Smoke inhalation injuries can cause both local pulmonary damage and systemic toxicity from inhaled chemicals. Thermal injuries damage mucous membranes while chemical injuries depend on particle size and solubility. Systemic toxins include carbon monoxide, which binds hemoglobin, and cyanide, which inhibits ATP production. Initial management focuses on airway support, 100% oxygen, and observation. Hyperbaric oxygen may benefit patients with significant carbon monoxide exposure. Burn depth depends on extent of skin layer damage. Minor burns are cleaned and covered while major burns require fluid resuscitation and potential transfer to facilities with specialized burn care resources.
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Smoke Inhalation and Fire Toxicology
1. SMOKE INHALATION AND
FIRE TOXICOLOGY
Steven A. Godwin MD
University of Florida /HSC
2. Background
• Account for 50% of fire deaths
• Multiple factors contribute to M
and M
– Local pulmonary insult
– Inhaled pulmonary and systemic
toxins
– Asphyxia
3. Mechanisms of Local
Pulmonary Injury
• Thermal Injury
• Chemical Injury
• Multifactorial
6. Physical Properties of
Chemical Inhalants
• Upper airway irritants
– Larger, highly water soluble particles
• Alveolar injury
– Associated with less water solubility
and smaller particles
7. Multifactorial Injury
• Respiratory epithelium necrosis
• Cilia inactivation
• Type II pneumocytes and alveolar
macrophage destruction
• Capillary leak syndrome
9. Chemical Asphyxiants
• Carbon monoxide
– Colorless, tasteless, odorless gas
– Leading cause of reported
toxicologic deaths
– Byproduct of incomplete combustion
– Pyrolysis of any carbon containing
material
10. Mechanism of CO Toxicity
• CO competes with oxygen binding
to hemoglobin, myoglobin, and
cytochrome oxidase
• Results in global hypoxia, muscle
ischemia, and cellular hypoxia
11. CO Toxicity
• Impaired O2 off-loading
• Leftward shift of oxygen
dissociation curve
• Fetal tissue at increased risk
• Neurologic and cardiovascular
systems primarily affected
12. Physical Findings and
Carboxyhemoglobin levels
• O % No symptoms
• 10 % Frontal HA
• 20 % HA, DOE
• 30 % N/V, dizziness, blurred
vision, poor judgement
• 40 % Confusion, syncope
• 50 % Coma, seizures
• 60-70 % Hypotension, death
13. Pediatric Exposures
• Up to 17 % of acute exposures die
• Up to 48 % of acute exposures may
require CPR
• Newborns at highest risk
• Confused for colic
• Implicated in some cases of SIDS
15. Mechanisms of CN Toxicity
• Inhibits ATP production by
binding with the ferric moiety of
cytochrome oxidase
• Blockade in the mitochondrial O2
• Severe hypoxia despite presence of
O2
16. Presentation of CN Toxicity
• Mimick signs of hypoxia without
cyanosis
• Physical signs are non-specific:
may include hyperventilation,
anxiety, decreased LOC, seizure,
coma, cardiac arrhythmias
17. Clinical Clues
• History most important clue
• Suspect in any patient found to be
comatose, bradycardic, and severely
acidotic w/o findings of cyanosis or
hypoxia
• Diagnosis supported by bright- red
retinal vessels, oral burns and odor
18. Initial Evaluation in Smoke
Inhalation
• History, History, History, History
• A,B,Cs
• PE:
HEENT: retinal veins, mucous
membranes, facial burns, singed nasal
hairs or presence of carbonaceous
sputum, dysphonia
19. Initial Evaluation in Smoke
Inhalation
• PE continued:
Neck: stridor
Cardiovascular: ectopy
Pulmonary: wheezing and rales
Skin: cherry red discoloration,
burns, chemical exposures, bullae
20. Airway Evaluation
• Fiberoptic evaluation
recommended in significant
exposures due to unreliable
physical signs
• Close observation with low
threshold for intubation
21. Laboratory
• Essential test:
ABG with co-oximetry COHb level
Urine pregnancy test Chest x-ray
• Additional test to consider
Electrolytes CPK levels
CBC Urine myoglobin
Coagulation studies
22. ABG and Pulse Oximetry
• Beware the saturation gap
– Ask for measured oxygen saturation
– May calculate poor man’s (UMC) COHb
level
• Evaluate severe acidosis
23. Initial Management
• 100 % Oxygen
• Airway evaluation with brochoscopy if
indicated
• Supportive care with treatment of burns
• No role for steroids or antibiotics
• Observation period depends on exposure
24. Initial Management
• Healthy asymptomatic patients with
normal blood gases may be discharged
• Exposure to agents with low solubility
(phosgene) need longer observation
• Exposure to local irritants (hydrogen
chloride, sulfur dioxide) treat
symptomatically and observe
25. CO Management
• Rules of thumb for the elimination half-
life of CO
Room air 240-320 minutes
100 % oxygen at 1 atm 60-90minutes
HBOT with 3 atm 23 minutes
26. Hyperbaric Therapy
• Dalton’s Law:
Pt=PO2 + PN2 + Px
– States the ratio of gases doesn’t change
despite the change in total pressure
– The individual partial pressures do
change
• Increases Oxygen content to 6.8 %
27. CO Management
• Guidelines for Hyperbaric therapy
– COHb > 25%
– COHb > 15% in patient with coronary dz
– COHb > 15% or with symptoms in pregnancy
– COHb > 15% in a young child
EKG changes pO2 < 60 mmHg
Metabolic acidosis Abnormal thermoregulation
28. CO Management
• Goals of oxygen therapy in mild
exposures:
– Treat until COHb level < 5 % and
asymptomatic
– Admit patients with cardiac dz for
observation
30. Mechanism of Action of
Antidote Kit
• Amyl nitrite and sodium nitrite converts
Hb > methemoglobin > binds CN >
cyanomethemoglobin > rhodenase
metabolizes CN to thiocyanate
(enhanced by sodium thiosulfate) >
renal excretion of sodium thiocyanate
31. Hydroxycobalamin
• Non- toxic
• Binds CN and is excreted by kidneys
as cyanocobalamin
• Used in Europe
• Awaiting FDA approval
32. Outpatient Burn Care
• 1st Degree
– Superficial Burns
• 2nd Degree
– Superficial Partial Thickness
– Deep Partial Thickness
• 3rd Degree
– Full Thickness
33. Superficial Burns
• Superficial epidermis only
• Painful, erythematous and w/o
blisters
• Usually due to sunlight or short
flash
• No Scar
34. 2nd Degree Burns
• Superficial Partial Thickness
– Full epidermis and may involve
dermis
– Red, blistered, weeping, and painfull
– Often scalds and short flashes
– No scarring
35. 2nd Degree Burns
• Deep Partial Thickness
– Usually spares deep dermal
structures
– Severe blistering or waxy
appearance
– Often confused with full thickness
– Scar on healing
36. 3rd Degree Burns
• Destruction of dermal layer
• Flames, scalds, and chemical and
electrical contact
• White, charred inelastic skin
• Thrombosed vessels
• Scar with contractures
43. Severe Burn Management
• Airway
– Assess for injury and establish control
early
• Breathing
• Circulation
– Fluid Resuscitation
– Monitor Urine Output
44. Fluid Resuscitation
• Rule of thumb:
– 1 ml of urine / kg / hr for children under
30kg
– 30-50 ml /kg / hr output for adults
45. Parkland Formula: Only a
Guideline
• Estimate of fluid requirements in
partial and full thickness burns
• 2-4 ml / kg / % BSA burn over first 24
hours
• 50% of Ringer’s Lactate give over 1st
8 hours with rest administered over
next 16 hours
46. Criteria for Transfer
• Partial / Full thickness burns greater than 10%
BSA in patients > 55 yo and < 10 yo.
• All other age groups with burns > 20 % BSA
• Partial / Full thickness burns to face, hands, eyes,
ears, feet, genitalia, or perineum or those
overlying major joints
• 5% Full thickness in any age group
• Significant electrical burns
• Significant chemical burns
47. Criteria for Transfer
• Inhalation injury
• Burn injury in patients with complicating co-
morbid illnesses
• Children in facilities lacking appropriate resources
to aid in rehab
• Patients requiring special long term support
including children in abuse cases