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
18
Q
Symptoms associated w/ specific COHgb levels
A
Symptoms noted at >20%
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
