Smoke inhalation Flashcards
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:
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
Acute neurologic dysfunction may be seen initially or as:
Significant dermal burn injury exacerbates:
immediate Tx. priority:
why:
supportive measures for:
prognosis:
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
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
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
three possible outcomes in pure, uncomplicated
carbon monoxide poisoning:
(1) complete recovery with possible transient hearing loss but no permanent effects
(2) recovery w permanent CNS abnormalities
(3) death
Carbon monoxide poisoning is the main cause of immediate death in humans, and death is due
cerebral and myocardial hypoxia
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
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.
MoA:
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
HCN cyanide tx:
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
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
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
UAO:
time:
Steam has a much greater heat capacity than
dry air and is therefore likely to produce more extensive injury
tracheostomy was required 2 of 27 dogs with smoke
24 and 72 hours after admission
Dermal Burn Injury- morbidity and mortality associated with smoke inhalation are greater when significant:
concurrent dermal burn injury is present
bc pulmonary pathophysiology associated w dermal burns (pulmonary edema, bacterial pneumonia, ARDS) and burn management requirements
patient’s neurologic status at the scene predominantly reflects the:
paroxysmal or intractable coughing suggests:
degree of carbon monoxide poisoning
inhalation of more irritating gases
cherry red
attributed to carboxyhemoglobinemia is rarely witnessed in clinical cases. This probably high level of preadmission mortality
PaO2 is
SpO2 is
dx:
AV gradient
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
high plasma lactate levels at admission independent of hypoxemia sensitive indicator:
indicator of HCN intoxication
dx
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
Tx:
O2 supplementation is immediate priority for CO
T1/2 of CO is:
reduced to _____:
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%
CO and fetus
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
Haldane effect
increased affinity for oxygen, causes the leftward shift of the oxygen hemoglobin dissociation curve
C/S
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
Hydrogen ion concentration may be a more sensitive and logical marker of tissue poisoning in CO
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.
Handheld breath analyzers are commercially available and are suitable for detection of carbon monoxide in human beings
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
closed-space fires with notable metabolic acidosis or elevated lactate levels should also be evaluated for possible concomitant
cyanide poisoning
tx:
100% oxygen facilitates
The half-life of carbon monoxide is reduced from more
Administration of 100% oxygen should not be employed for longer
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
in humans tx of choice
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.
