1. Toxic Injuries of Lung 호흡기내과 허진원

2. Inhalation Injury

3. Definitions of Types of inhaled Substances Gas Aerosol Vapor Fume (<0.1 um) Smoke (<0.5 um) SmokeFogSmog

4. Mechanisms of Lung Injury of Gaseous Respiratory Irritants Irritant GasMechanism of Injury AmmoniaAlkali burns Chlorine (Cl 2 )Acid burns, reactive oxygen species Hydrogen chlorideAcid burns Oxides of nitrogenAcid burns, reactive oxygen species OzoneReactive oxygen species PhosgeneAcid burns Sulfur dioxideAcid burns Deposition or formation of an acid, alkali, reactive oxygen species extensive cell damage

5. SMOG (PM 2.5)

6. Cause Coal : coal fires Transportation emissions airborne by-products from vehicle exhaust systems carbon monoxide (CO), nitrogen oxides (NO and NO x ), volatile organic compounds, sulfur dioxide, hydrocarbons sunlight, heat, ammonia, moisture, other compounds noxious vapors, ground level ozone, particles Photochemical smog chemical reaction of sunlight, nitrogen oxides and volatile organic compounds airborne particles and ground-level ozone

7. Health Effect harmful for senior citizens, children, and people with heart and lung conditions such as emphysema, bronchitis, and asthma. inflame breathing passages, decrease the lungs' working capacity, cause shortness of breath, pain when inhaling deeply, wheezing, and coughing Hospital admissions and respiratory deaths often increase during periods when ozone levels are high

8. SMOKE INHALATION AND THERMAL INJURY

9. Pathogenesis Smoke inhalation injury affects the entire respiratory tract ※ pulmonary irritants in smoke → directly toxic to respiratory epithelial or alveolar cells : aldehydes, acids, ammonia, nitrogen oxides, phosgene : Induce intense neutrophilic inflammation during 12 to 24 hours after injury : Mucosal edema and ulceration : Abnormally increased permeability of pulmonary capillaries with resultant capillary leak, and epithelial, alveolar, and immune cellular dysfunction : Bronchospasm or bronchorrhea : ARDS

10. Clinical manifestation 1) Thermal injury to upper airway mucosa → airway compromise (due to laryngeal edema) rapidly or during 12 to 24 hours 2) Burns to the face, mouth, and neck ; distort structures of the upper airway → airway compromise subacutely and late in the course 3) bronchospasm and bronchorrhea → cough, dyspnea, wheezing →respiratory failure 4) Accumulation of secretions, failure of mucociliary clearance and immune mechanisms, and epithelial necrosis predispose to pulmonary infection, particularly 3 to 5 days after injury 5) Late pulmonary complications; eschar formation and restriction of thoracic motion.

11. Diagnosis 1) Assessed emergently for airway patency 2) Immediate laryngoscopic evaluation of the oropharynx and supraglottic airway : head or neck burns, respiratory distress, stridor, or erythematous or edematous oral mucosa 3) Hypoxemia 4) Chest radiography : serially

12. Treatment 1) Endotracheal intubation : delay can result in increased edema and greater technical difficulty of intubation 2) Emergent tracheostomy : if cannot be intubated 3) ARDS or acute lung injury : mechanical ventilation 4) supplemental oxygen : high Fio2 5) Pulmonary toilet : maintain secretion clearance

13. CARBON MONOXIDE POISONING

14. Definition and Epidemiology 1) Carbon monoxide : a colorless, odorless gas produced by carbon-based fuels 2) CO inhalation : often coincident with smoke inhalation in fires : used in suicide attempts 3) Sources a) Endogenous production (during catabolism of Hb) : blood COHb level 0.4-0.7% b) Smoking: 1 pack/day smoker → COHb level 5-6% c) Automobile exhaust : lethal within 10 minutes in a closed space d) Heating equipment e) Fire (may reach up to 10% → COHb 75% in 1min) : most frequent cause of immediate fire death

15. Pathobiology 1) Carbon monoxide diffuses across the alveolar-capillary interface 2) Binds to hemoglobin with extremely high affinity → carboxyhemoglobin : ability of bound oxygen to dissociate and to be delivered to peripheral tissues is reduced 3) Tissue hypoxia → severe functional impairment & ischemic injury of oxygensensitive tissues : brain and heart.

17. Clinical Manifestations 1) Mild intoxication : nonspecific: headache, nausea, malaise, fatigue, and dizziness 2) Severe intoxications a) Neuropsychiatric symptoms : minor disturbances in attention and cognition to agitation : confusion, hallucination : seizures or frank coma 3) Physical findings : nonspecific a) tachycardia or hyperthermia b) classic “cherry-red” skin : rarely seen c) lactic acidosis, cardiac dysfunction with arrhythmia or ischemia d) pulmonary edema, rhabdomyolysis.

18. Diagnosis 1) A high index of suspicion is required for diagnosis 2) Arterial carboxyhemoglobin levels checked by co- oximetry : all patients known to have been involved in fires, suicide attempts, or other scenarios : symptoms generally occur at carboxyhemoglobin concentrations of 10% or higher 3) SpO2 at pulse oximetry : falsely normal

19. CO concentration (%) serum COHb level(%) symptoms 0.00710no symptom 0.01220 shortness of breath on moderate exertion occasional headache 0.02230 headache, dizziness, easy fatigue, judgement disturbance, dimness of vision 0.035-0.05240-50 Headache, confusion, collapse, fainting on exertion 0.080-0.12260-70 unconsciousness, convulsion, respiratory failure 0.19580rapidly fatal

20. Treatment 1) CO elimination enhancement : oxygen(100%) through tight-fitting mask or endotracheal tube until COHb < 10% 2) Hyperbaric oxygen treament (HBO) a) Indication: COHb > 40% or coma or COHb > 20% in preg with fetal distress b) 3 atm for 30min → 2 atm for 30 to 60min c) slow decompression( ∵ gas embolism) d) 3 hyperbaric oxygen treatments within 24 hrs of diagnosis reduce neurocognitive sequelae 4) Acid-base and electrolyte balance 5) Steroid and osmotic diuretics : ineffective in cytotoxic(hypoxic) cerebral edema

21. Prognosis 1) The mortality rate : 30% in severe cases 2) 2/3 of patients who survive ; without sequelae 3) Many of the remainder will suffer from long-term neuropsychiatric symptoms : cognitive dysfunction, abnormal mood or affect, memory disturbances, and other motor or sensory abnormalities

22. ORAGNOPHOSPHATE POISIONING

23. ETIOLOGY Malathion, parathion, dichlorvus 피부, 폐 및 위장관을 통해 흡수

24. 임상상 Acetylcholinesterase 를 비가역적으로 억제하여 muscarinic 및 nicotinic receptor 에 작용하는 아세틸콜린 의 양이 과대해짐 Muscarinic effect: 오심, 구토, 복통, 기관분비액 증가, 기 침, salivation, 서맥, 저혈압 Nicotonic effect: muscle twitching, weakness, 고혈압, 빈 맥, 호흡부전 CNS effect: 불안, 진전, 의식혼탁, 혼수

25. 치료 Decontamination: 피부, 위장관 세척 아트로핀 : muscarinic effect 치료 Pralidoxime(2-PAM): cholinesterase 를 reactivation 시키 면서 nicotinic symptom 치료제임