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Smoke inhalation
What’s the problem?

 Heat – Thermal Injury

 Smoke – Particulate

 Hypoxic gas inhalation (FiO2 <0.21) - Asphyxia

 Carbon Monoxide - Asphyxia

 Cyanide – Asphyxia

 Smoke inhalation better predictor of mortality
  than burn extent
Thermal Injury

 Obviously patients may have massive burn injury
  with or without trauma

 Dry Heat (from house fire) has very poor
  conveyance of heat beyond vocal cords

 Duration of exposure is important – flash burns
  usually only singe nasal hair and mucosa

 Stridor

 Difficulty managing secretions

 Hoarseness (count to 10)
Particulate matter

 Smoke is full of particulate matter, soot and ash

 Causes obstruction and sloughing in the small
  airways leading to atelectasis and shunt etc…

 Bronchospasm – due to direct toxic effects

 ARDS

 If their lung fall to pieces this is what will most
  likely kill them
Carbon Monoxide

 odorless, tasteless, colorless, nonirritating gas
  formed by the incomplete combustion of
  carbon-containing compounds

 Headache, malaise, confusion, angina, seizures,
  heart failure coma…
Pathophysiology
 Binds to Hb with 240
  times affinity than O2

 Reduces the other 3
  sites ability to offload
  O2 at tissue level

 Binds to myoglobin

 Interrupts
  mitochondrial function
How to pick it up
 ? Sats probe (depends how good your probe is)

 Work by two frequencies (940 and 660nm) – measure
  oxy and deoxy respectively

 COHb absorbs light at 660nm just like OxyHb therefore
  usually useless to differentiate

 (remember MetHb is similar)

 Co-oximetry is the way to do it (4 rather than 2
  wavelenghts)

 Your friendly blood gas machine has a nice co-
  oximeter in it

 What will the pO2 be?
What levels matter

 Normal <5%

 Smokers/COPD – allow up to 20%

 High levels DO NOT correlate with outcome
How to treat
 Lots of oxy

 Half life in FiO2 0.21 about 300 mins

 Half-life in FiO2 1.0 about 60-90 mins

 What about minute ventilation?

 ? Hyperbaric Oxygen – NEJM 2002 Volume 347:1057-
  1067

 Probably >25-40% and should be available within 6
  hours and most importantly not compromise care

 All pure COHb poisonings in single chambers on
  multiple occasions

 How do you apply the oxy?
Long term

 Poorly understood delayed neurosequelae (DNS)

 Cognition/personality/movement disorders

 3 days – 9 months post exposure

 Usually only if there was LOC with exposure

 Again - not correlated with COHb levels
Cyanide

 Not James Bond

 Commonly in house fires with plastic furniture

 Repeatedly missed due to lack of suspicion
How does it kill you?
 Mitochondrial toxin

 Cytochrome a3
How does it kill you?
 Stops oxidative phosphorylation and ATP production

 Switches to anaerobic production and subsequent
  lactic acid

  Glucose              Pyruvate
      In presence of
      O2
                                    In absence of O2




    Acetyl CoA


                                      Lactic
                                      acid
    Kreb’s cycle
                          LACTATE                       H+
                                          Dissociates
Clinically

 Sick and very sick

 LOC, seizures, BP, Acidosis
  •   TCAs, Aspirin, organophospates, meningococcal,
      eclampsia

 Collapse following gas exposure
  •   H2S, CO
Tests

 Mainly to exclude other causes
  •   ECG, BSL, Aspirin levels, HCG

 Specifically
  •   ABG
  •   Central venous pO2 to look for oxygen uptake
      (what else will affect this)
  •   Lactate (correlates with cyanide levels)
Treatment – Direct binding

 Hydroxycobalamin
  •   Binds to form cyanocobalamin – safely excreted
  •   Can interfere with co-oximetry

 Dicobalteditate
  •   Horrible toxic drug that at least works
Treatment – MetHb induction

 Sodium nitrite/Amyl Nitrite
  •   Cyanide has more affinity for fe3+ on MetHb than it
      does for Fe3+ on Cyt A3
  •   Has some rather obvious problems
Treatment – sulfur donors

 Body normally deals with cyanide with
  rhodanese – a sulfur requiring enzyme

 Sodium Thiosulfate

 Works reasonably and relatively safe
Treatment

 Most algorithms suggest:

1. Hydroxycobalamin

2. AND Sodium thiosulfate



 Have low threshold for treating in shocked
   house fire victim with profound lactic acidosis
Summary
 Smoke inhalation has 5 main aspects
  1.   Heat - airway
  2.   Particulate – wheeze/ARDS
  3.   Hypoxia – brain damage
  4.   CO – functional anemia
  5.   Cyanide – histotoxic hypoxia

 Usually with other catastrophic injuries

 Often associated with drug ingestions
Summary

 For CO
  1.   Co-oximetry – not sats probe
  2.   Get the oxy on
  3.   Levels don’t correlate

 For cyanide
  1.   Be suspicious
  2.   Shock/Seizures/Profound lactic acidosis
  3.   Central venous O2 useful
  4.   Hydroxycobalamin/Thiosulfate if good suspicion –
       these are safe.

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Smoke inhalation

  • 2. What’s the problem?  Heat – Thermal Injury  Smoke – Particulate  Hypoxic gas inhalation (FiO2 <0.21) - Asphyxia  Carbon Monoxide - Asphyxia  Cyanide – Asphyxia  Smoke inhalation better predictor of mortality than burn extent
  • 3. Thermal Injury  Obviously patients may have massive burn injury with or without trauma  Dry Heat (from house fire) has very poor conveyance of heat beyond vocal cords  Duration of exposure is important – flash burns usually only singe nasal hair and mucosa  Stridor  Difficulty managing secretions  Hoarseness (count to 10)
  • 4. Particulate matter  Smoke is full of particulate matter, soot and ash  Causes obstruction and sloughing in the small airways leading to atelectasis and shunt etc…  Bronchospasm – due to direct toxic effects  ARDS  If their lung fall to pieces this is what will most likely kill them
  • 5. Carbon Monoxide  odorless, tasteless, colorless, nonirritating gas formed by the incomplete combustion of carbon-containing compounds  Headache, malaise, confusion, angina, seizures, heart failure coma…
  • 6. Pathophysiology  Binds to Hb with 240 times affinity than O2  Reduces the other 3 sites ability to offload O2 at tissue level  Binds to myoglobin  Interrupts mitochondrial function
  • 7. How to pick it up  ? Sats probe (depends how good your probe is)  Work by two frequencies (940 and 660nm) – measure oxy and deoxy respectively  COHb absorbs light at 660nm just like OxyHb therefore usually useless to differentiate  (remember MetHb is similar)  Co-oximetry is the way to do it (4 rather than 2 wavelenghts)  Your friendly blood gas machine has a nice co- oximeter in it  What will the pO2 be?
  • 8. What levels matter  Normal <5%  Smokers/COPD – allow up to 20%  High levels DO NOT correlate with outcome
  • 9. How to treat  Lots of oxy  Half life in FiO2 0.21 about 300 mins  Half-life in FiO2 1.0 about 60-90 mins  What about minute ventilation?  ? Hyperbaric Oxygen – NEJM 2002 Volume 347:1057- 1067  Probably >25-40% and should be available within 6 hours and most importantly not compromise care  All pure COHb poisonings in single chambers on multiple occasions  How do you apply the oxy?
  • 10. Long term  Poorly understood delayed neurosequelae (DNS)  Cognition/personality/movement disorders  3 days – 9 months post exposure  Usually only if there was LOC with exposure  Again - not correlated with COHb levels
  • 11. Cyanide  Not James Bond  Commonly in house fires with plastic furniture  Repeatedly missed due to lack of suspicion
  • 12. How does it kill you?  Mitochondrial toxin  Cytochrome a3
  • 13. How does it kill you?  Stops oxidative phosphorylation and ATP production  Switches to anaerobic production and subsequent lactic acid Glucose Pyruvate In presence of O2 In absence of O2 Acetyl CoA Lactic acid Kreb’s cycle LACTATE H+ Dissociates
  • 14. Clinically  Sick and very sick  LOC, seizures, BP, Acidosis • TCAs, Aspirin, organophospates, meningococcal, eclampsia  Collapse following gas exposure • H2S, CO
  • 15. Tests  Mainly to exclude other causes • ECG, BSL, Aspirin levels, HCG  Specifically • ABG • Central venous pO2 to look for oxygen uptake (what else will affect this) • Lactate (correlates with cyanide levels)
  • 16. Treatment – Direct binding  Hydroxycobalamin • Binds to form cyanocobalamin – safely excreted • Can interfere with co-oximetry  Dicobalteditate • Horrible toxic drug that at least works
  • 17. Treatment – MetHb induction  Sodium nitrite/Amyl Nitrite • Cyanide has more affinity for fe3+ on MetHb than it does for Fe3+ on Cyt A3 • Has some rather obvious problems
  • 18. Treatment – sulfur donors  Body normally deals with cyanide with rhodanese – a sulfur requiring enzyme  Sodium Thiosulfate  Works reasonably and relatively safe
  • 19. Treatment  Most algorithms suggest: 1. Hydroxycobalamin 2. AND Sodium thiosulfate  Have low threshold for treating in shocked house fire victim with profound lactic acidosis
  • 20. Summary  Smoke inhalation has 5 main aspects 1. Heat - airway 2. Particulate – wheeze/ARDS 3. Hypoxia – brain damage 4. CO – functional anemia 5. Cyanide – histotoxic hypoxia  Usually with other catastrophic injuries  Often associated with drug ingestions
  • 21. Summary  For CO 1. Co-oximetry – not sats probe 2. Get the oxy on 3. Levels don’t correlate  For cyanide 1. Be suspicious 2. Shock/Seizures/Profound lactic acidosis 3. Central venous O2 useful 4. Hydroxycobalamin/Thiosulfate if good suspicion – these are safe.