October 28, 2003 Gases and Toxic Inhalation 1 Hazardous Material Medical Care Gas and Toxic Inhalation น. พ. สัมมน โฉมฉาย สาขาพิษวิทยาคลินิค

October 28, 2003

Gases and Toxic Inhalation

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Hazardous Material Medical CareGas and Toxic Inhalationน.พ . สั�มมน โฉมฉาย

สาขาพิ�ษวิ�ทยาคลิ�นิ�ค อาชี�วิเวิชีศาสตร์� แลิะ เวิชีศาสตร์�ส��งแวิดลิ�อม

ภาควิ�ชีาเวิชีศาสตร์�ป้�องกั นิแลิะส งคมคณะแพิทยศาสตร์�ศ�ร์�ร์าชีพิยาบาลิ

มหาวิ�ทยาลิ ย มห�ดลิ

[email protected]@hotmail.com

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Outline• Inhalation exposure• Asphyxiants

– Simple asphyxiants– Systemic asphyxiant

• Irritant gases• Smoke inhalation• Semiconductors gases

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Inhalation exposure

• The most common hazardous material exposure

• Involves large number of cases• Low potential for secondary

contamination• Asphyxiant:

– Simple asphyxiant– Systemic asphyxiants

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Simple asphyxiants• Displace oxygen from ambient air

• Decrease FiO2

• Inadequate oxygen for hemoglobin saturation• No pharmacological effects• Needs high ambient concentration to cause

asphyxia• Situations:

– Confined space– High ambient concentration -- compressed

liquefied gas

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Simple asphyxiants: Clinical manifestations• Symptoms of hypoxia• CVS and CNS effects predominate• No hypercapnia• No dyspnea until severe hypoxia• Many cases pass out and die

before developing obvious symptoms

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FiO2 (%) Manifestations

12-16 Tachypnea, hyperpnea, tachycardia, alteration ofconsciousness, euphoria, headache, mild incoordination

10-14 Incoordination, muscle fatigue, cyanosis

6-10 Nausea, vomiting, lethargy, air hunger, severein-coordination, coma

<6 Gasping respiration, seizure, coma, death

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Simple asphyxiants: specific agents• Noble gases: Helium, argon, xenon• Short chain-aliphatic hydrocarbon

gases: methane, ethane, propane, butane

• Carbon dioxide• Nitrogen gases

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Simple asphyxiants: treatment• Decontamination: not needed• Removal from exposure• Respiratory support

– Supplemental oxygen– Ventilation if needed– No role of hyperbaric oxygen

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Systemic asphyxiants

• Carbon monoxide• Cyanide• Hydrogen sulfide

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Carbon monoxide (CO)

• A leading cause of death from poisoning in western countries

• Carbon monoxide: product of combustion of organic materials

• Colorless, odorless and non-irritating gas• Major sources in Thailand:

– Smoke inhalation – Exposure to methylene chloride (paint remover):

•inhalation, skin, ingestion•conversion into carbon monoxide

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Carbon monoxide poisoning• CO is inhaled and absorbed at the rate proportional

to respiration• Confined to blood and 15% to tissue predominately

myoglobin• Elimination by gas exchange with half-life 4-6

hours at room air• CO 200-250 times affinity to hemoglobin when

compared to oxygen• Shift oxyhemoglobin dissociation curve leftward• CO 60 times affinity to myoglobin when compared

to oxygen

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Acute carbon monoxide poisoning• ‘Flu-like symptoms’• Headache and dizziness• Nausea, weakness, difficulty with

concentration• Mild tachycardia and tachypnea • Syncope, seizures, altered mental status• Acute metabolic acidosis• Cherry red skin

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• Anginal chest pain in patients with predisposing coronary artery disease

• Ischemic heart disease, cardiac arrhythmias and complications of IHD

Acute carbon monoxide poisoning

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Acute carbon monoxide poisoning: Diagnosis• History: exposure history• Acute unconsciousness/ acute

metabolic acidosis• Pulse oximetry may overestimate

oxygen saturation; thus ABG should be used.

• Confirmation: Carboxyhemoglobin

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• Normal (non-smoker): 5% or less/Normal smoker: up to 12%

• Serious toxicity with level 25% or more• A comatose person may have a level close to

zero.• Elevation of carboxyhemoglobin just confirms the

poisoning.• In a patient with altered mental status, CT scan

may show hypodensity change in globus pallidus and subcortical white matter as early as 6 hours after severe poisoning

Acute carbon monoxide poisoning: Carboxyhemoglobin

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• Removal from exposure• 100% oxygen therapy

– Promotes tissue oxygenation– Enhance CO elimination– Half-life of 1-2 hours– Treat until patients become

asymptomatic, CarboxyHb< 10%

Acute carbon monoxide poisoning: Management

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• 40% of cases– treated, completely recovered and appear fine.– Return of symptoms on day 20-40

• Headache, memory and learning problems• Parkinsonism• Symptomatic treatment• 50% recover and 50% permanent

symptoms

Acute carbon monoxide poisoning: long-term complications

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Cyanide poisoning• A powerful cellular poisoning• Inhalation exposure

– Hydrogen cyanide gas– Combustion products

• Other exposures: – Ingestion

•Cyanide salts•Cyanogenic plants

– Iatrogenic: infusion of degraded nitroprusside

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• Rapidly absorbed from respiratory tract• Distribute to RBC and tissues• Elimination by forming thiocyanate and

excrete in urine• Half-life of 2.5 days in persons with normal

renal function

• Binds to Ferric ion in cytochrome a-a3:

– enzyme in mitochondria – catalyzing electron transfer to oxygen

Cyanide poisoning

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Cyanide poisoning: Clinical manifestation

• Inhalation: Immediate onset• Low concentration (50 ppm or less): anxiety,

restlessness, dyspnea, palpitation, headache

• Higher concentration (100 ppm): death in 30 minute, tachycardia, tachypnea, syncope, seizures

• High dose (250 ppm): Immediate onset: seizures, bradycardia or asystole, CVS collapse, respiratory depression, coma

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Cyanide poisoning: Diagnosis• History

– Exposure: laboratories, jewelry, metal works

• Clinical manifestation– Rapid onset and progression of manifestations– Arterialization of veins in fundoscopy

• Severe type B lactic acidosis• Confirmation: erythrocyte cyanide level (<

50 mcg/L), retrospective

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• Removal from exposure• 100% oxygen• Cyanide antidote may not be needed for

inhalation victims who are asymptomatic or recovered before presentation

• Cyanide antidote kit:– Amyl nitrite– Sodium nitrite– Sodium thiosulfate

Cyanide poisoning: treatment

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Sodium nitrite• Induces ‘methemoglobinemia’: Hb with

Fe3+

• Cyanide binds with Fe3+

• Sodium nitrite 300 mg ( 10 ml of 3% NaNO2) IV over 5-10 minutes

• Hypotension due to vasodilation• Amyl nitrite in cases of

– Non-medical personal– No available IV line

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Sodium thiosulfate

• Enhances cyanide elimination from the body

• Sodium thiosulfate donates sulfur atom to rhodanase-catalyzed reactions to form thiosulfate

• Thiosulfate excreted in urine• Hemodialysis in renal failure• Sodium thiosulfate 12.5 g (50 ml of 25%

sodium thiosulfate)

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Hydrogen sulfide

• Colorless gas with sweet odor• Intermediate water solubility• Product of bacterial decomposition

of protein • Industries at risk: Liquid manure &

fertilizer, fishing, brewers, tanning, natural gas & oil exploration, sewer construction

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• Inhalation• Irritation of upper and lower respiratory

system• No bioaccumulation• Detoxification within 1 hour• Thiosulfate formation and renal excretion

• Inhibits cytochrome oxidase a3

• Inhibits aerobic metabolism

Hydrogen sulfide poisoning

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• Odor threshold 1 ppm characteristic sweet, rotten egg odor

• Olfactory fatigue within 10 minutes with 100 ppm; ‘loss of warning properties’

• Low level: 10 ppm muscle fatigue on chronic exposure

• 50 ppm: Rapid onset of upper respiratory mucosal irritation: ocular pain, keratitis, cough, sore throat, corneal ulceration


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• 250 ppm: systemic effects of cellular anoxia– Dyspnea, cough, tachypnea, chest pain– Headache, dizziness, lethargy, confusion,

delirium, seizures, coma– Hypotension, tachycardia, myocardial

ischemia and infarction, arrhythmias

• 1000 ppm: immediate death from respiratory depression and respiratory paralysis


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• No specific laboratory from biological sample

• History, clinical manifestations, metabolic acidosis and environmental sampling

• Environmental sampling: ambient hydrogen sulfide level


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• Removal from exposure• 100% oxygen• Do not perform mouth to mouth

resuscitation• Amyl nitrite and sodium nitrite for cases

with manifestations of cellular hypoxia• Methemoglobin binds with hydrogen

sulfide into sulfmethemoglobin


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Irritant gases

• Large variety of chemicals• Final common pathway:

destruction of the integrity of respiratory mucosal barrier

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• Rapid onset of symptoms (seconds to Rapid onset of symptoms (seconds to minutes)minutes)

• Signal to escape the exposureSignal to escape the exposure• Oral, nasal and pharyngeal pain• Mucosal edema, cough, stridor• Conjunctival injection, chemosis, skin

irritation• Gases with good water solubility• Upper airway obstructionUpper airway obstruction

Irritant gases: Clinical manifestationsShort exposureShort exposure

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Irritant gases: Clinical manifestationsProlonged exposureProlonged exposure• Gases without rapid onset of manifestation• Entry into lower respiratory tract• Tracheobronchitis, bronchiolitis,

bronchospasm• Acute lung injury, non-cardiogenic

pulmonary edema• Dyspnea, chest tightness, cough, frothy

sputum, wheezing, crackles• CXR: alveolar infiltration• Arterial hypoxemia

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Irritant gases: highly water-soluble gases

• Ammonia– Common industrial (plastic, fertilizer,

refrigeration, explosives, cleaning agents) and household gases

– Characteristic odor

– Dissolution: NH4OH

• Chloramine (NH2Cl)– Mixture of hypochlorite and ammonia– Dissolution: hypochlorous acid, ammonia,

oxygen radicals

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• Hydrogen chloride– Industrial acid, combustion product of

vinyl chloride– Dissolution: hydrochloric acid

• Hydrogen fluoride– Glassware and semiconductor industry– Hydrofluoric acid– Upper and lower airway irritation,

systemic hypocalcemia


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• Sulfur dioxide– Smelting and oil refining – Warning properties: odor– Dissolution: sulfurous and sulfuric

acids


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• Chlorine • Exposure: mixing hypochlorite with acid,

aged hypochlorite tablet, compressed chlorine gas for water chlorination

• Dissolution: Hypochlorous acid• Mild initial upper respiratory symptoms• Delayed symptoms of lower respiratory

tract injury for hours

Irritant gases: intermediate water-soluble

gases

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• Phosgene– Colorless gas, heavier than air– Musty odor– exposure

•Combustion products of polyvinyl or isocyanate compounds

•Chemical warfare

Irritant gases: poorly water-soluble gases

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• Phosgene– Slowly dissolves into hydrochloric

acid– Prolonged exposure – Upper and lower respiratory tract

irritation– Delayed non-cardiogenic

pulmonary edema up to 72 hours

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• Nitrogen dioxide– Reddish-brown color– Water insoluble– Heavier than air– Sources

•Silos: grains•Combustion: nitrocellulose in films and bed mattress

Irritant gases: poorly water-soluble gases

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Nitrogen dioxide

• Mild upper airway irritation• Dissolution into nitric and nitrous acids

in bronchiole, terminal bronchiole and alveoli

• Acute non-cardiogenic pulmonary edema

• Pulmonary inflammation and bronchiolitis obliterans 2-6 after the exposure

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Nitrogen dioxide

• 1-3 ppm odor• 15 ppm minimal irritation• 50-150 ppm mild irritation• LD50 for 1 hour exposure = 175

ppm• Acute phase: Mucosal irritation (may

last up to 2 weeks), methemoglobinemia

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• Delayed: 3-36 hours– Fever dyspnea rales hypoxemia

cyanosis– Perihilar infiltration on CXR

Nitrogen dioxide

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• Decontamination: Removal from gas exposure

• Airway management & intubation • Oxygenation and PEEP• Bronchodilator for bronchospasm

•Monitor ECG for patients with hydrocarbon exposure who receive bronchodilator

Irritant gases: management

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• Patient with hydrogen fluoride inhalation– Nebulization of 2.5% calcium

gluconate solution (1.5 mL of 10% calcium gluconate with 4.5 ml or NSS or water)

– Prevent fluoride induced hypocalcemia

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Smoke inhalation

• Another major mortality factor for patients with burns

• Half of all fire-related deaths are due to smoke inhalation

• Risk for smoke inhalation– Closed-space fire– Decreased mentation: overdose,

alcohol intoxication, drug abuse, head injury

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• Combustion or pyrolysis: the rapid decomposition or oxidation of a substance by heat

• Flame (light), heat, smoke• Components of smoke are unpredictable:

composition of the fuels, oxygen availability, heat• Components of exposure from smoke inhalation

– Particulate matters, fumes, aerosols, vapors– Toxic gases

Smoke inhalation

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• Heat: Thermal injury– Thermal injury occurs only at

upper airway levels– Quick onset and rapid

progression– Injury below vocal cord occur

only in cases of steam inhalation

Smoke inhalation

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• Particulate matters: – Diameter less than 0.5 micrometer

– Products of incomplete combustion of organic materials

– Bronchospasm – Edema of mucosa from upper respiratory

system down to terminal bronchiole– Onset of edema may be delayed up to

24 hours

Smoke inhalation

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• Toxic gases from smoke– Carbon monoxide: incomplete

combustion of organic substance– Hydrogen cyanide: Combustion

of nitrogen-containing organic substances: wool, silk, polyurethane, vinyl

Smoke inhalation

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Examples of combustion products from common household materials

Materials Combustion products

Wool Carbonmonoxide, hydrogen chloride, phosgene, cyanide

Nylon Ammonia, cyanide

Wood, cotton, paperCarbonmonoxide, formaldehyde

Plastics Cynaide, hydrogen chloride, aldehydes, ammonias, oxides of nitrogen, phosgene, chlorine

Polyvinyl chloride Carbonmonoxide, hydrogen chloride, phosgene, chlorine

Rubber Hydrogen sulfide, sulfur dioxide

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• Clues for diagnosis of smoke inhalation– History of closed-space fire– Physical signs

•facial burns, singed nasal hair, soot in the nose and throat, hoarseness, carbonaceous sputum, wheezing

– Carboxyhemoglobin level as a document of exposure to incomplete combustion in a enclosed space

– Chest x-ray may be normal at early stages

Smoke inhalation

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• Treatment should start before the definite diagnosis is made

• Early intubation may be needed to maintain airway: Indications for early intubation– Full-thickness burns of the face or perioral region– Circumferential neck burns– Progressive hoarseness– supraglottic edema or inflammation

• 100% humidified oxygen• Carboxyhemoglobin level

Smoke inhalation

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Empirical treatment for cyanide poisoning

• A patient with elevated carboxyhemoglobin

• Suspected cyanide poisoning:history, comatose, lactic acidosis

• Administration of sodium nitrite may worsen impaired oxygen transport

• IV Sodium thiosulfate alone

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Arsine

• A colorless, non-irritating gas• Heavier than air• Garlic-like odor• Semiconductor industry:

production of gallium arsenide• Reaction of acids with arsenical

compounds

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• Arsine depletes RBC glutathione• RBC cell membrane instability• Intravascular hemolysis• Absorbed into the body and is

oxidized to trivalent arsenic compounds and cause chronic arsenic poisoning

Arsine

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• Acute inhalation of level 250 ppm or more can cause death

• Long term exposure of level 10-50 ppm can cause acute symptoms

• Chronic low level exposure may cause arsenic poisoning

Arsine

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• Intravascular hemolysis• Headache, dizziness, malaise &

weakness• Nausea and vomiting, abdominal pain• Dark-red ‘Cola color urine’ in 4-6 hours• Jaundice in 24-48 • Acute (nephrotoxic) tubular necrosis:

secondary to deposition of RBC breakdown products

Arsine

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• Chronic arsenic poisoning• Malaise, nausea, headache• Painful peripheral neuropathy• Hepatitis• Bone marrow suppression• Mee’s line• Skin changes: hyper keratosis and

hyper pigmentation, Bowen’s disease

Arsine

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• History of exposure, cluster of cases

• Abdominal pain• Intravascular hemolysis• Garlic-like odor

Arsine

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• Acute cases: Transient elevation of urine arsenic levels

• Acute anemia with decreased haptoglobin• Negative Coomb’s test• Hemoglobinuria without hematuria• Hyperkalemia• Acute renal failure• Chronic cases: Elevation of urine arsenic

level

Arsine

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Arsine : Treatment

• Decontamination: Removal from exposure

• ABC: 100% oxygen• Supportive care:

– Blood transfusion in case of severe anemia

– Urine alkalinization and maintain urine flow

– Hemodialysis

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• No enhancement of elimination• Chelation therapy:

– No indications in acute cases– May be indicated for chronic exposure with

persistent elevation of urine arsenic level• Follow up

– Until stable hemolysis ceases and stable hematocrit

– Subacute and long-term follow up for renal function and chronic arsenic poisoning

• Asymptomatic exposed person should be observed for at least 6 hours

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Documents

October 28, 2003 Gases and Toxic Inhalation 1 Hazardous Material Medical Care Gas and Toxic Inhalation น. พ. สัมมน โฉมฉาย สาขาพิษวิทยาคลินิค