Chapter 36: Asphyxiants

36.1: Asphyxiants

• Asphyxiants: Are gaseous poisons, which produce respiratory embarrassment, leading to asphyxia.

Chemical Asphyxiants

• Chemical asphyxiants %%reduce the body’s ability to absorb, transport, or utilize inhaled oxygen.%% In other words by their specific toxic action they render the body incapable of utilizing an adequate oxygen supply.
  • They are often active at very low concentrations.
• Examples include: carbon monoxide, cyanides and hydrogen sulfide.

Simple Asphyxiants

• Simple asphyxiants are inert gases and they %%deprive tissue of oxygen by their ability to displace oxygen%%.
  • These asphyxiants displace the oxygen from the inspired gas mixture creating diminished uptake.
  • Examples include: carbon dioxide, helium, nitrogen, nitrous oxide, aliphatic hydrocarbon gases such as butane, ethane, methane, and propane, and noble gases.

Pulmonary Irritant Asphyxiants

• Respiratory or pulmonary asphyxiants are gases, which can %%damage the respiratory tract by destroying the integrity of mucosal barrier%% and %%produce non-cardiogenic pulmonary edema%%, which impairs the oxygen diffusion across the alveolar membrane.
  • Examples include ammonia, chlorine, formaldehyde, hydrogen sulfide, methyl isocyanate, and oxides of nitrogen, ozone, phosgene, and sulphur dioxide.

Systematic Asphyxiants

• Systematic asphyxiants are gases, which produce %%significant systemic toxicity by specialized mechanisms%%.
  • Examples include: Carbon monoxide, cyanide, and smoke.

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36.2: Carbon Monoxide

• Carbon monoxide is a colorless, tasteless, odorless and nonirritant gas, produced whenever there is incomplete combustion of carbon.
• It is soluble in water.
• It burns with a blue flame.

Sources

• The most important source is due to the %%incomplete combustion of almost all forms of fuel%% such as wood, charcoal, gas, kerosene, etc.
• Endogenous CO resulting from hem degradation constitutes another source of CO. It is an end product of normal metabolism and is formed during the conversion of heme into biliverdin.

Mechanism of Action

• Carbon monoxide has got 200 to 300 times more affinity for hemoglobin (Hb) than oxygen (O2) forming carboxyhemoglobin, which are quite stable.
  • This renders hemoglobin incapable of carrying oxygen resulting in tissue anoxia.
• As long as CO is in the atmosphere, %%it goes on accumulates and gets fixed in blood, leading to acute chemical asphyxia%%.
• The CO absorbed by the lung avidly combines with hemoglobin (85%). Elimination occurs exclusively through lungs.

Signs and Symptoms

• Acute Poisoning
  • The severity of poisoning usually depends on age of COHb.
  • Formation of carboxy Hb can lead to anoxemia resulting in weakening of the vascular walls; anoxia leading to the degeneration of nerve elements; weakening of the heart due to lack of nutrition and ultimately death due to deprivation of O2.
• Chronic Poisoning
  • This is due to frequent exposure to CO leading to tissue injury seen in people working in gas houses, automobile workers, traffic police, houses, and shops near heavy traffic roads.
• Delayed Deaths
  • Coma is accompanied by degenerative changes in the brain and capillaries. Neurological symptoms such as blindness, decerebrate rigidity, etc may also be developed.

Diagnosis

• Carboxyhemoglobin (COHb) level
  • 0 to 5% normally, but may be as high as 10% in heavy chain smokers.
• Pulse oximetry
  • This is a simple non-invasive technique of detecting oxygen saturation measured by discrete wavelengths of light corresponding to saturated and unsaturated hemoglobin (660 and 940 nm) by a photodetector.
• ECG
  • ST depression or elevation, T-wave flattening or inversion, dysrhythmias, etc. are diagnostic.
• Chest radiograph
  • This may reveal ground glass appearance, perihilar haze, parabronchial cuffing, and intra-alveolar edema.
• Bedside tests
  • Add a drop of blood suspected to contain CO to 10 to 15 ml of water and shake well. A pink coloration of water detects the presence of CO. With normal blood, color will not be pink.
  • Brownish coloration – Normal blood (due to the oxyhemoglobin – HbO2)
  • Straw yellow coloration – < 20% COHb
  • Pink coloration – > 20% COHb.

Treatment

• Shift the patient to fresh air immediately.
• Provide artificial respiration and provide 100% oxygen using a tight-fitting mask or endotracheal tube, until COHb falls to 15 to 20%.
• Gastric lavage in the early stage helps in preventing aspiration pneumonia.
• Monitoring the cardiac and respiratory status. Keep the patient at complete rest for minimum 48 hours.
• Prevent cerebral edema by hyperventilation (PCO 25 to 30 mm Hg), head elevation, infusion of mannitol (0.25 to 1 gm/kg of 20% solution for 30 minutes) and avoid administering steroids.
• Diazepam or phenytoin to control convulsions.
• In order to prevent lung infection antibiotics are given prophylactically.
• A whole blood transfusion is useful.
• Antidote:
  • Administration of hyperbaric oxygen (HBO): Considered, as a specific antidote by few authorities, may be helpful in reducing neuropsychiatric symptoms.

Postmortem Findings

• Cherry red discoloration of the skin, mucosa, postmortem lividity (hypostasis), blood, viscera, etc. If the blood is taken in a test tube and diluted with water and held against light or white background, the pink color will be better appreciated.
• Fine froth at nostrils/mouth.
• Pulmonary edema.
• Anoxic necrosis of muscles
• Necrosis of heart muscles.
• Necrosis and cavitations of basal ganglia, especially globus pallidum and putamen is usually seen in delayed deaths cases.

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36.3: Carbon Dioxide

• Carbon dioxide is a heavy, odorless, poisonous gas, produced by the %%complete combustion of carbon-containing compounds%%.
• It is also formed during respiration, combustion, fermentation, and decomposition of organic matter, mine explosion, and in refrigerating plants. In solid form, it is called dry ice.
• Atmospheric air usually contains 0.4% CO2. Occasionally, it is detected in certain %%unused wells or cellars or deep leach pits kept closed for long time%%. People die accidentally when they enter into such wells/cellars/leach pits for cleaning purposes.
• Signs vary with the concentration of gas.
• Fatal Dose and Period: Maximum concentration of CO2 in the atmosphere is 5000 ppm.
• Fatal Concentration:
  • Minimum — 25 to 30%
  • Maximum—60 to 80%
• Fatal Period: Instant collapse and death.

Treatment

• Shift to a fresh atmosphere.
• Maintain body warmth.
• Artificial respiration + O2 therapy.
• Cardiac stimulants—amphetamine sulfate.

Postmortem Findings

• Lack of oxygen such as:
  • Cyanosis
  • Marked capillary and venous congestion
  • Petechial hemorrhages
  • Froth at nostrils and mouth
  • Blood is dark and fluid
  • Deep congestion of viscera
• Preserve blood for chemical examination.

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36.4: War Gases

• War gases: Chemicals that are %%used only in warfare%%.
  • The term designates its applicability as an agent befitted to carry destruction or damage mostly in times of war or in dispersing unruly mobs.

Qualities of Ideal War Gas

• Should be capable of being manufactured cheaply in enormous quantities as any industrial byproduct.
• Must be highly toxic in low concentrations.
• Must be heavier than air.
• It must be capable of enough volatilization pervading assailed area.
• Gas should not corrode the containers used for storage.

Types of War Gases and Symptoms

• Lachrymators (Tear gases)
  • Chloracetophenon (CAP), Bromobenzyl cyanide (BBC), Ethyl iodoacetate (KSK)
  • These war gases are harmless to life.
  • They produce in their victims:
  • Severe lacrimation due to intense irritation of the eyes with a copious flow of tears, spasms of the eyelids and temporary blindness.
  • Irritation to respiratory passages.
  • Long continued exposure can result in nausea, vomiting, blistering and ulceration of the skin.
• Lung irritants
  • Chlorine (Cl2 ), Phosgene (CO Cl2), Diphosgene
  • These war gases can be fatal and kill the victim.
  • They mainly act on the alveoli. Inhalation can bring about dyspnoea, tightness in the chest, cough, irritation of conjunctivae followed by restlessness, rapid and stertorous respiration, cyanosis, followed by collapse and death within 1 to 2 days.
  • Cause of death is acute pulmonary edema.
• Nasal irritants (Sternutators)
  • Diphenyl chlorasine (DA), Diphenylamine chlorasine (DM), Diphenyl cyanarsine (DC)
  • Diphenyl chlorarsine can act upon the vomiting centre in the brain.
  • Vapors can result in intense pain and irritation in the nose and sinuses leading to sneezing, malaise, headache, and salivation followed by nausea, vomiting and chest pain.
  • Additional symptoms as those of arsenic poisoning may also be observed.
• Nerve gases
  • Chemical with acetylcholine-like action
  • They are compounds related to phosphate esters in action and toxicity. They are colorless and odorless volatile liquids.
  • They are absorbed from the lungs, gastrointestinal tract, skin and conjunctivae.
  • These nerve gases are chemicals with acetylcholine-like action or have the action of inactivating cholinesterase enzymes leading to the accumulation of acetylcholine.
  • Some of the known war gases are serin and tabun.
• Paralysants
  • Carbon monoxide (CO)
  • Hydrocyanic acid (HCN)
  • Hydrogen sulfide (H2S).
• Vesicants
  • Mustard gas, Lewisite.
  • Mustard gas can produce severe irritation of eyes, nose, throat, and respiratory passages.
  • It can also develop severe irritation of the skin especially over the oily areas, such as the face, axillae, pubis, scrotum, etc., especially over the moist areas.
  • There can be inflammation of the stomach leading to nausea, vomiting, pain abdomen, diarrhea, etc.
  • Rarely death can occur due to bronchopneumonia.
• Miscellaneous
  • Yellow/red rain, Methyl isocyanide.
  • Victims feel as if their body is getting blown up.
  • Cough and hemoptysis, followed by painful breathing.
  • Burning in the throat resulting in dysphagia.
  • Eyes may turn yellow, with the blurring of vision.
  • Nose-tingling as if hot pepper has been inhaled.
  • Necrosis of the gum with loosening of the teeth.
  • Skin may necrotize with red to blue coloration.
  • Rise in body temperature.

36.5: Methyl Isocyanate (MIC)

• Methyl isocyanate can be considered under several classifications, namely: agrochemicals, war gases, irritants and miscellaneous poisons.
• Methyl isocyanate has a pungent but sweet odor.
• It is a fairly stable liquid at room temperature (except in summer).
• Has a boiling point of 31°C.
• It reacts with water/moisture, alkaloids and most other common solvents. Hence, needs to be preserved under inert conditions.
• MIC is a deadly substance used in the pesticide and pharmaceutical industries.
  • Can kill in small doses.
  • Can get absorbed orally, through the respiratory tract or through intact skin.

Signs and Symptoms

• Acute Poisoning
  • MIC can produce irritation to skin, eyes and mucous membranes, resulting in a severe burning sensation in the throat, and unbearable irritation of the eyes followed by severe chest pain with labored breathing.
  • Death is usually due to pulmonary edema in untreated cases.
• Subacute poisoning
  • It occurs when a person survives for more than 5 to 6 days after acute poisoning.
  • The condition manifests now with more neurological effects such as motor weakness, paralysis, convulsions, coma, and cerebral edema leading to death.
• Delayed effects develop in a victim who survives for more than a week and manifests with dyspnoea, jaundice, weakness of limbs, etc. followed by exhaustion and death.
• In pregnant woman victims, the delayed effects of the poison may be abortion, congenital malformation, stillbirth, etc.

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36.6: Cyanide

• Cyanide occurs as a gas or a liquid or a solid.
• In a gaseous state is referred to as hydrogen cyanide (HCN).
• The liquid form which is called hydrocyanic acid or Prussic acid or cyanogen is a solution of either 2% or 4% of HCN in water.
• Pure acid is a colorless, transparent volatile liquid with a penetrating odor of bitter almonds.
• Cyanide salts occur as solids and these cyanides of sodium/ potassium are white powders.
• Cyanides are considered as a cardiac poison also.
• Cyanides are protoplasmic cytotoxic poisons. They act by inhibiting cytochrome oxidases for utilizing O2 in a cell, leading to internal asphyxia (cellular asphyxia), leading to death. It can also act on other enzymes mildly. It also acts as a corrosive on the mucosa.
• Fatal Dose:
  • Pure acid 60 mg
  • Any pharmacological preparation of 30 drops
  • Crude oil of bitter almond 60 drops
  • Potassium cyanide 200 mg
• Fatal Period:
  • In some cases—immediate death
  • An average for HCN acid is 2 to 10 minutes, and for potassium cyanide is 30 minutes.

Signs and Symptoms

• Acute Poisoning

  • All symptoms reflect cellular hypoxia and symptoms shift rapidly depending on the extent of cyanide exposure. Inhalation brings about death instantaneously by respiratory arrest.
  • Also cases with massive dose of oral poisoning present with a few voluntary acts such as corking a bottle or throwing a stone or even walking certain distance and then dropping down dead.

• Central Nervous System

  • Headache, giddiness, anxiety, agitation, confusion, convulsions, and coma. Eyes are glassy and prominent with unresponsive pupils.
  • Violent convulsions, clenched jaw, loss of muscle power and loss of consciousness, ultimately leading to death.

• Cardiovascular System: There will be hypertension with reflex bradycardia, sinus arrhythmia, followed by tachycardia and hypotension ventricular dysrhythmias, and cardiac collapse.

• Gastrointestinal System

  • When taken orally, the victim may complain of bitter, acid, burning taste; constriction and numbness of throat; salivation, nausea and rarely vomiting.
  • Frothing and corrosion of mouth may also be noticed.
  • There will be a smell of bitter almonds around mouth and breath.

• Respiratory System: Respiratory system shows initial tachypnoea followed by dyspnea, and bradypnea, with severe respiratory depression and cyanosis.

• Skin

  • Skin and mucosa will be brick red in color and characteristics. This is said to be due to increase in hemoglobin oxygen saturation in venous blood because of decreased utilization of oxygen by tissues. Skin will be cold and clammy to touch.
  • The skin turns cyanotic only in late stages.

• Chronic Poisoning

  • Headache, vertigo, nausea and vomiting
  • Visual defects.
  • Tropical ataxic neuropathy: This is a condition with clinical manifestations of peripheral sensory neuropathy, optic atrophy, ataxia, deafness, glossitis, stomatitis and scrotal dermatitis.

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36.7: Ammonia

• At room temperature, ammonia (NH3) is a highly water-soluble, colorless, irritant gas with a unique pungent odor.
• Ammonia has a boiling point of –33°C and an ignition temperature of 650°C.
• The farming industry uses anhydrous ammonia as a component of fertilizer and animal feed.
• Ammonia also is used in the production of explosives, pharmaceuticals, pesticides, textiles, leather, flame-retardants, plastics, pulp and paper, rubber, petroleum products, and cyanide.
• It is a major component of many common household cleaning and bleaching products.
• Fatal Dose:
  • Gaseous Form: 0.5% in air.
  • Liquid Form: 10 to 20 mL.

Signs and Symptoms

• Inhalation
  • Head, ears, eyes, nose, and throat (HEENT) symptoms include running nose and increased salivation.
  • Ammonia inhalation can produce tachypnoea, oxygen desaturation, stridor, drooling, cough, wheezing, rhonchi, decreased air entry asthma, severe upper respiratory tract irritation, pneumonia, pulmonary edema, bronchitis, and obstructive lung disease.
  • Death is usually due to bronchopneumonia.
• Ingestion
  • HEENT symptoms include edema of the lips, oropharynx, and upper airway.
  • Ammonia ingested can produce intense pain, and dysphagia followed by oesophageal stenosis.
  • The patient may experience epigastric tenderness; mediastinitis and peritoneal signs may be present with viscus perforation, which can occur as late as 24-72 hours post ingestion.
• Contact
  • Can result in skin burns (alkali burns) and cold injury.
  • Facial and oral burns and ulceration may be seen.
  • Alkali burns to the skin are yellow, soapy, and soft in texture. When burns are severe, skin turns black and leathery.
• Eye
  • Exposures results in watering of the eyes, corneal damage, conjunctivitis and palpebral edema.
  • Ammonia typically causes more corneal epithelium and lens damage than other alkalis.
  • Intraocular pressure and pH of the anterior chamber rise, resulting in a syndrome similar to acute narrow-angle glaucoma.
  • Other symptoms include iritis, corneal edema, semi dilated fixed pupil, and eventual cataract formation.
  • Blindness may be a serious consequence in severe cases.

Treatment

• Stomach wash and emetics use is not recommended.
• Giving demulcents, and dilute solution of vinegar are useful.
• Tracheostomy, oxygen administration and assisted ventilation may help to alleviate respiratory distress.
• Antibiotics and corticosteroids are controversial therapies following ammonia inhalation and ingestion exposures.
• Lesions of skin and eye needs thorough washing with a copious amount of water. Diluted vinegar may be applied to the skin after washing.

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