inhalational injuries

Inhalational Injuries

Ping-Wei ChenPGY -2

Emergency Medicine

Special thanks to Dr. Chris Hall and Dr. Yael Moussadji

Clinical Pearl

Objectives

• Mechanisms of injury– Determinants of Toxicity

• Classes of Inhalational Toxins– Simple Asphyxiants– Pulmonary Irritants– Cellular Poisons

Sources of Exposure

• Industrial/Occupational• Home/Community• War/Chemical Weapons

Mechanisms of Injury

• Direct Pulmonary Toxicity– Alter air/lung interface by invoking irritant or

inflammatory response• Dissolve to form acid/base• Oxygen free radicals

• Systemic Toxicity– Reduce inspired fraction of O2

– Alter oxygen transport– Uncoupling of electron transport chain/oxidative

phosphorylation

Determinants of Injury

• Exposure level• Water solubility• Particle size• Mixtures

Exposure Level

• Controlled vs Uncontrolled (explosion)• Confined vs Outdoors/Ventilated area• Duration of exposure

Water Solubility

• Determines level of respiratory tract involved and symptom onset– High water solublility

• Mucous membranes• Upper airway• Rapid irritation

– Poor water solubility• Lower airway• Delayed onset of symptoms

– Intermediate water solubility• Mixed presentation upper/lower airway

Particle Size

• Determines level of respiratory tract involved– Particles ≥ 10 microns are filtered in the nose

and/or deposited on the larynx– Particles ≤ 10 microns are deposited in the large

airways– Particles ≤ 5 microns are deposited in the distal

airways and alveoli

Mixtures

• Exposures commonly to mixture of substances– Synergistic toxics effects• Examples

– Smoke– Mixture of household cleaning products

Simple Asphyxiants

• Mostly inert substances• Toxicity from

displacement of O2 – Lowered FiO2

– Acute effects as result of hypoxia

• Examples:– propane, butane, nitrogen

• Mostly workplace related– Liquefied gases

Simple Asphyxiants

• Clinical symptoms due to hypoxia

Simple Asphyxiants

• Treatment– Removal from exposure– Supportive• Supplemental O2 preferred (room air suffices)

– Disposition• Mild symptoms – brief observation; discharge• Significant symptoms/comorbidities

– Admission for observation of post-hypoxic complications

Case 1

• 37yo female• Cleaning her bathroom with a combination of

bleach and disinfectants• Sudden onset of a strong odor• Developed marked irritation of eyes and

burning sensation in nose and throat• Immediately left the bathroom• Feels nauseated and slightly dyspneic

Pulmonary Irritants

• Destruction of integrity of mucosal barrier of respiratory tract– Acid/Base reactions– Free radical generation– Host response • Neutrophil recruitment• Cytokine activation

ACUTE LUNG INJURY

Ammonia

• High water solubility• Fertilizer, Cleaning

agent, Refrigerant• Dissolves to form

NH4(OH)

Chloramines

• High water solubility• Often from a mixture of

ammonia and sodium hypochlorite bleach

• Dissolves to form hypochlorous acid, ammonia, O2 free radicals

Sulfur Dioxide

• High water solubility• By-product of oil

refining and smelting• Dissolves to form

sulfuric acid• Cause of acid rain

Chlorine

• Intermediate water solubility– Mild initial symptoms– Prolonged exposure

• Swimming pools, mixing acids with bleach

• Dissolves to form HCL, hypochlorous acid, O2 free radicals

Other Pulmonary Irritants• Hydrogen Fluoride– High water solubility– Gasoline, Glassware, Building Renovation,

Semiconductor industries– Dissolves to form hydrofluoric acid– Systemic toxicity (hypocalcemia)

• Phosgene– Low water solubility– Pesticide production– Dissolves to form HCl– “fresh hay” scent

Management

• Airway evaluation– Swelling can be rapid or delayed (water solubility)– Signs of upper airway dysfunction mandate

visualization of the larynx ± airway stabilization• Symptomatic treatment– Bronchospasm: β-agonists– Chlorine/HCl: nebulized 2% NaHCO3 solution– ALI/ARDS: aggressive supportive care

Supportive Care

• Support airway patency• Pulmonary toilet – limit airway secretions• Maintain oxygenation• Ventilation Strategies:

– Prone– Inverse ratio– PEEP– Low Tidal Volume

• Currently, little to no evidence to support:– Cortisteroids (inhaled/systemic)– Antioxidants– Surfactant therapy

Disposition

• High Water Solubility Agents– Can be discharged if asymptomatic/improve with

treatment• Intermediate/Poor Water Solubility Agents– Observe asymptomatic patients for several hours– Symptomatic/High Risk features (comorbidities,

extremes of age, poor F/U) need to be observed for a minimum of 24 hours

Metal Fume Fever• Metal oxide fumes

– Onset hours post-exposure– Welding, galvanizing, smelting

• Recurrent influenza-like illness– fever/chills (38-39oC)– cough/dyspnea/CP– Headache– Myalgias– Metallic taste

• Immunologic/toxic etiology• 48hr natural history• Tx: Analgesic/antipyretics

Case 2

• 55 yo male construction worker• Involved in explosion, thrown backward 10

feet• Second and third degree burns to face, neck,

torso, arms and legs• Comes in with EMS on backboard in collar,

alert and screaming in pain• VSS

Case 2

Smoke Inhalation• Multiple etiologies of

injury– Irritant

• Combusted carbonaceous material increases exposure to adsorbed toxins

– Simple asphyxiant• Fire consume O2

– Chemical asphyxiant• Multiple substances

involved– Cyanide– Carbon monoxide

Smoke Inhalation

• Mortality rates of combined major burn injury and inhalation injury exceed that of either alone

• Inhalation injury is a predictor of prolonged ventilator dependence and death

• Twenty percent of those requiring admission to a burn unit carry a diagnosis of inhalation injury

Management

• Evaluate airway patency early!!– Airway Compromise• Edema (exacerbated by fluid resuscitation)• Intraluminal debris (soot)• Bronchospasm

– Diagnostic Tests• ABGs (beware pulse oximeters – CO)

– Serum lactate > 10mmol/L – suspect cyanide/CO poisoning

• CXRay – baseline study

Clinical Course• Early resuscitation phase – acute pulmonary insufficiency +/- critical airway

narrowing that can progress over 18-24 hours• Post-resuscitation phase (2-5 days) – characterized by mucosal necrosis, secretions, distal

airway obstruction, atelectasis, pulmonary interstitial edema, and bronchopneumonia

• Inflammatory-infection phase (5 days and beyond)– continues until there is lung healing and burn wound

closure; no role for prophylactic antibiotics

Chemical Asphyxiants

Oxygen Transport• Carbon Monoxide

Oxygen Utilization• Carbon Monoxide• Cyanide• Hydrogen Sulfide

Carbon Monoxide

• Generated by incomplete combustion of carbon containing material

• CO binds to Hgb to form carboxyhemoglobin– Slowly reversible reaction

Carbon Monoxide

• Uncouples oxidative phosphorylation/electron transport chain– Inhibits final cytochrome complex

Clinical Presentation• Signs/Symptoms consistent with asphyxia– CNS: mild to severe

• headache, N/V, dizziness, confusion• Altered LOC, seizures, coma

– CV:• Hypotension, dysrhythmias, cardiovascular collapse

• “Cherry-Red skin” is a post-mortem finding!• Delayed neurological sequelae – Appears after 2 – 40 days– Neurologic syndromes– Psychiatric/Cognitive findings

Treatment

Oxygen Tension Half-Life of Carbon MonoxideRoom Air 300 mins

100% FiO2 (normobaric) 60 mins

100% FiO2 (hyperbaric) 30 mins

•Prevention of delayed neurological sequelae•Severity of poisoning may not correlate with COHb levels •Oxygen is the mainstay of treatment•Achieve sufficient PO2 to sustain life in absence of normal Hgb•Shorten half-life of CO

Hyperbaric Oxygen Therapy

• Controversial• Cognitive sequelae less at 6 weeks and 12

months with HBOT (3 sessions)– 25% versus 46.1%

• Other studies: mixed/no benefit• Cochrane Review (2005)– “No evidence to support use of hyperbaric oxygen

for treatment of patients with carbon monoxide poisoning”

To HBOT or not HBOT

• Considerations:– Neurologic abnormality– Cardiovascular instability– COHb > 25%– Pregnant and COHb >15%

Cyanide

• Photography, Metallurgy, Synthetic manufacture, Fumigation

• “bitter almond” smell• Rapid absorption after inhalation• Uncouples oxidative phosphorylation/electron

transport

Hydrogen Sulfide

• Petroleum, Natural Gas, Waste Management

• Irritant + Systemic Toxicity– Uncouples oxidative

phosphorylation/electron transport chain

– Intermediate water solubility

• “rotten egg” smell

Clinical Presentation

• Signs/Symptoms consistent with asphyxia– CNS: mild to severe• headache, N/V, dizziness, confusion• Altered LOC, seizures, coma

– CV:• Hypotension, dysrhythmias, cardiovascular collapse

– May have persistent or delayed onset neurologic sequelae

Treatment

Hydrogen Cyanide• Re-activate cytochrome

oxidase system• Cyanide Antidote Kit:

– Create MetHb to bind cyanide• Inhaled amyl nitrite• IV sodium nitrite• NOT with CO poisoning

(MetHb + COHb = BAD)– Enhance

metabolism/elimination• Sodium thiosulfate

• Hydroxocobalamin– Cyanide binds to form Vit B12

Hydrogen Sulfide• Removal from exposure• Supportive Care• If severe toxicity

– Inhaled amyl nitrite– IV sodium nitrite

Don’t forget to warn others who are exposed!!