Lung Injury from hydrocarbon Flashcards

1
Q

Most common and serious complication

A

pneumonitis

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2
Q

aspiration high likely if

surface tension
low viscosity
volatility

A

low surface tension (adherance to surface)

low viscosity (spread easily, seep deeper in TISSUES)

HIGH VOLATILITY (rapid blood stream absorption; spread easily in ALVEOLI interfering gas exchange)

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3
Q

Chemical pneumonitis due to hydrocarbon may have radiologic signs within _____

A

2 hours (88%)
6-12 hrs (98%)

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4
Q

severe injury due to hydrocarbon

A

hemoptysis
pulmonary edema
respi failure within 24 hrs

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5
Q

radio signs

A

Punctate
mottled densities
pneumonitis
atelectasis

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6
Q

blood gas in hydrocarbon hypoxemia without hypercapnia suggesting

A

vq mismatch or diffusion block
*destruction of epithelium, bronchospasm

*displacement of alveolar gas

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7
Q

management

A

Intratracheal surfuctant
peep
ecmo / hfov
antibiotics

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8
Q

PULMO function in hydrocarbon

A

Increase RV/TLC
high volume of ISOFLOW
increased slope of phase III

low FEV1

suggest small airway obstruction

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9
Q

long term ff up showed residual injury to

A

peripheral airways

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10
Q

prognosis depends

A

ph
volume
type

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11
Q

hydrocarbon sniffing

A

results to acute hypoxemia
(displacement of alveolar gas)

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12
Q

3rd MC cause of poisoning deaths <5 yo
highest Morbidity and mortality <5 yo

A

Hydrocarbon aspiration and inhalational injury

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13
Q

common among
poor
african American
native american
<4 yo
and >85 yo

A

smoke inhalation

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14
Q

Blood gas of Carbon monoxide poisoning

A

O2 sat is low
Normal PaO2

*ABG obtained along COHb

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15
Q

Initial pathologic changes in smoke inhalation

A

Tracheobronchitis

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16
Q

Acute pulmonary edema caused by increased vascular permeability can occur within ____

A

30 minutes

17
Q

Upper airway obstruction occurs within ___ and can lead to alveolar hypoventilation

18
Q

VQ mismatch of carbon monoxide is due to

A

Inflammatory changes in the airways

19
Q

Bronchial and bronchiolar edema leads to _______ airway resistance

20
Q

Inhaled cyanide binds to _______ system
Inhibits cell metabolism and production of ATP

A

Cytochrome

21
Q

Clinical findings focus on

A

Hypoxemia, cyanosis

22
Q

How many % of COHb would lead to confusion, hallucination, ataxia, coma

A

40%

*increases cerebral blood flow
Permeability of cerebral capillaries
Cerebropspinal fluid pressure

23
Q

Sensitive indicator of cyanide poisoning

A

Plasma lactate concentration >10mM

24
Q

Manifestation of respi distress on cyanide develop within

A

12 hours-24 hours

25
Used in early assessment of the extent of supraglottic or tracheobronchial injury
Flexible fiberoptic nasopharyngoscopy or bronchoscopy
26
Chest Xray is not helpful in early diagnosis because in cyanide poisoning
Findings lag several hours
27
Should be done before head and neck swelling, which make this examination difficult
Direct laryngoscopy
28
Evaluate the extent of mucosal damage
Fiberoptic bronchoscopy
29
Administering 100% O2 may reverse CO poisoning reducing by _____ in about an hour
HALF *O2 for bronchiolitis and alveoliis with premature closure of small airways
30
Can cause increased airway resistance from edema and some reflex bronchoconstriction from airway receptors
Inhaled bronchodilators *smokers, CF
31
SIGNIFICANT decrease reintubation incidence and incidence of atelectasis Reduced mortality
Nebulized Heparin and N-acetylcysteine
32
Pulmonary damage from smoke inhalation shows within _____ hours
24
33
IV fluid can cause pulmonary edema by
Pulmonary vascular engorgement Increases vascular permeability with fluid leak
34
Increases risk for hypoventilation and atelectasis
Chest wall edema or eschar formation
35
Severity of pulmonary parenchymal injury depends on
Duration of exposure Type of inhalant
36
IMPACT of smoke inhalation on long term lung function depends on
Stage of lung developmenet AT THE TIME OF INJURY Confounding lung injury from (ARDS, pneumonia, acute lung injury)
37
PFT after 8 yrs following thermal injury
Obstructive Mixed obstructive and Restrictive