Tox: Inhaled toxins

Question 1

Examples of simple asphyxiants

Answer 1

CO2, methane, helium

Question 2

Sources of high concentrations methane gas

Answer 2

Bogs of decaying organic matter, natural gas

Question 3

Mechanism of toxicity of simple asphyxiants

Answer 3

Displace oxygen from the lungs resulting in hypoxia

Question 4

Signs/symptoms of simple asphyxiant toxicity

Answer 4

Pulm: rapid onset hypoxia, tachypnea, SOB
Neuro: Dizziness, confusion, coma.
CVD: tachy, possible arrest if prolonged high concentration exposure

Question 5

Tx of simple asphyxiant toxicity

Answer 5

Remove pt from source of exposure and administer oxygen

Question 6

How is CO produced

Answer 6

Odorless, colorless gas produced by incomplete combustion of fuels/organic materials.

Question 7

Sources of CO

Answer 7

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.

Question 8

Mxn of CO toxicity

Answer 8

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.

Question 9

Why is CO particularly concerning in pregnancy?

Answer 9

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

Question 10

Signs/symptoms of CO exposure

Answer 10

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.

Question 11

Long term neurological sequelae from CO exposure

Answer 11

Memory loss, parkinsonism, chorea

Question 12

When should CO poisoning be suspected

Answer 12

Any case with HA and n/v, ESPECIALLY if multiple people are affected

Question 13

How is CO poisoning diagnosed

Answer 13

Direct measurement of COHb in arterial or venous blood via co-oximetry.

Question 14

Normal COHb levels

Answer 14

Normal non-smoker: 2-3%

Smoker: <10%

Question 15

Expected sats/gas findings with CO toxicity

Answer 15

Normal pulse oximetry (cannot distinguish COHb from oxyHB). 
Metabolic acidosis (2* lactate from anaerobic metabolism/poor O2 delivery to tissues). 
Normal PaO2

Question 16

What other investigations should be ordered in the setting of CO toxicity

Answer 16

Troponin, ECG, lactate, CK

Question 17

Elimination half life of CO

Answer 17

Room air: 4-5hrs
100% 02: 1-1.5hrs
Hyperbaric O2: 20-30 min

Question 18

What is the ideal timing to treat someone with CO poisoning with hyperbaric O2

Answer 18

Ideally within 6 hrs. Unproven benefit after 12 hrs.

Question 19

How is CO poisoning treated

Answer 19

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.

Question 20

Purpose of using hyperbaric O2 tx in CO poisoning

Answer 20

Reduce risk of longterm neurocognitive deficits (memory loss, parkinsonism, chorea)

Question 21

Indications for hyperbaric O2 tx with CO poisoning

Answer 21

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)

Question 22

Sources of CN poisoning

Answer 22

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)

Question 23

How does CN cause toxicity

Answer 23

Inhibits cytochrome oxidase, disrupts oxidative phosphorylation –> cellular hypoxia and lactic acidosis

Question 24

Signs/symptoms of CN poisoning

Answer 24

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.

Question 25

DDx for CN poisoning

Answer 25

Hydrogen sulfide, seizure, post-cardiac arrest state

Question 26

Diagnosis of CN poisoning

Answer 26

Suspect if rapid onset coma, shock and marked LACTIC ACIDOSIS.
Blood CN levels can be measured but usually not available in timely manner.

Question 27

Clues to make you suspect CN poisoning

Answer 27

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.

Question 28

Antidote options for CN poisoning

Answer 28

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.

Question 29

What is hydrogen sulfide (H2S)?

Answer 29

Gas formed as a byproduct of organic decomposition as well as from many industrial processes. Has very strong, distinctive ‘rotten egg’ odor.

Question 30

Sources of H2S.

Answer 30

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)

Question 31

Mechanism of hydrogen sulfide toxicity

Answer 31

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.

Question 32

Typical presentation of H2S exposure

Answer 32

Rapid coma, shock, lactic acidosis (similar to CN) with spontaneous improvement after removal from source.

Question 33

Clues to H2S toxicity diagnosis

Answer 33

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

Question 34

Signs/Symptoms of H2S exposure

Answer 34

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

Question 35

Tx of H2S toxicity

Answer 35

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