SMOKE INHALATION AND FIRE TOXICOLOGY

Steven A. Godwin MD

University of Florida /HSC

Background

• Account for 50% of fire deaths

• Multiple factors contribute to M and M– Local pulmonary insult– Inhaled pulmonary and systemic toxins– Asphyxia

Mechanisms of Local Pulmonary Injury

• Thermal Injury

• Chemical Injury

• Multifactorial

Thermal Injury

• Rarely affects parenchyma

• Damages primarily mucous membranes

• Initial 24 hours is key

Chemical Injury

• Physical properties– anatomic location

– extent of absorption

• Length of exposure

Physical Properties of Chemical Inhalants

• Upper airway irritants– Larger, highly water soluble particles

• Alveolar injury– Associated with less water solubility

and smaller particles

Multifactorial Injury

• Respiratory epithelium necrosis

• Cilia inactivation

• Type II pneumocytes and alveolar macrophage destruction

• Capillary leak syndrome

Systemic Fire Toxins

• Chemical asphyxiantsCarbon monoxide

Cyanide

• Simple asphyxiantsNitrogen Argon Hydrogen

Methane Helium

Ethane Carbon dioxide

Chemical Asphyxiants

• Carbon monoxide– Colorless, tasteless, odorless gas

– Leading cause of reported toxicologic deaths

– Byproduct of incomplete combustion

– Pyrolysis of any carbon containing material

Mechanism of CO Toxicity

• CO competes with oxygen binding to hemoglobin, myoglobin, and cytochrome oxidase

• Results in global hypoxia, muscle ischemia, and cellular hypoxia

CO Toxicity

• Impaired O2 off-loading

• Leftward shift of oxygen dissociation curve

• Fetal tissue at increased risk

• Neurologic and cardiovascular systems primarily affected

Physical Findings and Carboxyhemoglobin levels

• O %

• 10 %

• 20 %

• 30 %

• 40 %

• 50 %

• 60-70 %

No symptoms

Frontal HA

HA, DOE

N/V, dizziness, blurred vision, poor judgement

Confusion, syncope

Coma, seizures

Hypotension, death

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

Cyanide Toxicity

• Suspect in fires involving synthetics– wool, silk, nylon, paper, upholstery,

plastics, polyurethane, asphalt

• Victims have bitter almond breath odor

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

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

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

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

Initial Evaluation in Smoke Inhalation

• PE continued:

Neck: stridor

Cardiovascular: ectopy

Pulmonary: wheezing and rales

Skin: cherry red discoloration, burns, chemical exposures, bullae

Airway Evaluation

• Fiberoptic evaluation recommended in significant exposures due to unreliable physical signs

• Close observation with low threshold for intubation

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

ABG and Pulse Oximetry

• Beware the saturation gap– Ask for measured oxygen saturation

– May calculate poor man’s (UMC) COHb level

• Evaluate severe acidosis

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

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

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

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 %

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

CO Management

• Goals of oxygen therapy in mild exposures:– Treat until COHb level < 5 % and

asymptomatic

– Admit patients with cardiac dz for observation

CN Management

• Lilly Cyanide Kit– Amyl nitrite

– Sodium nitrite

– Sodium thiosulfate

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

Hydroxycobalamin

• Non- toxic

• Binds CN and is excreted by kidneys as cyanocobalamin

• Used in Europe

• Awaiting FDA approval

Outpatient Burn Care• 1st Degree

– Superficial Burns

• 2nd Degree

– Superficial Partial Thickness

– Deep Partial Thickness• 3rd Degree

– Full Thickness

Superficial Burns

• Superficial epidermis only

• Painful, erythematous and w/o blisters

• Usually due to sunlight or short flash

• No Scar

2nd Degree Burns

• Superficial Partial Thickness– Full epidermis and may involve

dermis

– Red, blistered, weeping, and painfull

– Often scalds and short flashes

– No scarring

2nd Degree Burns

• Deep Partial Thickness– Usually spares deep dermal structures– Severe blistering or waxy appearance– Often confused with full thickness– Scar on healing

3rd Degree Burns

• Destruction of dermal layer

• Flames, scalds, and chemical and electrical contact

• White, charred inelastic skin

• Thrombosed vessels

• Scar with contractures

Second Degree Depth of Burn

Third Degree Depth of Burn

Minor Burn Management

• The 5 Cs:– Cut

– Cool

– Clean– Chemoprophylaxis - bacitracin, Silver

Sulfadiazine

– Cover

Don’t Forget Pain Control!!

Major Burn Evaluation

• Adult Body Surface Area: “Rule of Nines”

Major Burn Evaluation

• Pediatric Body Surface Area: “Rule of Nines”

Severe Burn Management

• Airway– Assess for injury and establish control

early

• Breathing

• Circulation– Fluid Resuscitation

– Monitor Urine Output

Fluid Resuscitation

• Rule of thumb:– 1 ml of urine / kg / hr for children under

30kg

– 30-50 ml /kg / hr output for adults

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

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

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

Questions

THE END