- dysphagia
- hemoptysis
- tachypnea
- accessory muscle usage
- wheezing
- carbonaceous sputum
- increased CO levles
13
Q
Types of inhalational burns?
A
- Most commonly associated with thermal burns
- likely in closed space burn; suspect in pt unconscious at scene
- 3 types
- 1) Upper airway injuries- inhalation of superheated air/steam
- may spare lower airway d/t reflexive VC closure
- 2) Lower airway/parenchymal
- soot particle/chemical inhalation
- acute phase will have significant bronchopasmsbronchodilator therapy always required
- may need epi b/c refractory to other treatment
- 3) metabolic asphyxiation- carbon monoxide, etc.
- 1) Upper airway injuries- inhalation of superheated air/steam
14
Q
Pathophys of inhalational injury?
A
- microvascular changes
- heat denatures proteins, activates complements
- causes release of histamine
- histamine causes release of xanthin oxidase
- enzyme involved in breakdown of purine–> uric acid
- ROS released ROS combine with NO–> reactive nitrogen species formed
- causes edema in burned area
- increases microvascular pressure and permeability to protein
- release proinflammatory cytokine and oxygen free radical/interleukin
- attract polymorphonuclear cells to area and neutrophils applify release of oxygen radicals, proteases and other materials
- becomes vicious cycle
15
Q
Consequence of inhalational injury?
A
- Coagulopathy
- Bronchospasm
- mucus secretion–> airway obstruction
- airway epithelial exfoliation because of neutrophil migration
- increased airway blood flow
- causes airway wall edema
- upregulation of adhesion molecules, ROS, superoxide
- end up with lots of cellular dysfunction, pulmonary edema, V/Q mismatch, loss of hypoxic vasoconstriction
- causes airway wall edema
- All major burns are going to have change in pulmonary physio even with no direct inhalational injury
16
Q
Indications for ealy trahceal intubaiton after inhalation injury
A
- Extensive burn over face/neck
- over s/s of airway obstruction by edema
- inability to protect the airway
- sig toxicity from CO or cyanide
- Respiratory failure
- hemodynamic instability
17
Q
What is carbon monoxide poisoning?
A
- Carbon Monoxide Poisoning
- Suspect w/ inhalation injuries
- Detected by measurement of arterial COHgb levels
- Severity of symptoms correlates w/ CO Hgb levels
- > 30% CO Hgb NEED:
- High FiO2 to reduce COHb half life Elimination of COHgb dependent on alveolar O2 pressure (not alveolar ventilation)COHb ½ life
- 21% FiO2 (RA): 4 hrs
- 100% FiO2: 60-90 min
- High FiO2 to reduce COHb half life Elimination of COHgb dependent on alveolar O2 pressure (not alveolar ventilation)COHb ½ life
- > 30% CO Hgb NEED:
- Why problem: Affinity for Hgb: CO > O2
- 200x greater affinity for hemoglobin than O2
- Oxygen-Hgb Dissociation Curve→ shift to left/reduces O2 release
- Affinity of CO:
- Myoglobin > Hgb (greater affinity for myoglobin than Hgb***)
- Binding cardiac myoglobin leads to →
- Myocardial depression
- HypoTN
- Arrythmias
- Metabolic acidosis at cellular level
- D/t O2 delivery being impacted
- FALSELY HIGH pulse ox readings
- Tx:
- Hyperbaric oxygen may be considered if COHgb is > 30%
- If suspected, intubation is recommended until eval can be completed
18
Q
Symptoms associated w/ specific COHgb levels
A
Symptoms noted at >20%
19
Q
What is cyanide poisoning?
Symptoms?
Treatment?
A
- Blocks intracellular use of O2 → leads to tissue hypoxia
- Binds to the terminal cytochrome of ETC
- Result:
- Hypoxia
- lactic acidosis
- ↑ mixed venous O2 sat (bc not using O2 that’s being delivered)
- Result:
- S/S Neuro:
- loss of consciousness, mydriasis (pupil dilation), seizures
- CV/pulm:
- HoTN
- tachypnea (then →) apnea
- ↑ lactate levels
- ANTIDOTE: Hydroxocobalamin (Vit B12)
- Actively binds cyanide by forming cyanocobalamin
- Directly excreted via the kidney
- Other treatment to combine w/ B12: amyl nitrate, sodium nitrite, sodium thiosulfate
- **anything with furniture → think cyanide poisoning
20
Q
What are pharmacokinetic changes involved in the burn shock phase? hypermetabolic phase?
A
- Biphasic response to injury
- Burn shock developed 6-8 hours after injury
- hypermetabolic phase develops in several days to weeks after
- Burn shock phase: generally decreased requirements
- reduction in hepatic and renal blood flow
- prolonged rate of drug distribution
- prolonged onset of clinical effects
- Hypermetabolic: phase: generally increased requirements
- Decreased albumin
- increased alpha 1-acid glycoprotein
- denervation phenomenon with spreading of acetylcholine receptors
- increased nicotinic acetylcholine receptors and decreased function
21
Q
Anesthetic considerations for patients with burn injuries?
A
- Fluids
- crystalloid mainstay for early phase
- colloid considered after 24 hours
- Succinylcholine
- succ okay <24 hours
- avoid if >24 hours and up to 18 months after burn injury
- Nondepolarizing muscle relaxants
- increase dose frequency and requirements (2-5 fold)during hyperdynamic phase
- no change in reversal requirements
- Consider rocuronium > 24 hours after burn injury for RSI
- IV anesthetics
- decrease dose early phase
- increase dose hyperdynamic phase
- use multimodal therapy
- Inhalation agents
- Decrease MAC early phase
- Increase MAC hyperdynamic phase
- may be beneficial for inhalation injury (bronchodilator)
- Beta blocker
- attenuate hyperdynamic phase
- Insulin
- attenuate hyperdynamic phase burn injury
22
Q
CV changes in early vs late phase?
A
- Early:
- hypovlemia
- decrease cardiac output
- increase SVR
- decrease contractility
- Late
- increase cardiac output
- tachycardia
- systemic HTN -Depleted catecholamine
- decrease SVR
- decrease contractility
23
Q
Pulmonary changes in burn early vs late phase?
A
- Early:
- Airway obstruction and edema
- pulmonary edema
- carbon monoxide poisoning
- Late:
- chest wall restriction due to scar formation
- tracheal stenosis due to repeat/prolonged intubation
24
Q
Renal and hepatic changes in burn injury early vs late phase?
A
Renal
- Early
- decrease GFR
- myoglobinuria
- Late
- increase GFR
- Increase tubular dysfunction
Hepatic
- Early
- decrease perfusion
- Late
- increase perfusion
- increase metabolism
25
Q
Endocrine and metabolic early vs late?
A
- Early
- no changes
Late
- increase metabolic rate
- increase core body temperature
- increase muscle catabolism
- increase insulin resistance
- increase lipolysis
- increase glucolysis
- decrease thyroid and PTH hormone
26
Q
Hematologic changes early vs late
A
- Early
- hemoconcentration (increase Hct)
- hemolysis
- thrombocytopenia
- Late
- anemia
27
Q
GI changes in early vs late phase?
Neuro changes?
A
GI
- Early
- decrease perfusion with mucosal damage
- late
- stress ulcers
- adynamic ileus
Neuro
- early
- increase cerebral edema
- increase ICP
- Late
- hallucination
- personality change
- delirium
- seizure
- coma
28
Q
Initial Airway assessment and management in burn patients?
A
consider inhalational injury likelihood
- facial burn
- hoarseness
- evidence smoke exposure
- insepct neck and oral cavity
- gold standard airway assessment: fiberoptic bronch
- CXR is usually normal in early phase
- Early intubation when upper airway injury suspected- do not wait for decompensation
- intubation will be easier if not delayed
- always cuffed ETT
- awake, spontaneously breathing fiberoptic intubation if any airway abnormality suspectedtopical anesthesia plus hypnotic that preserves spontaneous ventialtion
- ketamine
- dexmedetomidine
- opioids/sedatives judiciously
- If no airway abnormality, rapid sequence techniques can be used however NO SUCCINYLCHOLINE permitted beyond 1st 24 hours after injury
- severe airway burns may require immediate surgical airway/trach
- Potential difficult airway
- face
- neck
- upper chest burn
29
Q
Initial managmeent in burn shock phase?
Fluid resusitation? Target fluid resusitation?
When is fluid loss the greatest?
What complications can over-resuscitation cause?
A
- Combination of distributive, hypovolemic, and cardiogneic shock
- priorities
- airway managmenet
- fluid resus
- crystalloid only in first 24 hours
-
Fluid resusitation: All based on pt weight and % TBSA burned
- parkland formula most widely used foruma in world
- recommended fluid is LR
- 4mL/kg per percentage of TBSA in 1st 24 hours
- 1/2 of calculated volume in first 8 hours
- remained of fluid over next 16 hours
- 4mL/kg per percentage of TBSA in 1st 24 hours
- may need dextrose containing fluid for children in early phase d/t depletion of glycogen stores
-
target fluid resus
- normal BP
- UOP 1-2mL /kg/hr
- blood lactate
- base deficit
- gastric intramucosal pH >7.32
- normal CVP/CI/O2 delivery index
- fluid loss greatest in first 12 hours; stabilizes at 24 hours
-
over-resus can lead to complication
- intraabd HTN ( intra abd > 12 ,mHg)
- Abd compartment syndrome (intra-abd pressure >20 mmHg)
- see organ damage and death at this point
- pericardial effusion/pleural effusion
- pulmonary edema
- conversion of partial thickness to full thickness lesion
- crystalloid fluid of choice in 1st 24 hours
30
Q
Physio behind of hypermetabolic phase of burns?
Symptoms?
Treatment?
A
- Develops over several days to weeks; changes persist long term
- Caused by an immense surge in catecholamines and corticosteroids (10-50x baseline)
- increase myocardial O2 consumption and cardiac work
- cardiac output/HR increase 150% above non-burn patient
- can stay elevated 2 years post burn
- Caused by an immense surge in catecholamines and corticosteroids (10-50x baseline)
- S/S
- Persistent tachycardia
- systemic HTN
- Tachypnea
- increased muscle protein degradation
- insulin resistance
- elevated core temp
- liver dysfunction
- increased risk of infection
- can lead to physical exhaustion and death without treatmnt
-
Treatment:
- Early excision and grafting
- warming strateigies
- nutritional support
- insulin
- beta blockers
31
Q
What are escharotomies and grafting considerations?
A
- Early debridement is preferred with closure/grafting
- decreases rate of sepsis
- surgeries often stagedusually started on 2nd day to 2nd week after injury
- burn has to establish itself
- indications to suspend surgery and return later:
- 20% BSA excised (may extend to larger area if stable)
- time of 2-3 hours
- temperature drop to 35C
- blood los requiring 10 units or more of PRBC
- Surgery done every 2-3 days
- blood loss can be significant
- up to 2L in 15-20 min
- anticipate need for massive transfusion
- manage fluid/electrolyte abnormalities
32
Q
NPO status in burn patients?
A
- Adequate caloric intake is critical in ongoing mgmt
- NPO after MN NOT appropriate
- enteral feeds
- intubated pt ;no need to D/C enteral feeds before sx
- Unintubated pt: feeds stay on up to 4 hours before sx
- once in OR: decompress NG tube
- check gastric residuals
- Parenteral feeds: continue intraop and do not use the line for lipids and hyperalimentation
33
Q
Preop setup for burn patients?
A
- Warm the OR ahead of time
- should not exceed 95 degree
- Check availability of blood products and order more if needed
- based on preop Hgb, size of burn, extent of planned debridement
- have blood products immediately available in OR as surgical debridement is initiated. critical for ped patient
- have at least one blood warmer primed, plugged in, and turned on
- if burn large, have two
- make sure you have adequate IV access before srugoen begins debriding burn
- have adequate supply of narcs/MR
- know and plan ahead of time if invasive lines needed
- plan for airway mgmt and ventilation both intraop/postop as needed
- have a plan but be willing to modify it if necessary
34
Q
Induction for burn patient?
A
- All standard monitorschallenges: ECG lead, NIBP, SPo2 placement
- suture/staple ECG leads in
- may need invasive BP
- Rare to see pt in OR in 1st 24 hours
- urgent surgery needed at outset you must reduce dosage of inducitona gents secondary to shock
- NO SUCCINYLCHOLINE after 1st 24 hours
- Expect resistance to NDNMB- higher/more frequent dosing
- if unable to take off ICU vent, consider TIVA
- consider benefits of VA
- helpful with bronchospasm
- no ideal anesthetic mgmt but ketamine helpful
- increase SVR
- maintain airway reflex preservation
- analgesic
- use anticholinergic along with ketamine
35
Q
Intraop considerations for burn patient?
A
- ABP required if >20-30% TBSA involved
- Accurate temp monitoring essential/avoid hypothermia/actively warm
- HME
- Low flows
- OR 28-33 degree celsius
- plastic to retain heat
- continue ICU infusions (including narcs) and O2 during transport
- ensure ETT securement is infalliable
- may not be able to secure tube to face as usual
- blood loss can be rapid and tremendous- need adequate product immediately available and checked in room
- start unit immediately after induction or even prior
- don’t only look at suction, look at drape too
- anticipate use of epi-soaked gauze, may see systemic effects
- pain control
- may need co-oximeter to look at metHgb and CarboxyHgb concentration
36
Q
Burns and NMB considerations?
A
- Proliferation of extrajunctional nicotinic Ach receptors
- increased resistance to NDNMB
- Increased sensitivity to depolarizing MR
- succinylcholine >24 hours postburn injury is prohibited
- potentially lethal hyperkalemic response
- may persis for 18 months p injury
- resistance to NDNMB may develop within week of burn injury
- persist for up to a year
- 2-5 fold dose increase
- roc in large doses up to 1.2 mg/kg can be used RSI
- Resistane does not prolong recovery times or alter efficcy of reversal agnets
37
Q
Ventilator management for burn patients?
A
- Anticipate pulmonary compromise
- RAD
- Laryngospasm
- bronchospasm
- V/Q mismatch
- decrease pulm compliance
- PNA
- ALI
- ARDS
- HIgh fio2 and frequent sucitoning needed (thick/copious secretion)
- Lung protective ventilation
- target TV 4-8 mL/kg
- plateau pressure <30 cm H2o
- permissive hypercapnia up to pH 7,2
- HFOV (if needed) may require TIVA
38
Q
A 37 year old female was in a house fire. She has extensive burns to her face/ neck/ torso & arms.
VS:
- Heart rate: 145
- BP 100/50
- RR 32
- SpO2 93%
- She is confused and complaining of a headache
What is the TBSA you estimate for her burns?
What would you expect her physiological response to be from the burns in this acute phase?
How would you treat her in this acute phase?
A
63%
Physiological response –> burn shock phase
Treat: Fluids
- parkland formula
- intubate early
- suspicion of inhalational injury
- respiratory distresss/failure probable
- CO or cyanide poisoning
- treatment: high FiO2 and Vit B12
- Temp management (examples)
39
Q
A 37 year old female was in a house fire. She has extensive burns to her face/ neck/ torso & arms. Her burn was 3 hours ago.
- VS:
- Heart rate: 145
- BP 100/50
- RR 32
- SpO2 93%
- She is confused and complaining of a headache
What is your plan on induction?
A
High FiO2
Succs ok (< 24 hrs)
Roc ok
Reduce doses of induction agents –> shock phase!
Ketamine: helpful!
- increase SVR
- maintain airway reflex preservation
- analgesic
- use anticholinergic along with ketamine
