Severe burn injury, burn shock, smoke inhalation parts 1 and 2 JVECC. 2012

Question 1

How do you differentiate local burn injury versus severe burn injury?

Answer 1

severe burn injury involves >20-30% TBSA and results in burn shock with systemic involvement

local burn injury does not typically cause systemic disease

Question 2

What are the 2 phases of burn shock?

Answer 2

• resuscitation phase (immediately after injury, lasts 24-72 hours)
• hyperdynamic hypermetabolic phase (begins 3-5 days after injury, can last up to 24 months)

Question 3

name 4 types of burn injury most commonly encountered in small animals

Answer 3

• thermal injury
• radiation injury
• chemical injury
• electrical injury

Question 4

What are the different classifications of burn depth, list the dermal layers involved, wound characteristics and healing

Answer 4

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

Question 5

What are the 3 zones of burn injuries?

Answer 5

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

Question 6

What main mediators are implicated in the development of the resuscitation phase of severe burn injuries?

Answer 6

• Prostaglandins, prostacycline
• TXA-2
• ROS
• NFK-b, TNF-alpha, IL-1, IL-6
• Histamine
• caspases
• macrophage migration inihbitor factor

Question 7

How much does the CO in the hyperdynamic phase of patients with severe burn injuries increase?

Answer 7

1.5 x CO of a healthy person

Question 8

What is the metabolic rate of a patient in the hyperdynamic phase of a patient with severe burn injuries?

Answer 8

3 x basal metabolic rate

Question 9

List the 3 counterregulatory hormones driving the hypermetabolic state in severe burn injury patients

Answer 9

• cortisol
• glucagon
• catecholamines

Question 10

Explain how burn patients develop hyperglycemia and the risk factors associated with hyperglycemia in patients with severe burn injury

Answer 10

hyperdynamic and hypermetabolic phase
* increased gluconeogenesis
* cortisol, glucagon, catecholamines –> insulin resistance

hyperglycemia –> increased risk of bacterial or fungal infection, decreased wound healing, increased mortality

Question 11

How does severe burn injury lead to hepatomegaly?

Answer 11

hypermetabolic state during the hyperdynamic state:
counteregulatory hormones (cortisol, glucagon, catecholamines) –> lipolysis –> increased triglyceride –> fatty liver –> hepatomegaly

Question 12

Explain the pathophysiology of airway injury from smoke inhalation (include time line)

Answer 12

• 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
• bronchiolar obstruction peaks at 72 hours
• distal migration of particulate matter + bacteria –> pneumonia (in 50% of people with smoke inhalation injury)

Question 13

Besides Hb binding, what complications are associated with CO poisoning?

Answer 13

• induction of lipid peroxidation
• direct cellular damage
• reperfusion injury
• CNS demyelination

Question 14

What is the expected timing of pharyngeal edema post burn injury with smoke inhalation?

Answer 14

occurs within first 24-48 hours and resolved after a few days

Question 15

What is the time frame of pesudomembrane cast formation and secondary lower airway obstruction in patients with smoke inhalation?

Answer 15

48-72 hours

Question 16

What are the two causes for neurologic signs after a patient sustained burn injuries or smoke inhalation?

Answer 16

carbon monoxide toxicity
cyanide toxicity

Question 17

During carbon monoxide poisoning, what are the expected SpO2 and PaO2 findings

Answer 17

falsely higher peripheral oxygen saturation reading –> SpO2 cannot differentiate between oxyhemoglobin and carboxyhemoglobin

normal PaO2, unless pulmonary disease present as well

Question 18

What is the likely diagnosis in a patient sustaining burn injuries with neurologic signs, normal co-oximetry, lactic acidosis, and normal PaO2?

Answer 18

Cyanide toxicity

Question 19

What ocular injuries may occur from burn exposure?

Answer 19

exposure keratopathy
corneal ulceration
less common: corneal burn

orbital compartment syndrome (subsequent optic neuropathy and blindness)

Question 20

What is the half-life of carboxyhemoglobin on room air, 100% oxygen administration, or 100% in hyperbaric conditions (HBOT)?

Answer 20

• 5 hours
• 1 hour
• 20 min

Question 21

How soon after burn injury does hemodynamic instability typically ensue?

Answer 21

1-2 hours later

Question 22

Describe the “Parkland” aka “Censensus” formula for fluid therapy in burn patients

Answer 22

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

Question 23

What are the antimicrobial properties of honey?

Answer 23

• low pH
• hydrogen peroxide production
• high osmolality

Question 24

Why is an elevated temperature not a reliable marker for secondary infections in patients with severe burn injury?

Answer 24

because during the hyperdynamic hypermetabolic phase, the set point temperature may be elevated by 2 C or 3.6 F