Gas/Gaseous Poisoning

Classification of Toxic Gases

1. Carbon Monoxide (CO) Poisoning

Properties

• Colorless, tasteless, odorless gas (sometimes described as having a garlicky odor from utility gas admixtures)
• Slightly lighter than air
• Sources: incomplete combustion (charcoal, coal fires, motor exhausts, blast furnaces, house fires, gas engines); car exhaust in closed garages produces enough CO to poison a small space in under 10 minutes

Mechanism

1. Displaces O2 from hemoglobin, forming carboxyhemoglobin (COHb) - a stable compound that cannot carry oxygen
2. Causes a leftward shift of the oxyhemoglobin dissociation curve (impairs O2 unloading)
3. Acts as a direct cellular poison - inhibits mitochondrial cytochrome oxidase and the electron transport chain, blocking ATP synthesis
4. Has direct cardiotoxic effects

Clinical Features by COHb Level

Key Signs

• Cherry-red skin/mucosae - classic but not always present; due to COHb (which is bright red)
• Bullous skin lesions - discrete, isolated, containing thick cellular fluid; pathognomonic when present; caused by sudden hypoxia
• ECG changes: prolonged PR interval, AV block, bundle branch block, prolonged QT, ST depression
• Retinal hemorrhages, papilloedema
• Glycosuria, albuminuria

Chronic CO Poisoning

• Frontal headache, nausea/vomiting, palpitations, dyspnoea
• Memory loss, ataxia, visual disturbances, mental symptoms
• Anaemia, polycythemia, tachycardia, hepatomegaly, angina

Diagnosis

• Co-oximetry (pulse oximetry is unreliable - reads COHb as oxyHb, giving a falsely normal saturation)
• Blood COHb level
• Smell of utility gas on clothing
• History of exposure (closed space, fire, faulty heating)

Treatment

1. Remove from exposure immediately - bring to fresh air
2. 100% high-flow O2 via tight-fitting non-rebreather mask - halves CO half-life from ~5 hours (room air) to ~60-90 minutes; some advocate 5% CO2 + 95% O2
3. Airway management - suction, intubation if needed
4. Hyperbaric oxygen (HBO) - the definitive treatment in severe cases:
   • Reduces CO half-life to ~20-30 minutes
   • Indications for HBO:
     • COHb > 25% without clinical findings
     • COHb > 15% or signs of fetal distress in pregnancy
     • Any COHb elevation + syncope, coma, altered mental status, abnormal cerebellar function, or prolonged exposure
   • Salt Lake City protocol: 3 ATA x 60 min (two air breaks) then 2 ATA x 65 min; two more treatments at 6-12 hour intervals
   • Philadelphia protocol: 2.8 ATA x 30 min then 2.0 ATA x 90 min (single session)
5. Correct dehydration, treat cardiac complications (IV digoxin for acute heart failure), antibiotics for infection

Medicolegal Importance

• Most cases are accidental (poorly ventilated rooms, faulty gas fittings, car exhausts)
• Suicidal - especially in Western countries (closing a room with fire, garage exhaust inhalation)
• The wild/agitated behavior of the dying person can be mistaken for a violent quarrel (homicide suspicion)
• In deaths due to fire, COHb > 50% is expected; levels of 15-20% mimic drunkenness
• CO poisoning can be confused with vehicular accident victims

2. Cyanide (HCN) Gas Poisoning

Sources

• Burning of synthetic materials (plastics, polyurethane) in house fires
• Industrial exposures (electroplating, mining, fumigation)
• Combustion of nitrogen-containing materials

Mechanism

Clinical Features

• Rapid onset: anxiety, headache, dizziness, then seizures and coma
• Bitter almonds odor on breath (not always detectable)
• Cardiovascular collapse, lactic acidosis (lactate > 10 mmol/L strongly suggests cyanide)
• Concomitant CO + cyanide poisoning is common in fire victims and produces synergistic toxicity

Diagnosis (empirical)

• Patient is a fire victim
• Cardiovascular instability (hypotension) + altered mental status
• Serum lactate > 10 mmol/L

Treatment

• Hydroxocobalamin (preferred antidote) - binds cyanide to form cyanocobalamin (vitamin B12); safe even in co-existing CO poisoning; dose: 5g IV
• Sodium thiosulfate - can be given concomitantly as adjunct; provides a sulfur donor for rhodanese enzyme to convert cyanide to thiocyanate
• Sodium nitrite - induces methemoglobin which competes with cytochrome oxidase for cyanide; use with caution in CO co-poisoning (further reduces O2 carrying capacity)
• High-flow O2; HBO may augment antidote treatment

3. Hydrogen Sulfide (H2S) Poisoning

Sources

• Sewers, manure pits, petroleum refineries, volcanic areas, and mining
• "Sewer gas" - the classic occupational gas poisoning

Mechanism

Key Clinical Feature

• Rotten eggs odor at low concentrations; paradoxically, at high concentrations, olfactory paralysis occurs and the smell cannot be detected - highly dangerous
• Oxygen saturation gap (pulse oximetry may show sulfmethemoglobin)
• Rapid loss of consciousness, respiratory failure

Treatment

• Remove from exposure - the most critical step
• Ventilatory support - most patients respond to this
• Sodium nitrite - can be used if patient is not recovering after removal from source (induces methemoglobin to bind H2S)
• HBO and methylene blue have no role in H2S poisoning

4. Simple Asphyxiant Gases (CO2, N2, Helium, Methane)

• These gases are inert and produce toxicity only by displacing O2, lowering the fraction of inspired oxygen (FiO2)
• No direct toxic action on cells
• As FiO2 falls from 21% to 15%: tachycardia, tachypnoea, dyspnoea, ataxia, dizziness
• Below FiO2 10%: lethargy, cerebral edema
• Below FiO2 6%: life-threatening
• Treatment: removal from the environment; oxygen supplementation; supportive care

5. Irritant Gases

• High-solubility gases warn the victim immediately; low-solubility gases are more dangerous because the victim feels fine initially but then develops pulmonary edema hours later.

Quick Reference: Distinguishing Key Gas Poisonings