16-Irrespirable_gases
Irrespirable Gases
Carbon Monoxide (CO)
Formation:
Produced by incomplete combustion of carbon-based materials.
Properties:
Colorless, odorless, tasteless, non-irritating, and lighter than air.
Chemical Reactions:
Combines with chlorine to form carbonyl chloride (phosgene, CoCl2).
Sources:
Automobile exhaust
Industrial smoke
Tobacco smoke
Coal gas
Signs and Symptoms:
Commonly occur after mine explosions (damp, choke damp).
Safety Limit: 0.01% (100 ppm) upper limit in air.
Mechanism of Action:
Combines with hemoglobin to form carboxyhemoglobin, causing anemic hypoxia.
Has 200-300 times more affinity for hemoglobin than oxygen, inhibiting Cytochrome A3 oxidase and Cytochrome P450, affecting intracellular respiration.
15% of CO bonds with myoglobin.
Symptoms Progression:
Symptoms correlate with CO saturation in blood:
Common acute symptoms include headache, dizziness, nausea, confusion.
Recovery depends on the clearance of CO from the blood.
Effects Mimic Hypoxia:
Liver: Enlarged liver, bleeding tendency.
CNS: Spastic paraplegia, intellectual impairment, personality changes, retrograde amnesia, parkinsonism.
CVS: Dysrhythmias, myocardial infarction.
Skin: Bullous lesions due to hypoxia.
Signs & Symptoms by Carboxyhemoglobin Levels (% in blood):
COHb % | Symptoms |
|---|---|
0-10% | No symptoms |
10-20% | Mild headache, lassitude, breathlessness on moderate exertion |
20-30% | Throbbing headache, breathlessness, muscular weakness, incoordination |
30-40% | Severe headache, nausea, vomiting, dim vision, confusion |
40-50% | All symptoms intensified |
50-60% | Syncope or coma, convulsions, rapid respiration, rapid weak pulse |
60-70% | Deep coma, incontinence of urine and feces |
70-80% | Respiratory paralysis and death |
Notes:
Victims may exhibit erratic movements, potentially mistaken for assault.
Children saturate CO more rapidly than adults.
Severity varies by blood concentration:
10-30%: Mild
30-40%: Moderate-Severe
40%: Very severe
Differential Diagnosis:
Alcohol intoxication
Uremia
Hypoglycemic coma
Head injury >20%
Diagnosis:
Often misinterpreted due to vague symptoms.
Methods for Diagnosis:
Patient history and clinical signs.
Lab Findings:
COHb Analysis: Spectroscopy identifies carboxyhemoglobin (COHb).
Kunkel's Test: Shows crimson red coagulum with diluted blood and tannic acid.
Hoppe-Seyler's Test: Produces pink/red color with blood and 10% NaOH if COHb is present.
Treatment Options:
Immediate Care:
Remove patient to fresh air.
Specific Treatments:
Blood transfusion if required.
Hyperbaric oxygen for COHb above 25%: PO2 at 2-3 atmospheric pressure.
Gastric lavage to prevent aspiration pneumonia.
Supportive measures for cerebral edema (20% mannitol solution IV).
Postmortem Findings:
External Findings:
Cherry-red color in hypostasis and mucous membranes.
Fine froth at mouth/nasal areas.
Blisters over bony pressure points (buttocks, calves, wrists, knees).
Internal Findings:
Lungs: Congested and edematous.
Heart: Possible petechial hemorrhages.
Brain: Congested and edematous, bilateral necrosis in basal ganglia.
Circumstances of Poisoning:
Suicidal: Starting car in neutral in a closed garage.
Accidental: Exposure to exhaust gases from burning buildings or gas mines.
Safety Note: Safe CO level in air is 0.1%. Inhalation risks in confined spaces during explosions.
Homicidal Cases: Rare unless the victim is incapacitated or a child.
Carbon Dioxide (CO2)
Properties:
Heavy, colorless, odorless, slightly irritating gas.
Solid form: Dry ice.
Sources:
Unused wells, putrefied organic matter.
Actions:
Pure CO2 may cause glottic spasm due to vagal inhibition, potentially leading to sudden death.
Symptoms of CO2 poisoning arise from lack of oxygen.
Signs and Symptoms by Blood Concentration:
CO2 % | Symptoms |
|---|---|
2-10% | Throbbing headache, tachypnea, tinnitus, mental confusion, muscle tremors |
10-20% | Slow respiration, blood pressure drops |
20-40% | Dyspnea, muscular weakness |
40-60% | Drowsiness, coma, convulsions, and death |
Postmortem Findings:
Asphyxia symptoms:
Froth at nostrils.
Cyanosis.
Blue hypostasis.
Petechiae on face and in pleural/pericardial surfaces.
All internal organs congested; brain congested and edematous.
Circumstances of Poisoning:
Rare in suicides and homicides, common in accidents (e.g., mining).
Historical context: "Ghost wells" due to certain beliefs about deaths in abandoned wells.
Testing CO2 concentration: Use soda lime in a bottle lowered into the well; a milky white indicates calcium carbonate formation.
Hydrogen Sulphide (H2S)
Properties:
Colorless gas with a rotten egg smell.
Dissolves in water & burns with a pale blue flame.
Sources:
Sewage, putrefying bodies, petroleum, silk, rayon, paper industries.
Action:
H2S combines with methemoglobin instead of hemoglobin, asphyxiating by disrupting oxygen use in the cytochrome oxidase system.
Comparable toxicity to cyanide and rapid onset.
Signs and Symptoms of H2S Poisoning:
Respiratory: Rhinitis, breathlessness, cyanosis, pulmonary edema, pneumonia.
Cardiovascular: Arrhythmia, myocardial depression.
CNS: Giddiness, headache, nystagmus, muscular weakness, poor concentration, delirium, coma, convulsions.
Ocular: Lachrymation, photophobia, conjunctivitis.
Death: Results from respiratory center paralysis.
Treatment Options:
Remove victim to fresh air.
Provide artificial respiration & 100% oxygen.
Administer amyl nitrite inhalation and sodium nitrite infusion to form sulfmethemoglobin.
Break amyl nitrite ampoules and hold over the nose for 30 seconds.
Infuse sodium nitrite in 10cc of sterile water slowly IV.
Supportive measures for electrolyte imbalances and pulmonary edema.
Postmortem Appearances:
Signs of asphyxia: cyanosis, froth at nostrils, petechial hemorrhages, pulmonary edema.
Greenish discoloration of postmortem stains, blood, and visceral organs.
Rotten egg smell at the mouth and nostrils.
Circumstances of Poisoning:
Accidental Poisoning: Common in industrial workers and sewage cleaners.
Detergent Suicide/Chemical Suicide: Involves household items (bath sulfur + toilet cleaner), resulting in toxicity via inhalation.
Chronic Exposure to H2S:
Symptoms include:
Headache, nausea, weakness, weight loss, ataxia, tremors, nasal mucosa anesthesia, conjunctivitis, pharyngitis.
Green Line on Gingiva and allergic bronchitis.
War Gases
Categories of War Gases:
Vesicants/Blistering Gases
Asphyxiants/Lung Irritants
Lachrymators/Tear Gases
Sternutators/Nasal Irritants
Paralysants
Nerve Gases
i) Vesicants or Blistering Gases:
Examples: Mustard Gas, Lewisite.
Symptoms: Irritation of eyes, nose, throat; nausea, abdominal pain; skin irritation and vesication.
Treatment:
Wash affected area with soap and water.
Eye wash with sodium bicarbonate.
BAL (British Anti-Lewisite) for systemic treatment.
ii) Asphyxiants or Lung Irritants:
Examples: Carbon Monoxide, Carbon Dioxide, Chlorine, Phosgene, Diphosgene.
Properties: Phosgene is 4x more toxic than chlorine, acts primarily on pulmonary alveoli.
Symptoms: Watering eyes, nausea, vomiting, cough, dyspnea, cyanosis, collapse.
Treatment:
Eye wash with saline.
Oxygen therapy.
Antibiotics to prevent infection.
iii) Lachrymators or Tear Gases:
Examples: Chloracetophenone, Ethyliodoacetate.
Symptoms: Severe eye irritation, temporary blindness, nausea, skin blistering.
Treatment:
Remove patient to fresh air.
Wash eyes with normal saline.
Antibiotics to prevent infection.
iv) Sternutators or Nasal Irritants:
Examples: Diphenyl chlorarsine, Diphenylamine chlorarsine.
Symptoms: Intense nasal/sinus irritation, rhinitis, sneezing, chest tightness.
Treatment:
Removal to fresh air.
Nose irrigation with sodium bicarbonate.
Antibiotics to prevent infection.
v) Paralysants:
Types of Paralysants:
Hydrogen sulphide (H2S)
Hydrocyanic acid (HCN)
Carbon monoxide (CO)
Methyl isocyanate (MIC)
Methyl Isocyanate (MIC):
Bhopal Gas Tragedy:
Occurred in 1984; over 2000 deaths, 200,000 injuries, 50,000 blindness cases. Phosgene was released, which is 10 times more toxic than MIC.
Physical Properties:
State: Liquid.
Boiling Point: 31°C.
Reactivity: Violently reacts with water; requires inert storage conditions.
Usage: Intermediate product in carbamate pesticide production.
Mechanism of Action:
Local Effects: Irritant to eyes and respiratory system.
Systemic Action: Carbamylation of enzymes.
Fatal Dose: >21 ppm for 1-5 minutes. Fatal Period: 5 minutes to 2 days.
Clinical Features:
Symptoms include irritation, blindness, pulmonary edema (common complication), bronchopneumonia, uremia, hypotension, hypothermia, psychological disturbances in ~10% cases.
Treatment:
Decontamination of skin/eyes; oxygen therapy; bronchodilators; antibiotics to prevent pneumonia.
vi) Nerve Gases:
Types: Tabun (GA), Sarin (GB), Soman (GD), Cyclosarin (GF), VX.
Chemical Nature: Derivatives of phosphoric acid, functioning like organophosphates.
Properties: Colorless, odorless, absorbed through lungs, skin, GIT, conjunctiva.
Mechanism: Inhibit acetylcholinesterase.
Signs and Symptoms:
Similar to organophosphate (OP) poisoning; loss of consciousness within seconds from large doses; convulsions; respiratory paralysis leading to death.
Treatment: Similar to OP poisoning.