Smoke inhalation Flashcards

1
Q

most common cause of immediate death w smoke inhalation is -

Direct thermal injury to the upper respiratory tract =

lower respiratory tract injury from irritant
gases and superheated particulate matter can result

Bacterial bronchopneumonia typically occurs:

A

CO poisoning
high incidence of preadmission mortality reflected in limited studies/data

laryngeal obstruction

atelectasis, pulmonary edema, decreased lung compliance, ARDS

later in the course of the condition and is usually secondary to therapeutic interventions or sepsis

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2
Q

Acute neurologic dysfunction may be seen initially or as:

Significant dermal burn injury exacerbates:

immediate Tx. priority:

why:

supportive measures for:

prognosis:

A

delayed syndrome

morbidity & mortality - worse px.

aggressive oxygen supplem. immediate priority

hasten carbon monoxide elimination

respiratory & neurologic complications follow

if CO poisoning resolves, the prognosis is
good in the absence of significant dermal burn injury,
bronchopneumonia, or acute neurologic signs

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3
Q

CO poisoning:
Carbon monoxide is a ____ gas that competitively and ______binds to hemoglobin at the same sites as oxygen but with ____X affinity

produced by:

therefore most significant in:

COHb shifts the O2-hg dissociation curve to the:

left, which results in less offloading at the tissue

A

nonirritant gas
reversibly binds to hemoglobin
230 to 270 X

incomplete combustion of carbon-containing materials

enclosed fires bc there is LESS oxygen available

left
less offloading at the tissue
stability of the hemoglobin-O2 bond. Thus the fixation of carbon monoxide on any one of the four oxygen-binding sites of hemoglobin increases the oxygen affinity at the remaining sites

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4
Q

three possible outcomes in pure, uncomplicated

carbon monoxide poisoning:

A

(1) complete recovery with possible transient hearing loss but no permanent effects
(2) recovery w permanent CNS abnormalities
(3) death

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5
Q

Carbon monoxide poisoning is the main cause of immediate death in humans, and death is due

A

cerebral and myocardial hypoxia

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6
Q

Hydrogen cyanide (HCN) is most prevalent in fires involving

It is a _____ gas that interferes with the ____

incidence and significance of cyanide toxicity in vet

A

wools, silks, and synthetic nitrogen-containing polymers (e.g., urethanes, nylon)

nonirritant
cellular cytochrome oxidase and thereby causes histotoxic hypoxia

undefined

Throughout history there have also been some popular examples including the mass suicide at Jonestown and Heaven’s gate, it was also commonly used by the Nazi’s including Hitler. However, the most likely situation in your emergency department will be a house fire. Cyanide is produced from melting plastics and those enclosed in house fires are at considerable risk.

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7
Q

MoA:

A

Cyanide binds to ferric ion (Fe3+) of
cytochrome oxidase
inhibits oxidative metabolism (essentially blocking the electron transport chain)
end result is a lactic acidosis

Biogenic amines are also released which result in pulmonary and coronary vasoconstriction.
In the CNS cyanide triggers the release of NMDA which leads to seizures

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8
Q

HCN cyanide tx:

A

Lilly cyanide antidote kit (Sodium thiosulphate/Amyl Nitrite/Sodium Nitrite):

  • rhodanese enzyme in the liver converts cyanide to the less toxic thiocyanate which can be excreted in the urine
  • toxic ingestion overwhelmes and needs more sulphur donors – sodium thiosulphate acts as this donor
  • its use is for only mild ingestions and to make it more effective the kits contain sodium nitrite/amyl nitrite to form methaemoglobinaemia. This is because Cyanide binds avidly to methaemoglobinaemia, forming cyanmethemoglobin, thus releasing cyanide from cytochrome oxidase
  • downside is now you have an additional hypoxic state in your patient. However, in some cases you could just use the sodium thiosulphate on its own
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9
Q

CO
common cause of poisoning of lower socioeconomic groups. It can be quite obvious if a fire has occurred or the patient admits to a suicide attempt. Symptoms can be a little more insidious and subtle if exposure has been chronic and hyper-vigilance is required

A

Correlation of COHb levels and clinical features

Used to confirm the diagnosis but are a poor indicator for outcome and are altered by any previous oxygen that has been applied or delayed presentation.

<10% = Background level in a smoker
10% = Usually asymptomatic, slight headache
20% = Dizziness, nausea, dyspnoea, headache
30% = Vertigo, ataxia, visual disturbance
40% = Confusion, coma, seizures, syncope
50% = Cardiovascular compromise, respiratory failure, seizures, death
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10
Q

UAO:
time:

Steam has a much greater heat capacity than
dry air and is therefore likely to produce more extensive injury

A

tracheostomy was required 2 of 27 dogs with smoke

24 and 72 hours after admission

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11
Q

Dermal Burn Injury- morbidity and mortality associated with smoke inhalation are greater when significant:

A

concurrent dermal burn injury is present
bc pulmonary pathophysiology associated w dermal burns (pulmonary edema, bacterial pneumonia, ARDS) and burn management requirements

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12
Q

patient’s neurologic status at the scene predominantly reflects the:

paroxysmal or intractable coughing suggests:

A

degree of carbon monoxide poisoning

inhalation of more irritating gases

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13
Q

cherry red

A

attributed to carboxyhemoglobinemia is rarely witnessed in clinical cases. This probably high level of preadmission mortality

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14
Q

PaO2 is
SpO2 is

dx:

AV gradient

A

normal l
also normal bc SpO2 does not differentiate between COHb and oxyhemoglobin

Co-oximetry allows direct measurement of oxyhemoglobin and COHb

suggestive of significant HCN toxicity
>lactate

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15
Q

high plasma lactate levels at admission independent of hypoxemia sensitive indicator:

A

indicator of HCN intoxication

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16
Q

dx

A

COHb co-oximetery
TTW and BAL - presence of carbonaceous particulate matter in the airway confirms the diagnosis, and direct visualization of the anatomic level and extent of airway injury is possible along with sample collection

17
Q

Tx:
O2 supplementation is immediate priority for CO

T1/2 of CO is:

reduced to _____:

A

significant clinical improvement within min

approximately 250 min w normal respiratory
exchange breathing room air

but is reduced to 26 to 148 minutes at
a fraction of inspired oxygen (FiO2) of 100%

18
Q

CO and fetus

A

exaggerated leftward shift of fetal carboxyhemoglobin makes tissue hypoxia more severe because less oxygen is available to fetal tissue

fetal elimination of carbon monoxide takes 3.5 times as long as maternal elimination of the poison

19
Q

Haldane effect

A

increased affinity for oxygen, causes the leftward shift of the oxygen hemoglobin dissociation curve

20
Q

C/S

A

humans as many as 5% of those treated for influenza are thought to be actually suffering from subclinical CO

-dyspnea. However, the earliest signs in mild exposures are nausea, vomiting, and dizziness. In moderate exposures, serious signs appear, including tachycardia, tachypnea, weakness, and ataxia

21
Q

Hydrogen ion concentration may be a more sensitive and logical marker of tissue poisoning in CO

A

provide additional information as to the severity of the toxic episode. Furthermore, animals with such an acidosis should be thought to have significant carbon monoxide exposure even if carboxyhemoglobin levels are low.

22
Q

Handheld breath analyzers are commercially available and are suitable for detection of carbon monoxide in human beings

A

inexpensive, easy to perform, and fairly accurate and provides an answer in a reasonably short time frame. Breath sampling methods should be further investigated to determine

23
Q

closed-space fires with notable metabolic acidosis or elevated lactate levels should also be evaluated for possible concomitant

A

cyanide poisoning

24
Q

tx:
100% oxygen facilitates

The half-life of carbon monoxide is reduced from more

Administration of 100% oxygen should not be employed for longer

A

dissociation of carbon monoxide from hemoglobin

240 minutes at room air to 60 minutes when 100% oxygen is delivered via endotracheal tube.

18 hours to prevent subsequent oxygen toxicity
initiation - ROS antiox depl
inflamm - wbc edema permeablitity
destruction- most death
prolif - type II pn
Fibrosis
25
Q

in humans tx of choice

A

hyperbaric oxygen can shorten T1/2 23 minutes. In several studies hyperbaric oxygen benefits the brain more than normobaric oxygen, because it improves energy metabolism, prevents lipid peroxidation, and decreases neutrophil adherence. In humans hyperbaric oxygen therapy is the treatment of choice for patients severely poisoned by carbon monoxide.