[216B] Trauma: Thermal Injury Flashcards
How well do pediatric patients compensate? Which failure happens first?
- Compensate well but decompensate quickly
- Resp. failure
How well do adult patients compensate? Which failure happens first?
- Not well due to comorbidities + aging
- Cardiac failure
What are 5 causes of thermal cell injury?
- Nutritional deficits
- Mechanical forces
- Chemical injury
- Radiation injury
- Extreme temp.
What are the 4 main mechanisms of the pathophysiology of cellular injury?
- Inflammation
- Hypoxia
- Cellular calcium dysfunction
- Free radicals
What are some examples of damage caused by excessive inflammation?
- Edema
- Ischemia
- Hypotension
- Hypoperfusion
- DIC
- Metabolic/lactic acidosis
- Hyperkalemia/glycemia
- Necrosis
What is the difference between hypoxia, hypoxemia, and ischemia:
Hypoxia: Low tissue O2
Hypoxemia: Low blood O2
Ischemia: Impaired O2 delivery due to low perfusion
What are 4 causes of hypoxia?
- Low air content
- Constriction/obstruction
- Altered cellular permeability
- Hypermetabolic states
The brain will be injured in _ mins if hypoxia is present.
4 mins.
The kidneys will be injured in __-__ mins if hypoxia is present.
15-20 mins.
How will Na+, K+ and Ca2+ be impacted in cell damage?
High intracellular Na+ (hyponatremia).
Low intracellular K+ (hyperkalemia).
High intracellular Ca2+ (hypocalcemia).
Electrolyte imbalances d/t cell injury will result in a fluid shift into the ________ space, which we will see as:
intracellular; cellular edema.
Hypoxia will cause the cell to use _______ metabolism for energy. Why is this bad?
Anaerobic: lactic acid byproduct will cause acidosis.
List 3 causes of calcium dysfunction.
- Hypoxia.
- Stimulation of the parathyroid gland.
- Inflammation.
What happens when the parathyroid gland is stimulated?
Ca2+ released into blood from bone.
Why would we see stimulation of the parathyroid gland in cell damage?
To compensate for low blood calcium (hypocalcemia) (despite there being high intracellular calcium, but the parathyroid doesn’t know this)
Free radicals will react with endogenous substances such as (3):
- Lipids (cell membranes).
- Enzymes.
- Cell structures/mechanisms (ex: proteins, DNA).
When free radicals combine with endogenous substances, they create:
ROS (reactive oxygen species).
ROS are endogenous byproducts of (2):
respiration & cell metabolism.
ROS are balanced by (2); give an example of each.
- Antioxidants (ex: Vit C)
2. Endogenous scavengers (ex: catalase)
List 6 examples of acute causative agents of free radicals.
- Radiation.
- Drugs.
- Pathogens.
- Inflammation.
- Chemicals (cytokines).
- Nicotine.
Oxidative stress is direct damage to individual cells via:
electron reactions.
Oxidative stress results in (3):
- Decreased function.
- Cytokine release = inflammation.
- Alteration of cellular metabolites.
Chronic oxidative stress results in:
ageing.
List 3 antioxidant agents.
- Ascorbate (vitamin C).
- Flavonoids.
- Carotenes (vitamin A).
Name 4 types of drug exposures that can cause cell damage. Give an example of each.
- Overdoses (ex: Tylenol d/t toxic metabolites).
- Drugs with narrow TIs (ex: aminoglycosides).
- Toxic exposures (ex: arsenic).
- CO (carbon monoxide).
Arsenic causes cell necrosis by _________ cellular ATP production. List 4 ways it does so.
Decreasing cellular ATP production:
- Imitates/replaces cellular phosphate.
- Inhibits pyruvate production.
- Inhibits cellular glucose uptake & gluconeogenesis.
- Directly induces oxidative stress.
Why is chelation therapy helpful in substance poisonings (ex: arsenic)?
It binds with the substance to prevent further damage, then the compound is excreted.
Why is polonium harmful to our cells? (3)
- Binds cell electrons = destruction > necrosis.
- Ionizes cells & H2O molecules > ROS formation.
- Direct DNA damage d/t electron binding.
Polonium will affect cells that:
multiply quickly (ex: bone marrow, WBCs, hair).
_______ is used in chelation therapy for polonium poisoning.
Dimercaprol.
Half life of polonium:
140 days.
Which UV rays are most skin damaging?
UVB.
UVB causes cellular damage in (3):
Melanin, Langerhans cells & immune cells.
UVB rays cause oxidative stress via:
ROS formation.
List 4 s&s of a superficial sunburn.
- Erythema (redness).
- Peeling of damaged skin.
- Dryness.
- Itchiness.
List 2 s&s of a moderate sunburn.
- Extensive blistering.
2. Oozing (“wet” appearance).
List 4 systemic effects of severe sunburn.
- Fever.
- Chills.
- Malaise.
- Dehydration.
How do we prevent sunburn?
Sunscreen!
What are the 2 types of sunscreens?
- Absorb UVR.
2. Reflect UVR.
What is the active ingredient in sunscreens that absorb UVR?
Benzones (ex: benzophenone, oxybenzone).
What is the main ingredient in sunscreens that reflect UVR?
Zinc (or zinc-like materials).
Are burns usually uniform in depth?
No :0
How long can it take to classify a burn? Why?
Several days: burns are dynamic and may progress to deeper wounds as time goes on.
Regeneration is present on _______ tissue. What should we do if this tissue is completely damaged or unavailable?
Dermal tissue: if none, graft.
List the 4 burn classifications. Which layers do each of them involve?
- Superficial: epidermis.
- Partial thickness: epidermis & dermis.
- Full thickness: full dermis & subcutaneous tissue.
- 4th degree: underlying structures (ex: bone, muscle, joints).
Which burn(s) blister?
Partial-thickness.
Which burn(s) are the most painful? Why?
Superficial: only burn type where pain nociceptors will be fully intact.
What is the healing time for superficial & partial thickness burns?
Superficial: 6 days.
Partial thickness: 7-21 days.
Partial thickness burns can be further classified into 2 categories:
Superficial or deep.
Dead black tissue in burns is called:
Eschar.
List 5 “do”s with superficial burns.
- Stop the burning with cool water or a cool compress.
- Relieve pain with analgesics or soothing lotions.
- Protect by loosely covering.
- Rehydrate for fluids & electrolytes.
- Keep blisters intact.
List 2 “don’t”s with superficial burns.
- No ice (further damage).
2. No oils/butter (trap heat, enhance burning).
Which type of burn is not counted by the rule of 9’s.
Superficial burns.
According to the rule of 9s, hypovolemia is present if >_% of the body is affected by the burn.
15%.
According to the rule of 9s, severe burn effects are likely if >_% of the body is affected by the burn.
40%.
List 3 severe burn effects in the burn zone.
- Direct cell membrane disruption > cell injury.
- Inflammation.
- Necrosis of affected tissue.
List 7 consequences of inflammation d/t tissue damage (ex: burns).
- Vascular injury/permeability.
- Hypoxia.
- Cellular Ca2+ dysfunction.
- Oxidative stress.
- Insulin resistance.
- Fluid shift ( > hypovolemia, hypoproteinemia)
- Stimulation of platelets > coagulation.
List 4 systemic severe burn effects.
- Hemodynamic instability (d/t loss of water & electrolytes).
- Hypermetabolic state (increased cell demand, stress response).
- Respiratory system dysfunction (ex: secondary inhalation injuries).
- Immune dysfunction > risk of infection/sepsis.
Which will we see first in a burn pt: hemodynamic instability or the hypermetabolic state?
Hemodynamic instability.
During hemodynamic instability, the pt is at risk for __________ ________, which will cause a ______ in CO.
hypovolemic shock; decrease in CO.
What 3 endogenous substances are released in the hypermetabolic state?
- Catecholamines.
- Cortisol.
- Inflammatory mediators.
List 5 inflammatory mediators released in a burn pt. Which is specific to burn stress?
- Bradykinin.
- Histamine.
- NO.
- Cytokines.
- Hydrogen sulfide (produced in liver in response to burns).
When will the hypermetabolic state start? How long can it last?
Starts 24-72 hrs post-burn, but may last up to 2 years.
What will the body do to overcompensate in a hypermetabolic state? (3)
- Have high CO.
- Induce high cellular metabolic rates.
- Induce fever.
List 3 things we would see in a metabolic crises.
- Protein catabolism (breakdown) d/t injury.
- Hyperglycemia d/t extreme glucose mobilization but insulin resistance.
- Electrolyte imbalance.
List 11 treatments for burns.
- ABCs.
- Oxygenation (possibly intubation).
- Hemodynamic stability via IV fluids & electrolytes.
- Thermoregulation (initial cooling, warm room after).
- Treat lactic acidosis (O2, sodium bicarb, glucose admin).
- Nutrition (enteral feeds).
- Manage hyperglycemia with insulin/oral antidiabetics.
- Prevent infection (sterile dressings, isolation).
- Escharotomy.
- Wound grafting asap.
- Manage hormonal imbalances d/t hypermetabolic responses (check labs & correct).
Do we give prophylactic abx to burn pts?
No d/t risk of creating resistant organisms.
What is escharotomy?
Debridement/making an incision in the eschar to relieve pressure & prevent compartment syndrome.
What 3 additional txs might we need for electrical burns?
- Tx of the exit wound,
- Arrhythmias (asystole, heart block, vfib)
- Seizures (changes to CNS depolarization).
List 3 possible associated injuries in burn pts. Which is most common?
- Fractures (most common: 50-60%).
- Head injuries (up to 25%).
- Inhalation injuries (ex: cyanide poisoning).
