Tox: Inhaled toxins Flashcards
Examples of simple asphyxiants
CO2, methane, helium
Sources of high concentrations methane gas
Bogs of decaying organic matter, natural gas
Mechanism of toxicity of simple asphyxiants
Displace oxygen from the lungs resulting in hypoxia
Signs/symptoms of simple asphyxiant toxicity
Pulm: rapid onset hypoxia, tachypnea, SOB
Neuro: Dizziness, confusion, coma.
CVD: tachy, possible arrest if prolonged high concentration exposure
Tx of simple asphyxiant toxicity
Remove pt from source of exposure and administer oxygen
How is CO produced
Odorless, colorless gas produced by incomplete combustion of fuels/organic materials.
Sources of CO
vehicle exhaust, ovens, house fires, furnaces, portable generators.
Methylene chloride is metabolized in vivo to CO following absorption and is found in paint thinners, degreasers, similar products.
Mxn of CO toxicity
Binds to HgB –> COHB which is incapable of binding O2 –> impaired O2 delivery, cellular hypoxia, lactic acidosis.
COHb shifts oxyHB dissociation curve left –> decreased release of O2 to tissues from normal Hb.
Binds to heme groups in mitochondria and triggers oxidative injury.
Why is CO particularly concerning in pregnancy?
CO has an even greater affinity for fetal HgB and thus, there are higher fetal levels of CO and toxicity for any given maternal exposure
Signs/symptoms of CO exposure
SS are often vague/nonspecific and if not severe, will resolve shortly after removal from CO source.
cardiopulm: tachycardia, syncope, CP, angina, dyspnea, cardiac arrest.
GI: n/v
MSK: rhabdo
Neuro: HA, dizziness, weakness, confusion. Ataxia, cerebellar symptoms, coma, seizure.
Long term neurological sequelae from CO exposure
Memory loss, parkinsonism, chorea
When should CO poisoning be suspected
Any case with HA and n/v, ESPECIALLY if multiple people are affected
How is CO poisoning diagnosed
Direct measurement of COHb in arterial or venous blood via co-oximetry.
Normal COHb levels
Normal non-smoker: 2-3%
Smoker: <10%
Expected sats/gas findings with CO toxicity
Normal pulse oximetry (cannot distinguish COHb from oxyHB). Metabolic acidosis (2* lactate from anaerobic metabolism/poor O2 delivery to tissues). Normal PaO2
What other investigations should be ordered in the setting of CO toxicity
Troponin, ECG, lactate, CK
Elimination half life of CO
Room air: 4-5hrs
100% 02: 1-1.5hrs
Hyperbaric O2: 20-30 min
What is the ideal timing to treat someone with CO poisoning with hyperbaric O2
Ideally within 6 hrs. Unproven benefit after 12 hrs.
How is CO poisoning treated
Remove patient from CO source.
100% O2 by non-rebreather (if low risk, NRB x4hrs then can d/c if no symptoms and HBCO negative).
Hyperbaric O2 for some.
Purpose of using hyperbaric O2 tx in CO poisoning
Reduce risk of longterm neurocognitive deficits (memory loss, parkinsonism, chorea)
Indications for hyperbaric O2 tx with CO poisoning
1) Any hx of LOC
2) COHb >25%
3) Coma
4) Fetal distress in pregnancy (or pregnancy in general?)
5) Persistent neurological symptoms/cerebellar dysfunction
6) Prolonged CO exposure (>24hrs)
7) Seizure
8) Signs of end organ damage (e.g. +troponin)
Sources of CN poisoning
1) Combustion of plastics, synthetic fibers, wool, house fires (smoke inhalation of listed)
2) Prolonged infusion of nitroprusside
3) Industry including mining, plastics manufacturing, welding, fumigation, chemical synthesis, research
4) Pits and seeds of certain fruits (apricots, bitter almonds) that contain amygdalin (releases CN in vivo during metabolism)
How does CN cause toxicity
Inhibits cytochrome oxidase, disrupts oxidative phosphorylation –> cellular hypoxia and lactic acidosis
Signs/symptoms of CN poisoning
Effects w/in seconds of hydrogen CN gas exposure, minutes of salt ingestion.
If toxicity from amygdalin pulverized seeds, may be delayed by hours.
Initially: HA, n/v, confusion, HTN, tachypnea.
Late: seizures, coma, pulmonary edema, dysrhythmias, hemodynamic collapse, cardiac arrest.
DDx for CN poisoning
Hydrogen sulfide, seizure, post-cardiac arrest state
Diagnosis of CN poisoning
Suspect if rapid onset coma, shock and marked LACTIC ACIDOSIS.
Blood CN levels can be measured but usually not available in timely manner.
Clues to make you suspect CN poisoning
1) Hx of smoke inhalation or occupational access to CN
2) ABG evidence of reduced tissue extraction of O2 (AGMA, arterial appearance of venous blood and elevated venous oxygen sat >90% due to inability to extract O2)
3) Marked lactate (>8)
4) Pt has distinctive bitter almond-like odor.
Antidote options for CN poisoning
1) Hydroxocobalamin (B12a): reacts w/ CN to form cyanocobalamin (B12), non-toxic compound, excreted in urine. Used as single agent.
2) Cyanide antidote kit (3 components):
- Sodium thiosulfate: Binds CN and forms thiocyanate.
- Amyl nitrite pearls (IN): for inhalation prior to IV access. Induces methemoglobinemia. should NOT be used if concurrent CO poisoning.
- Sodium nitrite (IV): also induces methemoglobinemia. May worsen tissue deoxygenation if CO poisoning.
What is hydrogen sulfide (H2S)?
Gas formed as a byproduct of organic decomposition as well as from many industrial processes. Has very strong, distinctive ‘rotten egg’ odor.
Sources of H2S.
1) Sewers
2) Manure gas
3) Chemical/industrial processes (tanning, rubber vulcanizing, manufacture of paper, silk, rayon, refridgerants, soap, petroleum products).
4) natural sources (hot springs, volcanic eruptions)
Mechanism of hydrogen sulfide toxicity
Strong inhibitor of cytochrome oxidase -> disrupts oxidative phosphorylation -> cellular hypoxia/lactic acidosis.
Spontaneous dissociation from cytochrome oxidase.
Direct mucous membrane irritant.
High concentrations may overwhelm olfactory system and extinguish odor.
Typical presentation of H2S exposure
Rapid coma, shock, lactic acidosis (similar to CN) with spontaneous improvement after removal from source.
Clues to H2S toxicity diagnosis
1) Relevant occupational setting
2) rapid LOC
3) odor of rotten eggs on scene
4) silver jewelry on scene may be darkened
5) ABG evidence of reduced tissue extraction of O2 (AMGA, arterial appearance venous blood, high o2 sat in venous blood)
6) Marked lactic acidosis
Signs/Symptoms of H2S exposure
Low concentration exposure -> mainly mild mucous membrane irritation.
CVD: hypoTN, brady, dysrhythmias, arrest.
GI: n/v
MM irritation: conjunctivitis, rhinitis, bronchorrhea, pulmonary edema
Neuro: HA, seizures, rapid LOC, coma
Tx of H2S toxicity
1) Remove from source
2) Acute stabilization
3) 100% O2
4) Observe for several hours (delayed pulmonary edema)
5) Antidote: sodium nitrite (if prolonged symptoms, limited effectiveness)
Most pts do not require further therapy
