Smoke Inhalation Flashcards

1
Q

T/F 50% of fire related deaths are from smoke inhalation and not from the burns.

A

FALSE–80% from smoke inhalation

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2
Q

What does smoke include?

A

vapors, gases, fumes, heated air, particulate matter, liquid and solid aerosoles

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3
Q

_____ animals are more likely to present for smoke inhalation.

A

younger (pets

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4
Q

What factors play into the LD50 for smoke inhalation?

A

substances burning, combustion products, temp of fire, length of exposure, availability of oxygen, size of animal

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5
Q

Toxicity of smoke inhalation is due to?

A

burns in resp tract enhance toxicity, super heated air and steam cause thermal burns to resp tract (higher temp and humidity increase injury), benzopyrene (carcinogen)

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6
Q

Name the 3 categories that combustion products are classified as.

A

simple asphyxiants, irritants and chemical asphyxiants

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7
Q

MOA of simple asphyxiants?

A

space occupying at the expense of oxygen, combined w/ consumption of environmental oxygen by the combustion

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8
Q

MOA of irritants?

A

chemically react on contact w/ MM to cause local effects–ex: sulfur oxide–>sulfurous acid

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9
Q

MOA of chemical asphyxiants?

A

produce toxic systemic effects at tissue distant from lung

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10
Q

Simple asphyxiants include?

A

CO2, methane, oxygen deprived environment

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11
Q

Irritants include?

A

High water solubility (upper airway injury)–>acrolein, sulfur dioxide, ammonia, hydrogen chloride
Intermediate water solubility (upper and lower airway injury)–>chlorine, isocyanates
Poor water solubility (pulmonary parenchymal injury)–>phosgene, nitrogen oxides

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12
Q

Describe soot?

A

finely divided carbonaceous particulate matter suspended in the gases and hot air of smoke–contains carbon, aldehydes, acids, reactive radicals–sulfur dioxide adheres highly to soot

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13
Q

Effects of inhaling soot?

A

enhances effect of other irritant toxins, soot binds to resp mucosa allowing materials to adhere and react, small particles (1-3 microns) reach alveoli

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14
Q

T/F Solubility of the toxin is the most important determinant of respiratory injury.

A

TRUE

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15
Q

MOA of highly soluble particles?

A

injury to mucosa, inflammatory mediators, free radicals–>increased permeability–>edema (affect the upper airways)

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16
Q

MOA of low water soluble particles?

A

slower reaction, delayed effect (affect the lungs)

17
Q

Initial injury from smoke inhalation causes?

A

inflammatory response, increased secretions, bronchospasm, mucosal sloughing

18
Q

Chemical asphyxiants include?

A

CO, hydrogen cyanide, hydrogen sulfide, nitrogen oxides

19
Q

What is the most serious systemic agent w/ smoke inhalation?

A

carbon monoxide–changes oxygen-hemoglobin binding

20
Q

Clinical signs of smoke inhalation?

A

resp signs, cardiovascular signs, signs of irritation, CNS signs, resp compromise, surface burns

21
Q

Respiratory clinical signs of smoke inhalation?

A

cough, dyspnea, tachypnea–on auscultation: rales, wheezing, decreased breath sounds (bronchospasm), crackles (edema)

22
Q

Cardiovascular clinical signs of smoke inhalation?

A

tachycardia, hypoxemia, hypotension, dysrhythmias

23
Q

Signs of irritation due to smoke inhalation include?

A

conjunctivitis, pharyngitis, rhinitis, drooling, dysphagia, hoarseness–edema, mucosal ulcerations, soot on nose/mouth/throat–corneal abrasions common

24
Q

CNS signs due to smoke inhalation include?

A

agitation, confusion, ataxia, abnormal posturing, transient loss of consciousness, seizures

25
Q

Initial workup for smoke inhalation includes?

A

history (type of combustibles) and initial presentation (altered mentation, ataxia, collapse–>CO, cyanide)–vitals–oxygenation status (hypoxia, hypercapnia, SPO2)–thorough ophthalmic evaluation–acid/base status–carboxyhemoglobin or methemoglobin measurement–thoracic rads (recheck 24-36 hrs)

26
Q

Lesions due to smoke inhalation?

A

burns (skin, MM), pulmonary changes (presence of soot, pulmonary edema, pneumonia, chronic sequelae–fibrosis, bronchiolitis, neoplasia), cerebral edema and lesions attributed to CO poisoning (caudate nucleus, globus plaids and substantial nigra, cerebellum, cerebral cortex, dorsal thalamus)

27
Q

Treatment of smoke inhalation?

A

removal from smoke, oxygen support, inhaled B2 agonist to tx bronchoconstriction, remove soot from skin surface, early intubation, NSAIDs, antioxidants, inhaled nitric oxide, hyperbaric oxygen, hydroxocobalamin, methylene blue, IV fluids

28
Q

What is contraindicated in the treatment of smoke inhalation?

A

cough suppressants, opioids (bc suppress cough), steriods (higher mortality and infection rates)–also don’t give prophylactic abx wait until pneumonia develops

29
Q

Purpose of hydroxocobalamin in treatment of smoke inhalation?

A

tx cyanide toxicosis–displaces the hydroxo ligand to form cyanocobalamin

30
Q

Purpose of methylene blue in treatment of smoke inhalation?

A

tx methemoglobin

31
Q

Potential indications for early intubation after smoke inhalation?

A

aggressive fluid therapy (edema), SPO2 50mmHg), pulmonary edema, depressed mentation, full thickness neck or facial burns, failure to improve with oxygen mask

32
Q

Monitor closely for _____ hrs post exposure and recheck within ____ hrs.

A

6-8 hrs–72 hrs