smoke and thermal injury Flashcards

1
Q

what caused direct thermal injury

A

caused by the inhalation of hot gases

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2
Q

What is the effect of direct thermal injury on distal airway

A

they are spared due to:
– Ability of upper airways to cool hot gases
– Reflex laryngospasm
– Glottic closure

usually do not occur below the level of the larynx

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3
Q

what are the local toxins contain in smoke that cause direct airway damage

A

acolein, formaldehyde, sulphur dioxide and nitrogen dioxide

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4
Q

what is the result of local toxin on direct airway?

A

an acute inflammatory process mediated by leukocytes, especially neutrophils

Symptoms appear until 24 hours after

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5
Q

what are two systemic toxin that cause systemic effect?

A

CO: most frequent to cause death from inhalation injury

Cyanide: inhibition of cellular oxygenation, causing tissue anoxia through inhibition cytochrome oxidase enzymes (Fe3+)

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6
Q

what is the definition of smoke inhalation injury?

A

the aspiration of superheated gases, steam or noxious substances of incomplete combustion

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7
Q

what lead to smoke

A

pyrolysis: smoldering in a low-oxygen environment
combustion: burning, with visible flame, in an adequate-oxygen environment

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8
Q

what cause the pathologic change in distal airways and alveoli

A

–Irritating and toxic gases
–Suspended soot particles
–Vapors associated with incomplete combustion and smoke

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9
Q

what happens at early stage (0-24hr after inhalation)

A

tracheobronchial tree becomes more inflamed resulting in bronchospasm

overabundance of bronchial secretions to move into the airways, resulting in further airway obstruction.

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10
Q

smoke effect on mucosal ciliary transport

A

slow the activity of the mucosal ciliary transport mechanism, causing further mucous retention

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11
Q

what else can smoke inhalation cause

A

ARDS

noncardiogenic high-permeability pulmonary edema –> “leaky alveoli.”

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12
Q

what else can cause Noncardiogenic pulmonary edema

A

overhydration resulting from overzealous fluid resuscitation.

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13
Q

what happens during the intermediate stage ( 2 - 5 days)?

A
  1. upper airway injury improve
  2. pathologic change deep in leak usually peak
  3. mucosa of the tracheobronchial tree frequently becomes necrotic and sloughs (usually at 3 to 4 days).
  4. mucous accumulation often leads to bacterial colonization, bronchitis, and pneumonia.
  5. ARDS may develop
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14
Q

what happen in late stage of smoke inhalation injury (5 or More Days after)

A

Infections resulting from burn wounds on the body surface are the major concern during this period.

–> can lead to sepsis MODS,pulmonary embolism

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15
Q

what are the Anatomic Alterations of the Lungs Thermal Injury?

A
  • Blistering
  • Mucosal edema
  • Vascular congestion
  • Epithelial sloughing
  • Thick secretions
  • Acute upper airway obstruction
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16
Q

how is burning classified?

A

1st degree burn
2nd degree burn
3rd degree burn

17
Q

what is 1st degree burn

A

Red with no blister

6-10 day heal to normal

18
Q

what is 2nd degree burn

A

Damage to epidermis and dermis

Red and blisters

time is between 7 and 21 days.

normal to a hairless and depigmented skin with a texture that is normal, pitted, flat, or shiny.

19
Q

what is 3rd degree burn

A

Full thickness; dermis, epidermis & underlying tissue

Tissue charred and coagulated
•Healing after 21 days to scarring or may never occur without skin grafting, poor ROM
•May not heal without grafting

resultant damage heals with hypertrophic scars (keloids) and chronic granulation

20
Q

What suggest inhalational injury

A

facial burns
soot/black mucous
singed nasal hair
wheezing, crackles

21
Q

what suggest upper airway

obstruction

A
oral & laryngeal edema
painful swallow
stridor
hoarseness
difficulty speaking
22
Q

what are 2 complication associated with inhalation injury

A

CO poisoning

hydrogen cyanide poisoning

23
Q

what are the Treatment of Inhalational Injury

A
Mainly supportive:
–100 % O2
–Humidity
–Pain medication
–Monitor for edema or respiratory failure
42
24
Q

how to manage CO Poisioning

A

o2 reduces half life of CO

Via: hyperbaric chamber and/or 100% O2

half life breathing 21%: 5 hours
half life with 100% : 1 hour
half life breathing 100% at 3 atm: < 1 hour

25
Q

what is Cyanide poisoning?

A

inability to utilize O2 at cellular level, and shock (vasodilation)

26
Q

what are the treatment protocol for Cyanide poisoning

A

amyl nitrate inhalation

sodium nitrate injection

27
Q

how does IV sodium thiosulphate

A

help with clearance of MetHb by forming thiocyanate which can be easily excreted in urine

28
Q

what is the result of HCN?

A

shift to anaerobic metabolism
metabolic acidosis
decrease O2 transport

29
Q

what is the lab findings for inhalation injury

A

ABG: Acute Alveolar Hyperventilation (Acute Respiratory Alkalosis)

PFT: primarily restrictive lung pathology then combined (+ obstructive) after recovery

30
Q

what are the radiological findings

A

• Usually normal (early stage)
• Pulmonary Edema/ARDS
(intermediate stage)
• Patchy of segmental infiltrate (late stage)