INHALED TOXINS


Simple Asphyxiants

Simple Asphyxiants
Simple asphyxiants include carbon dioxide, nitrogen dioxide (silo filler’s disease), nitrous oxide, methane gas, and helium. Methane gas is present in high concentrations in bogs of decaying organic matter and in natural gas.

MECHANISM/TOXICITY

  • Produce toxicity by displacing O2 → hypoxia

SYMPTOMS/EXAM

  • Rapid onset
  • Tachycardia, tachypnea, shortness of breath
  • Dizziness and confusion to coma
  • If untreated may lead to cardiac arrest

DIAGNOSIS

  • Clinical diagnosis is based on history of exposure

TREATMENT

  • Remove patient from source of exposure.
  • Supportive care
  • Administration of O2

Carbon Monoxide Poisoning

Carbon Monoxide
Carbon monoxide (CO) is an odorless and colorless gas produced by incomplete combustion of fuels or organic material. Common sources of CO include vehicle exhaust, ovens, house fires, furnaces, and portable generators. Methylene chloride, a solvent found in paint removers, degreasers, and other similar products, is metabolized in vivo to CO following absorption.

MECHANISM/TOXICITY

  • Binds to hemoglobin → carboxyhemoglobin (COHb), which is incapable of carrying O2 → impaired O2 delivery, cellular hypoxia, lactic acidosis
  • Shifts the oxyhemoglobin dissociation curve to left → ↓ release of O2 to tissues from normal hemoglobin
  • Binds to heme groups in mitochondira and triggers oxidative injury
  • CO has even greater affinity for fetal hemoglobin → higher fetal levels and toxicity for any given maternal exposure.

SYMPTOMS/EXAM

  • The symptoms and signs of CO toxicity are vague and nonspecific, and, if not
    severe, will resolve shortly after removal from CO source.
    • Headache, dizziness, weakness
    • Tachycardia, chest pain
    • Dyspnea
    • Nausea/vomiting (no diarrhea)
    • Confusion, memory impairment (delayed)
    • In severe cases: Myocardial ischemia, seizures, syncope, coma, cardiac arrest

DIAGNOSIS

  • Direct measurement of COHb in either arterial or venous blood via cooximetry
    • Normal nonsmoker = 2–3%
    • Smokers = <10%.
  • Pulse oximetry cannot distinguish COHb from Oxyhemoglobin.
  • Expected ABG findings:
    • Normal PaO2 (measuring dissolved O2)
    • Metabolic acidosis (from lactate accumulation)
    • Normal calculated O2 saturation (calculated from PaO2)

TREATMENT

  • Removal of the patient from CO source
  • Acute stabilization as required
  • Administration of 100% O2:
    • Reduces the elimination half-life of CO from approximately 4–5 hours (room air) to 1 hour
    • Continue until COHb level is ≤ 5%.
  • Hyperbaric O2 (HBO)
    • Further reduces the elimination half-life of CO to 20–30 minutes
    • Indications for HBO Treatment of CO Poisoning:
      • Any history of syncope
      • Evidence of major end-organ damage
      • Persistent neurologic symptoms
      • Pregnancy
      • COHb level > 20—25%

COMPLICATIONS

  • Delayed or persistent neurocognitive deficits on neuropsychiatric testing.
  • HBO therapy may prevent the development of these effects but studies are not conclusive.
CO poisoning:
Normal pulse oximetry ABG with metabolic acidosis and normal PaO2
Elimination half life of CO
Room air: 4-5 hours
100% O2: 1 hour
Hyperbaric O2 :20-30 minutes

Cyanide Poisoning

Cyanide
 Cyanide (CN) is a rapid-acting, highly toxic poison found in a wide variety of chemicals. Poisoning is rare in the United States as few household products contain CN.

Sources of CN include:
Burning of: wool, nylon, silk, acrylic, polyurethane, melamine, polyacrylonitrile, polyamide plastics
Industries: fabrication of plastics, electroplating, mining, photography, precious metal reclamation, solvents, hair removal from hides
Fumigants and fertilizers
Vermin extermination: cyanide spread into burrows and dens
Chemistry laboratories
Medicinal: Laetrile,* sodium nitroprusside
Plants: seeds from Prunus species (apricots, cherries, plums, peaches), cassava
Illicit phencyclidine manufacturing
Cigarette smoke
Vehicle exhausts

MECHANISM/TOXICITY

  • Inhibits cytochrome oxidase, disrupting oxidative phosphorylation →cellular hypoxia and lactic acidosis

SYMPTOMS/EXAM

  • Effects are very rapid following CN inhalation or absorption.
  • In contrast, toxicity due to amygdalin may be delayed by hours as CN is released by metabolism.
  • Early symptoms of N/V, headache, and confusion are followed rapidly by seizures and coma.
  • Cardiovascular findings include hypertension and tachypnea (initially), dysrhythmias, pulmonary edema, and cardiac arrest.
  • Skin may appear flushed or cyanotic.
Cardiovascular
Tachycardia Mild
Hypertension  
Bradycardia
Hypotension
Cardiovascular collapse
Asystole Severe
Central nervous system
Headache Mild
Drowsiness  
Seizures
Coma Severe
Pulmonary
Dyspnea Mild
Tachypnea  
Apnea Severe

DIFFERENTIAL

  • Any other cause of coma, shock, or lactic acidosis

DIAGNOSIS

  • CN poisoning should be considered in any patient presenting with rapid onset of coma, shock, and marked lactic acidosis.
  • ABG findings are similar to severe CO poisoning.
  • Clues to the diagnosis include:
    • A history of smoke inhalation or occupational access to CN
    • Evidence of decreased tissue extraction of O2:
      • Arterial appearance of venous blood
      • Elevated measured venous O2 saturation (>90%)
      • Marked lactic acidosis
    • Patient has a distinct, almond-like smell. Many individuals are genetically incapable of detecting this odor.
  • Blood CN levels can be directly measured, but are not available in a timely manner.
Anticipated Laboratory Findings in Cyanide Poisoning
Test Result Cause
Serum electrolytes Elevated anion gap Lactic acidosis from anaerobic metabolism
Arterial blood gases Metabolic acidosis Oxygenation initially normal
Normal PaO2
 
Lactate >10 mmol/L Correlates with toxic cyanide level
Measured oxygen saturation by co-oximetry Normal Hemoglobin retains normal oxygen-carrying capacity
Measured arterial-mixed venous oxygen difference Decreased Decreased tissue oxygen consumption
Whole-blood cyanide level Toxic >0.5 mcg/mL Note: plasma cyanide levels are roughly one tenth of the whole-blood cyanide levels
Fatal >2.5 mcg/mL
Fire victims Elevated carboxyhemoglobin level Carbon monoxide generated by incomplete combustion
Synergistic toxicity with cyanide


TREATMENT

  • Acute stabilization as required
  • Surface decontamination, if indicated
  • Antidote = cyanide antidote kit; three components:
    • Amyl nitrite pearls (for inhalation)
      • Use until IV access is obtained.
      • Induces methemoglobinemia
      • Methemoglobin strongly binds CN, pulling it away from cellular enzymes.
      • Is used illicitly as “poppers”
  • IV sodium nitrite
    • Induces methemoglobinemia
  • IV sodium thiosulfate
    • Binds to CN to form thiocyanate, a much less toxic compound that is renally excreted
  • A smoke inhalation victim with suspected CN poisoning should only receive sodium thiosulfate. There is the potential for worsening tissue oxygenation from nitrite-induced methemoglobinemia.
  • Antidote = hydroxycobalamin.
    • 2 vials, each 2.5 g reconstituted in 100 mL NS, give over 7.5 min (for a total dose of 5 g over 15 min).
    • Can be repeated within 15 min as clinically indicated
    • Recently approved as an antidote for cyanide poisoning in the United States
    • It reacts with CN to form cyanocobalamin (vitamin B12), a nontoxic compound which is readily excreted in urine.
    • It may replace the cyanide antidote package in the future due to its ease of use and improved risk profile.
Treatment of Cyanide Poisoning in Adults:
100% oxygen
Amyl nitrite inhaler; crack vial and inhale over 30 s
Sodium nitrite 3% solution: 10 mL (300 mg) IV given over no < 5 min
Sodium thiosulfate 25% solution: 50 mL (12.5 g) IV
Repeat sodium thiosulfate once at half dose (25 mL) if symptoms persist

Treatment of Cyanide Poisoning in Children:
100% oxygen
Sodium nitrite 3% solution: adjusted according to hemoglobin level, given IV over no less than 5 min*
Hemoglobin (grams/100 mL) Sodium Thiosulfate 3% solution (mL/kg)
7 0.19
8 0.22
9 0.25
10 0.27
11 0.30
12 0.33
13 0.36
14 0.39
Sodium thiosulfate 25% solution: 1.65 mL/kg IV
Repeat sodium thiosulfate once at half dose (0.825 mL/kg) if symptoms persist
Monitor methemoglobin and keep level <30%

 

Laboratory clues to CN poisoning: Marked lactic acidosis, arterial appearance of venous blood, elevated measured venous O2 saturation
Sodium thiosulfate should be administered empirically if CN poisoning is considered.
Avoid using sodium nitrite in smoke inhalation victims with suspected CO poisoning.
-- Use sodium thiosulfate alone.

Hydrogen Sulfide Poisoning

Hydrogen Sulfide
Hydrogen sulfide (H2S) is a gas formed as a byproduct of organic decomposition. It has a very strong, distinct “rotten egg” odor.

Sources of H2S include:

  • Sewer or manure gas
  • Chemical or industrial processes, such as tanning, rubber vulcanizing, mining, and manufacture of paper, silk, rayon, refrigerants, soap, and petroleum products
  • Natural sources include hot springs and volcanic eruptions.

MECHANISM/TOXICITY

  • H2S is a stronger inhibitor of cytochrome oxidase than CN → disruption of oxidative phosphorylation → cellular hypoxia and lactic acidosis.
  • Spontaneously dissociates from cytochrome oxidase
  • Direct mucous-membrane irritant

SYMPTOMS/EXAM

  • Severity of symptoms depends on the concentration and duration of exposure. Low concentration exposure may only produce mild mucous membrane irritation. Brief exposures to very high concentrations can cause
    immediate loss of consciousness.
  • Mucous membrane irritation: Conjunctivitis, rhinitis, bronchorrhea, pulmonary edema
  • Headache, seizures, loss of consciousness, coma
  • Hypotension, bradycardia, dysrhythmias, cardiac arrest
  • N/V

DIAGNOSIS

  • H2S poisoning should be considered in any patient presenting with rapid onset of coma, shock, and marked lactic acidosis.
  • Clues to the diagnosis include:
    • Relevant occupational setting
    • Odor of rotten eggs at scene
    • Evidence of decreased tissue extraction of O2:
      • Arterial appearance of venous blood
      • Elevated measured venous O2 saturation (>90%)
      • Marked lactic acidosis
      • Blood levels of sulfide and thiosulfate can serve as markers of H2S exposure, but are not readily available in most clinical laboratories.

TREATMENT

  • Acute stabilization as required
  • Administer 100% O2.
  • Most patients will not require further therapy.
  • Antidote = sodium nitrite (if prolonged symptoms).
    • Induces methemoglobinemia
    • Methemoglobin binds H2S, producing sulfmethemglobin.

 

Sewer or manure gas exposure? Rotten egg odor? Think hydrogen sulfide toxicity.
Hydrogen sulfide toxicity: Rapid coma, shock, and lactic acidosis (as with CN); spontaneous improvement after exposure is ended