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• A 43 y/o woman presents with a 3-week history of
  intermittent headache, nausea, and fatigue. Her
  husband and children also have similar symptoms.
  They all were diagnosed with a viral syndrome by a
  private doctor. The symptoms began when it started
  to get cold. The symptoms are worse in the morning
  and improve while she is at work. Her V/S: 123/75,
  83, 37.0, O2 98%. PE – unremarkable. What is the
  most appropriate next step to confirm your
  suspicion?
   a)   A mono spot test
   b)   Nasal pharyngeal swab for influenza test
   c)   COHb level
   d)   Lead level
• A 35-year-old man presents complaining of
  headache, weakness, nausea, and vomiting after
  working with paint remover in an enclosed space.
  Which of the following statements regarding
  management of this patient’s problem is TRUE?
   a) A special antidote kit is required
   b) Carboxyhemoglobin level is not helpful in this case
   c) Treatment must continue longer in patients with this
      exposure than from other sources
   d) The patient’s oxygen–hemoglobin dissociation curve is
      shifted to the right
   e) Severe metabolic acidosis may be present
Carbon Monoxide
Carbon Monoxide (CO)
• an odorless, colorless, tasteless gas
• produced by incomplete combustion of carbon
  materials
• normally present in air at < 10 parts per million (ppm)
  or less; toxicity begins at 100 ppm
• also an endogenous substance (normal breakdown of
  heme)
• 200-250 times greater affinity for hemoglobin than O2
• reversible binding at the iron-porphyrin center of
  hemoglobin, producing carboxyhemoglobin (COHb)
Sources of Carbon Monoxide
Automotive exhaust
Motorboat exhaust
Propane-fueled heaters
Wood- or coal-burning stoves or heaters
Structure fires
Gasoline-powered generators or motors
Natural gas–powered heaters/furnaces/generators
Methylene chloride
Forklifts
Pathophysiology
• Half-lives of COHb
  – room air: 249 - 320 minutes
  – 100% oxygen: 74 - 80 minutes
  – methylene chloride exposure: up to 13 hours
• COHb level increase  relative anemia &
  hypoxia
• There is a separate toxicity to carbon
  monoxide irrespective of the level of COHb.
Pathophysiology
• 10-15% of CO is dissolved unbound into
  plasma >>move>> intracellular
• CO inhibits cytochrome oxidase, interfering
  with cellular respiration and ATP generation
   a relative uncoupling of oxidative
  phosphorylation
   lactic acidosis
Pathophysiology
• Release of guanylate cyclase & nitric oxide 
  endothelial dysfunction & vasodilatation 
  hypotension
• Relative hypoxia + hypotension  ischemia-
  reperfusion injury in cardiac myocytes, neuronal
  tissue
• Rhabdomyolysis, acute myocardial infarction,
  neuronal cell death
• Cells in the basal ganglia are particularly sensitive
Clinical Features
• Clinical presentation is highly variable
• Clinical scenarios:
  – unconscious patient pulled from a house fire, or
    from a running car in a closed garage
  – the patient with "flu-like" symptoms
  – the elderly person presenting with syncope and
    ischemic ECG changes
Shannon: Haddad and Winchester's Clinical Management of Poisoning and Drug
                                                         Overdose, 4th ed.
Shannon: Haddad and Winchester's Clinical Management of Poisoning and Drug
                                                         Overdose, 4th ed.
• CO poisoning should always be in the dDx for
     1. comatose patients
     2. patients with mental status changes
     3. patients with an elevated anion gap
        metabolic acidosis or otherwise
        unexplained lactic acidosis
• A comatose pt removed from a fire scene
   should be assumed to have CO poisoning
   until proven otherwise, even in the absence
   of cutaneous or airway burns.
Diagnosis
• blood COHb levels (using co-oximetry )
• COHb serves as a marker of severity and helps
  to stratify pts at risk for delayed sequelae
• SaO2 appear artificially high in routine ABG
• Correlation between arterial and venous
  COHb levels is excellent  VBG sample
  analyzed with co-oximetry is usually sufficient
Diagnostic Study Findings Associated with CO Poisoning
↑ COHb level (normal 0-5%; not correlate well w/
symptoms)
Artificially elevated oxyhemoglobin saturation using pulse
oximetry (higher than the saturation on the ABG, pulse
oximetry gap)
↑ lactate
↑ anion gap metabolic acidosis
↑ CPK (rhabdomyolysis > cardiac source)
↑ troponin (diffuse cardiac myonecrosis > focal CAD)
Variable ECG findings—ranges from normal to injury pattern
Bilateral globus pallidus lesions on MRI
Not recommend to rely solely on pulse co-oximeters to detect
CO poisoning
Neuroimaging
• CT brain: change in 12 h of CO exposure + LOC
• Symmetric low-density areas at globus
  pallidus, putamen, caudate nuclei
• CT changes in 24 h  poor outcome
• Not influence patient management
• Reserved for patients who show poor
  response or have an equivocal diagnosis
• MRI appears to be superior
www.learningradiology.com
Bilateral hypodensity in the globus pallidus and hippocampal regions on admission CT.




                                    Coric V et al. J Neurol Neurosurg Psychiatry 1998;65:245-
                                    247


©1998 by BMJ Publishing Group Ltd
Other Tests
• Neuron-specific enolase or S100B and CSF
  myelin basic protein are markers for CO
  neurotoxicity
• More useful to determine prognosis than
  diagnosis
Treatment
• Immediate removal from the contaminated
  environment
• Initial resuscitation steps
• Supplemental oxygen (conc. ≈ FiO2 1.0)
  immediately …and for at least 4 hours
• Severely poisoned pts >> continuous cardiac
  monitoring, an IV line established, and an ECG
  performed.
Hyperbaric Oxygen (HBO) Therapy
• Enhance elimination of COHb (reduces the half-
  life to ≈ 30 min)
• Increases amount of dissolved O2 in plasma
• Reduces CO binding to other heme-containing
  proteins
• Questionable benefit over normobaric oxygen
• May reduce incidence of neurologic sequelae
• The question of who will benefit most, and when
  to refer, remains controversial.
Commonly Utilized Indications for Referral for
Hyperbaric Oxygen Treatment
Syncope
Confusion/altered mental status
Seizure
Coma
Focal neurologic deficit
Pregnancy with COHb level >15%
Blood level >25%
Evidence of acute myocardial ischemia


       Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7th ed.
HBO Therapy
• The patient needs to be clinically stable (+
  secure airway, stable hemodynamic) before
  referral or transport for HBO.
• Complications:
  – Pneumothorax
  – Barotrauma to the ears
  – Seizures from oxygen toxicity (usually with
    prolonged or multiple treatments)
  – Gas embolism
Disposition Considerations
Symptom Severity         Disposition                   Comments
Minimal or no         Home                  Assess safety issues
symptoms
Headache              Home after            Administer 100% O2 in ED
Vomiting              symptom               Observe 4 h
Elevated CO level     resolution            Assess safety issues
Ataxia, seizure,      Hospitalize           Administer 100% O2 in ED
syncope, chest        Consult with          CO level, comorbid
pain, focal           hyperbaric            conditions—including
neurologic deficit,   specialist            pregnancy—and age; stability
dyspnea, ECG                                of the patient must be
changes                                     considered if considering
                                            transfer for hyperbaric
                                            oxygen
           Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7th ed.
Special Populations
• Children:
  – more susceptible (↑fetal hemoglobin,
    ↑metabolic rate)
  – HBO - good safety profile
• Elderly:
  – higher risk from poisoning (esp. serious comorbid)
  – CAD – low COHb (4-6%) can cause ECG changes &
    myocardial ischemia
Special Populations
• Pregnant pts:
  – HBO therapy if they meet criteria or if there are
    signs of fetal distress
  – Normobaric oxygen therapy should be prolonged
    (slower elimination of CO from the fetus)
Thank You
• A 43 y/o woman presents with a 3-week history of
  intermittent headache, nausea, and fatigue. Her
  husband and children also have similar symptoms.
  They all were diagnosed with a viral syndrome by a
  private doctor. The symptoms began when it started
  to get cold. The symptoms are worse in the morning
  and improve while she is at work. Her V/S: 123/75,
  83, 37.0, O2 98%. PE – unremarkable. What is the
  most appropriate next step to confirm your
  suspicion?
   a)   A mono spot test
   b)   Nasal pharyngeal swab for influenza test
   c)   COHb level
   d)   Lead level
• A 35-year-old man presents complaining of
  headache, weakness, nausea, and vomiting after
  working with paint remover in an enclosed space.
  Which of the following statements regarding
  management of this patient’s problem is TRUE?
   a) A special antidote kit is required
   b) Carboxyhemoglobin level is not helpful in this case
   c) Treatment must continue longer in patients with this
      exposure than from other sources
   d) The patient’s oxygen–hemoglobin dissociation curve is
      shifted to the right
   e) Severe metabolic acidosis may be present

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Carbon monoxide poisoning

  • 1. • A 43 y/o woman presents with a 3-week history of intermittent headache, nausea, and fatigue. Her husband and children also have similar symptoms. They all were diagnosed with a viral syndrome by a private doctor. The symptoms began when it started to get cold. The symptoms are worse in the morning and improve while she is at work. Her V/S: 123/75, 83, 37.0, O2 98%. PE – unremarkable. What is the most appropriate next step to confirm your suspicion? a) A mono spot test b) Nasal pharyngeal swab for influenza test c) COHb level d) Lead level
  • 2. • A 35-year-old man presents complaining of headache, weakness, nausea, and vomiting after working with paint remover in an enclosed space. Which of the following statements regarding management of this patient’s problem is TRUE? a) A special antidote kit is required b) Carboxyhemoglobin level is not helpful in this case c) Treatment must continue longer in patients with this exposure than from other sources d) The patient’s oxygen–hemoglobin dissociation curve is shifted to the right e) Severe metabolic acidosis may be present
  • 4. Carbon Monoxide (CO) • an odorless, colorless, tasteless gas • produced by incomplete combustion of carbon materials • normally present in air at < 10 parts per million (ppm) or less; toxicity begins at 100 ppm • also an endogenous substance (normal breakdown of heme) • 200-250 times greater affinity for hemoglobin than O2 • reversible binding at the iron-porphyrin center of hemoglobin, producing carboxyhemoglobin (COHb)
  • 5. Sources of Carbon Monoxide Automotive exhaust Motorboat exhaust Propane-fueled heaters Wood- or coal-burning stoves or heaters Structure fires Gasoline-powered generators or motors Natural gas–powered heaters/furnaces/generators Methylene chloride Forklifts
  • 6. Pathophysiology • Half-lives of COHb – room air: 249 - 320 minutes – 100% oxygen: 74 - 80 minutes – methylene chloride exposure: up to 13 hours • COHb level increase  relative anemia & hypoxia • There is a separate toxicity to carbon monoxide irrespective of the level of COHb.
  • 7.
  • 8. Pathophysiology • 10-15% of CO is dissolved unbound into plasma >>move>> intracellular • CO inhibits cytochrome oxidase, interfering with cellular respiration and ATP generation  a relative uncoupling of oxidative phosphorylation  lactic acidosis
  • 9. Pathophysiology • Release of guanylate cyclase & nitric oxide  endothelial dysfunction & vasodilatation  hypotension • Relative hypoxia + hypotension  ischemia- reperfusion injury in cardiac myocytes, neuronal tissue • Rhabdomyolysis, acute myocardial infarction, neuronal cell death • Cells in the basal ganglia are particularly sensitive
  • 10. Clinical Features • Clinical presentation is highly variable • Clinical scenarios: – unconscious patient pulled from a house fire, or from a running car in a closed garage – the patient with "flu-like" symptoms – the elderly person presenting with syncope and ischemic ECG changes
  • 11. Shannon: Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose, 4th ed.
  • 12. Shannon: Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose, 4th ed.
  • 13. • CO poisoning should always be in the dDx for 1. comatose patients 2. patients with mental status changes 3. patients with an elevated anion gap metabolic acidosis or otherwise unexplained lactic acidosis • A comatose pt removed from a fire scene should be assumed to have CO poisoning until proven otherwise, even in the absence of cutaneous or airway burns.
  • 14. Diagnosis • blood COHb levels (using co-oximetry ) • COHb serves as a marker of severity and helps to stratify pts at risk for delayed sequelae • SaO2 appear artificially high in routine ABG • Correlation between arterial and venous COHb levels is excellent  VBG sample analyzed with co-oximetry is usually sufficient
  • 15. Diagnostic Study Findings Associated with CO Poisoning ↑ COHb level (normal 0-5%; not correlate well w/ symptoms) Artificially elevated oxyhemoglobin saturation using pulse oximetry (higher than the saturation on the ABG, pulse oximetry gap) ↑ lactate ↑ anion gap metabolic acidosis ↑ CPK (rhabdomyolysis > cardiac source) ↑ troponin (diffuse cardiac myonecrosis > focal CAD) Variable ECG findings—ranges from normal to injury pattern Bilateral globus pallidus lesions on MRI Not recommend to rely solely on pulse co-oximeters to detect CO poisoning
  • 16. Neuroimaging • CT brain: change in 12 h of CO exposure + LOC • Symmetric low-density areas at globus pallidus, putamen, caudate nuclei • CT changes in 24 h  poor outcome • Not influence patient management • Reserved for patients who show poor response or have an equivocal diagnosis • MRI appears to be superior
  • 18. Bilateral hypodensity in the globus pallidus and hippocampal regions on admission CT. Coric V et al. J Neurol Neurosurg Psychiatry 1998;65:245- 247 ©1998 by BMJ Publishing Group Ltd
  • 19. Other Tests • Neuron-specific enolase or S100B and CSF myelin basic protein are markers for CO neurotoxicity • More useful to determine prognosis than diagnosis
  • 20. Treatment • Immediate removal from the contaminated environment • Initial resuscitation steps • Supplemental oxygen (conc. ≈ FiO2 1.0) immediately …and for at least 4 hours • Severely poisoned pts >> continuous cardiac monitoring, an IV line established, and an ECG performed.
  • 21. Hyperbaric Oxygen (HBO) Therapy • Enhance elimination of COHb (reduces the half- life to ≈ 30 min) • Increases amount of dissolved O2 in plasma • Reduces CO binding to other heme-containing proteins • Questionable benefit over normobaric oxygen • May reduce incidence of neurologic sequelae • The question of who will benefit most, and when to refer, remains controversial.
  • 22. Commonly Utilized Indications for Referral for Hyperbaric Oxygen Treatment Syncope Confusion/altered mental status Seizure Coma Focal neurologic deficit Pregnancy with COHb level >15% Blood level >25% Evidence of acute myocardial ischemia Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7th ed.
  • 23. HBO Therapy • The patient needs to be clinically stable (+ secure airway, stable hemodynamic) before referral or transport for HBO. • Complications: – Pneumothorax – Barotrauma to the ears – Seizures from oxygen toxicity (usually with prolonged or multiple treatments) – Gas embolism
  • 24.
  • 25. Disposition Considerations Symptom Severity Disposition Comments Minimal or no Home Assess safety issues symptoms Headache Home after Administer 100% O2 in ED Vomiting symptom Observe 4 h Elevated CO level resolution Assess safety issues Ataxia, seizure, Hospitalize Administer 100% O2 in ED syncope, chest Consult with CO level, comorbid pain, focal hyperbaric conditions—including neurologic deficit, specialist pregnancy—and age; stability dyspnea, ECG of the patient must be changes considered if considering transfer for hyperbaric oxygen Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7th ed.
  • 26. Special Populations • Children: – more susceptible (↑fetal hemoglobin, ↑metabolic rate) – HBO - good safety profile • Elderly: – higher risk from poisoning (esp. serious comorbid) – CAD – low COHb (4-6%) can cause ECG changes & myocardial ischemia
  • 27. Special Populations • Pregnant pts: – HBO therapy if they meet criteria or if there are signs of fetal distress – Normobaric oxygen therapy should be prolonged (slower elimination of CO from the fetus)
  • 29. • A 43 y/o woman presents with a 3-week history of intermittent headache, nausea, and fatigue. Her husband and children also have similar symptoms. They all were diagnosed with a viral syndrome by a private doctor. The symptoms began when it started to get cold. The symptoms are worse in the morning and improve while she is at work. Her V/S: 123/75, 83, 37.0, O2 98%. PE – unremarkable. What is the most appropriate next step to confirm your suspicion? a) A mono spot test b) Nasal pharyngeal swab for influenza test c) COHb level d) Lead level
  • 30. • A 35-year-old man presents complaining of headache, weakness, nausea, and vomiting after working with paint remover in an enclosed space. Which of the following statements regarding management of this patient’s problem is TRUE? a) A special antidote kit is required b) Carboxyhemoglobin level is not helpful in this case c) Treatment must continue longer in patients with this exposure than from other sources d) The patient’s oxygen–hemoglobin dissociation curve is shifted to the right e) Severe metabolic acidosis may be present