Burns (JVECC review 1+2, Henrikkson papers, CCM 130) Flashcards
How do you differentiate local burn injury versus severe burn injury?
severe burn injury involves >20-30% TBSA and results in burn shock with systemic involvement
local burn injury does not typically cause systemic disease
What are the 2 phases of burn shock?
- resuscitation phase (immediately after injury, lasts 24-72 hours)
- hyperdynamic hypermetabolic phase (begins 3-5 days after injury, can last up to 24 months)
name 4 types of burn injury most commonly encountered in small animals
- thermal injury
- radiation injury
- chemical injury
- electrical injury
What are the different classifications of burn depth, list the dermal layers involved, wound characteristics and healing
Superficial
* Epidermis only
* erythematous desquamation, dry flaky appearance, may not be immediately visible
* heals within 3-5 days via re-epithelialization, minimal scar formation
Superficial partial thickness
* Epidermis + upper 1/3 of dermis (papillary layer)
* erythematous, moist blances, painful blisters, edema may present eschar formation
* heals in 1-2 weeks via re-epithelialization, minimal scar formation
Deep partial thickness
* Epidermis + all dermis
* red-waxy white, reduced pain sensation, blisters, eschar
* heals in 2-3 weeks, surgical intervention recommended to prevent significant scar formation
Full-thickness
* Epidermis + dermis + subcutaneous tissue
* bloodless pearl-white eschar formation
* hair easily plugged
* requires surgical intervention for healing
What are the 3 zones of burn injuries?
Zone of coagulation
* area of initial and most severe thermal injury
* most cellular damage
* thermal injury –> coagulation of constituent proteins –> irreversible tissue loss –> primary location of eschar formation
Zone of stasis
* capillary vasoconstriction –> decreased tissue perfusion –> ischemia
* mixture of viable and nonviable cells
* tissue damage potentially reversible (need to restore blood flow, e.g., fluid therapy) –> otherwise becomes zone of coagulation
Zone of hyperemia
* viable cells
* local inflammatory mediators –> vasodilation
What main mediators are implicated in the development of the resuscitation phase of severe burn injuries?
- Prostaglandins, prostacycline
- TXA-2
- ROS
- NFK-b, TNF-alpha, IL-1, IL-6
- Histamine
- caspases (myocardial apoptosis!)
- macrophage migration inihbitor factor
- kallikrein-kinin system»_space; bradykinin
How much does the CO in the hyperdynamic phase of patients with severe burn injuries increase?
1.5 x CO of a healthy person
What is the metabolic rate of a patient in the hyperdynamic phase of a patient with severe burn injuries?
3 x basal metabolic rate
List the 3 counterregulatory hormones driving the hypermetabolic state in severe burn injury patients
- cortisol
- glucagon
- catecholamines
Explain how burn patients develop hyperglycemia and the risk factors associated with hyperglycemia in patients with severe burn injury
hyperdynamic and hypermetabolic phase
* increased gluconeogenesis
* cortisol, glucagon, catecholamines –> insulin resistance
- hyperglycemia + high insulin cc for up to 4-5 weeks after SBI
hyperglycemia –> increased risk of bacterial or fungal infection, decreased wound healing, increased mortality
How does severe burn injury lead to hepatomegaly?
hypermetabolic state during the hyperdynamic state:
counteregulatory hormones (cortisol, glucagon, catecholamines) –> lipolysis –> increased triglyceride –> fatty liver –> hepatomegaly
Explain the pathophysiology of airway injury from smoke inhalation (include time line)
- direct thermal injury to the upper airway - effects seen within 24 hours
- soot adheres to the respiratory mucosa –> irritant binding
- inflammation –> edema –> airway obstruction and bronchospasms (peaks at 24 hours, can resolve over a few days)
- damaged mucosal cells –> exudate rich in protein, inflammatory cells, necrotic debris
- neutrophilic chemotactic response within 4 hours of injury –> inflammation –> inhibits the mucociliary apparatus
- exudate, mucus, cellular debris etc can move distally –> obstruction of lower airways
- within 3-5 day - exfoliation of the tracheal and bronchi lining –> pseudomembrane casts –> block lower airways –> inactivate surfactant –> segmental atelectasis (48-72 hours after smoke inhalation)
- bronchiolar obstruction peaks at 72 hours
- distal migration of particulate matter + bacteria –> pneumonia (in 50% of people with smoke inhalation injury)
Note: often appear better initially and full extend of injury take 24-36 hours to show
Besides Hb binding, what complications are associated with CO poisoning?
- induction of lipid peroxidation
- direct cellular damage
- reperfusion injury
- CNS demyelination»_space; delayed neurologic sequelae - 2 to 40 days after initial improvement
What is the expected timing of pharyngeal edema post burn injury with smoke inhalation?
occurs within first 24-48 hours and resolved after a few days
What is the time frame of pesudomembrane cast formation and secondary lower airway obstruction in patients with smoke inhalation?
48-72 hours
What are the two causes for neurologic signs after a patient sustained burn injuries or smoke inhalation?
carbon monoxide toxicity
cyanide toxicity
During carbon monoxide poisoning, what are the expected SpO2 and PaO2 findings
falsely higher peripheral oxygen saturation reading –> SpO2 cannot differentiate between oxyhemoglobin and carboxyhemoglobin
normal PaO2, unless pulmonary disease present as well
What is the likely diagnosis in a patient sustaining burn injuries with neurologic signs, normal co-oximetry, lactic acidosis, and normal PaO2?
Cyanide toxicity
What ocular injuries may occur from burn exposure?
exposure keratopathy
corneal ulceration
less common: corneal burn
orbital compartment syndrome (subsequent optic neuropathy and blindness)
What is the half-life of carboxyhemoglobin on room air, 100% oxygen administration, or 100% in hyperbaric conditions (HBOT)?
- 5 hours
- 1 hour
- 20 min
How soon after burn injury does hemodynamic instability typically ensue?
1-2 hours later
Describe the “Parkland” aka “Censensus” formula for fluid therapy in burn patients
administer 4mL/kg/%TBSA burned
50% of this over first 8 hours, rest 50% over next 16 hours
reduce by 25 to 50% in cats
e.g., cat 5kg 40% TBSA burned –> 4mL x 5 x 40 = 800 mL - 25% reduction 600 mL –> 300/8 = 37 mL/hr first 8 hours, then 300/16 = 19 mL/hr next 16 hours
What are the antimicrobial properties of honey?
- low pH
- hydrogen peroxide production
- high osmolality
Why is an elevated temperature not a reliable marker for secondary infections in patients with severe burn injury?
because during the hyperdynamic hypermetabolic phase, the set point temperature may be elevated by 2 C or 3.6 F
