T H E R M A L I N J U R Y Flashcards

1
Q

Most common cause of burn injury

A

Scald (80% treated as outpatient)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Most common cause of burn injury requiring admission to burn unit

A

FLAME due to house fire or clothing ignition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

American Burn Association Criteria for Admission to Burn Center

A

2nd or 3rd degree burns of >10% BSA in pots 50 y.o.
2nd or 3rd degree burns of >20% BSA
Significant burns to face, hands, feet, genitalia, perineum, or skin of major joints
Full thickness burns of >5% BSA at any age
Significant electrical injury (inc. lightning)
Significant chemical injury
Lesser burn injury in conjunction with inhalation injury, trauma, or pre-existing medical conditions
Burns in patients requiring special social, emotional, or rehab assistance (i.e., child or elder abuse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

If burns are <25% BSA, what is initial tx for analgesia?

A

Cold saline soaks. Watch for hypothermia. Cover burns with clean sheet and then warm blanket.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When assessing severity and extent of burns, which degree burns do you use to calculate %BSA burnt?

A

Only 2nd and 3rd degree burns.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Palm of patients hand is roughly equivalent to what % BSA?

A

1% BSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Parkland formula for fluid estimates in burn victims

A

For first 24 hours, LR at rate of 4 mL/kg/%BSA burn. Give half of 24-hour requirement in first 8 hours from time of burn and remainder over next 16 hours. If pediatric, use 3 mL/kg/%BSA burn.
In the second 24 hour period, change fluid to D5 1/2 normal saline, and give albumin is <3.0 and patient is hypotensive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Use crystalloid as fluid replacement in burn victims unless?

A

Fluid requirement based on urine output is >2 times estimated in first 12 hours.
By 48 hours, both are equally effective at restoring intravascular volume and CO, but colloid is associated with more pulmonary complications and higher mortality.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

%BSA of head/neck at birth

A

19%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

%BSA of head/neck of adults 15+

A

9%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

%BSA of each arm

A

9%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

%BSA of anterior trunk

A

18%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

%BSA of each leg in adult 15+

A

18%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Adequate UO in adults (indicative that resuscitation is good)

A

30-50cc/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Adequate UO in children <30 kg

A

1 cc/kg/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When should you adjust fluids in burn victims?

A

UO >33% different (in either direction) from recommended over 2-3 hours.

17
Q

In oliguric patients, when should diuretics be considered?

A

When you are concerned about myoglobinuria – seen with high voltage injury, soft tissue mechanical injury, deep burns involving muscle, extensive burns with excess fluid.
If mannitol is used, patient requires central venous pressure line because UO ceases to be adequate assessment of fluid status.

18
Q

4 types of injuries that require increased fluid requirements

A

High voltage electrical injury
Inhalational injury
Delayed resuscitation
Intoxicated at time of injury

19
Q

3 types of patients that require decreased fluid requirements

A

Patients >50, <2 y.o., or with cardiac or pulmonary disease

20
Q

Effect of burns on CV system pre-resuscitation

A

Increased microvascular permeability secondary to released vasoactive materials (via arachidonic acid pathway, substance P, IL-1, IL-6, IL-8, histamine)
Decreased CO but overall hyper dynamic state with increased EF.
Increased hct due to decreased blood volume, increased blood viscosity.
Increased PVR
Oliguria because decreased blood volume and CO lead to decreased RBF and decreased GFR.

21
Q

Effect of burns on CV system after resuscitation

A

Persistent hyperdynamic state:
CO increased, leading to increased RBF and GFR. Elevated metabolic requirements. Elevated catecholamines and glucagon. Decreased levels of insulin and thyroxin. Result in catabolic state.
EDEMA (peaks 8-12 hrs) as fluid is lost from intravascular compartment

22
Q

Effect of burns on pulmonary system

A

In absence of thoracic burns or inhalation injury, hypovolemia may result in rapid but shallow respirations.
After resusc., hyperventilation occurs with or without modest parenchymal dysfunction, leading to a mild respiratory alkalosis.
Increased pulmonary vascular resistance but no change in pulmonary capillary permeability.
With circumferential thoracic burns, the constricting eschar and edema cause a restrictive defect and may necessitate escharotomy.

23
Q

Effect of burns on hematologic system

A

Plasma loss.
RBC destruction in proportion to extent of burn: cell lysis secondary to heat, microvascular thrombosis in areas with tissue damage.
Early: decreased platelets and fibrinogen, increased fibrin degradation products.
Later, levels return to normal and the become elevated, though antithrombin III and protein C are decreased.

24
Q

Effect of burns on GI system

A

Most puts with >25% TBSA will have an ileum that resolves between day 3-5. GI permeability is increased with increased bacterial translocation. Patients generally require NG tube and GI pox with H2 blocker.

Burn patients are susceptible to CURLINGS ulcer which is due to lack of the normal mucosal barrier.

25
Q

Effect of burns on endocrine system

A

Increased glucagon, cortisol, catecholamines. Decreased insulin, T3.

26
Q

Immunologic effect of burns

A

Loss of skin barrier function.
>20% BSA, cell mediated immunity decreases in proportion to burn size.
Early decrease in WBC (esp. lymphocytes) then agranulocytosis and B-lymphocytosis with T-cell activation.
Decreased IL-2, IgG, NK cells.
Increased IL-6, TNF-a.
PMN dysfunction: immunosuppression, increased susceptibility to infection, decreased chemotaxis, dysfunction related to size of burn.

27
Q

Metabolic and nutritional effect of burns

A

Hypermetabolism: increased O2 consumption, increased CO, increased minute ventilation volume, increased temperature, increased urinary nitrogen.
Greatly increased blood flow to wound.
Catecholamine release, especially NE.
Increased UUN (VC1) secondary to breakdown of muscle protein to glucose because of greatly increased need for glucose.
Increased protein and calorie needs.
Start PO supplementation by NG tube day 3 or 4 if no oral intake but ileum resolved.

28
Q

Tx of invasive burn infection

A

Change to Sulfamylon (Mafenide acetate) and start systemic abx. IT penetrates eschar well.

29
Q

Tx of pseudomonas or pediatric burn infections

A

Infuse subeschar piperacillin and plan for emergent operative debridement within 12 hours.

30
Q

Tx of Aspergillus-infected burns

A

If it crosses the fascia, amputation fof extremity required

31
Q

Tx of viral infection with HSV-1 infected burns

A

7 days of 5% acyclovir ointment

32
Q

Cause of death in over half of fatal burns

A

Pneumonia–usually s. aureus or gram negatives such as E. coli and enterococcus. Usually onset after day 10.

33
Q

Burn scar cancer

A

Marjolin’s ulcer
Usually SCC which metastasizes. Dx made by biopsy.
Tx is wide excision of all involved tissue.

34
Q

Which type of burn injury is most likely to require fasciotomy?

A

Electrical injury – deep tissue edema may be extensivee causing compartment syndrome.

35
Q

3 priorities in tx of chemical injury

A

Removal of clothing to prevent further contact.
Copies water lavage-irrigation for at least 30 minutes for acid burns and longer for alkali burns bc they penetrate deeper into tissue.
Check pull status for edema, mucosal desquamation, bronchospasm.

36
Q

Smoke inhalation injury leads to what kind of toxicity, and what are the major clinical mx? PS not talking about CO poisoning.

A

HCN!! Produced from the combustion of nitrogen-containing synthetic polymers. HCN is a potent and fast acting poisoon, and blood levels cannot be measured rapidly to confirm dx. Exposure to moderate-to-high concentrations causes sx to develop rapidly. Earlly causes neurologic and cardiorespiratory stimulation and patients develop headache, vertigo, dizziness, hyperventilation, tachycardia, nausea and vomiting. Neurologic, respiratory, and cardiovascular depression eventually occurs and mx as coma, seizures, bradycardia, hypotension, and cardiorespiratory arrest. Cy

37
Q

Tx for cyanide tox

A

Hydroxocobalamin or sodium thiosulfate which directly binds cyanide molecules. Alternatively, can induce methemoglobinemia with nitrites to increase ferric iron (Fe3+) in circulating hemoglobin. Cyanide binds avidly to Fe3+ and so methemoglobinemia provides an alternate binding site.

38
Q

Best tx plan for pt with frostbite injuries to extremities

A

Rapid rewarming with warm water (40-44 C). This results in less tissue damage than treatment with slow rewarming. The extremity should be immersed in the warm water which is continuously circulated.