Non-invasive Carboxyhemoglobin Monitoring: Implications for Carbon Monoxide (CO) Toxicity Screening Following Major Disasters

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Non-invasive Carboxyhemoglobin Monitoring
Implications for Carbon Monoxide (CO) Toxicity
Screening Following Major Disasters

• Selim Suner MD, MS
• Assistant Professor of Emergency Medicine,
  Surgery and Engineering
• Brown University
• Team Leader
• RI-1 DMAT

Brown Medical School Emergency Medicine Medical
Simulation Center
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Objectives

• To understand the epidemiology of carbon monoxide
  toxicity
• To review the pathophysiology and treatment of
  carbon monoxide toxicity
• To report results of COHb screening in a large
  urban tertiary care emergency department

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Simulation Center
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Outline

• Epidemiology
• Mechanisms of toxicity
• Diagnosis
• Treatment
• NBO
• HBO
• Data from recent study

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Disclaimer
Equipment used at RIH provided by Masimo No
content directed by Masimo Publishable data
remains in PI possession
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Sources of CO

• Exogenous incomplete combustion of fossil fuels
• coal and wood burning
• oil heaters
• kerosene burners
• gasoline fires

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Sources of CO

• Endogenous enzymatic conversion of methylene
  chloride to CO
• significant CO toxicity by this source is not
  common
• Physiological breakdown of heme
• Giving the non-smoker person a 1-2 normal level

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Epidemiology of CO Poisoning

• Cases are mostly sporadic and isolated
• Clusters are seen more often in the winter
• About 500 deaths every year
• 46 suicide, 28 fires, 21 unintentional, 5
  homicide
• Association between immigrants who do not speak
  English and unintentional CO toxicity
• Association with ice storms and severe weather
• Association with disaster management from
  generator use

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Smoke Inhalation Mortality Distribution
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Major Morbidity

• Neurological or Psychiatric sequelae are seen in
  2/3 of patients who survive CO toxicity.
• Increased morbidity and mortality from cardiac
  disease following CO toxicity
• Tibbles PM, Perrotta PL Treatment of carbon
  monoxide poisoning a critical review of human
  outcome studies comparing normobaric oxygen with
  hyperbaric oxygen. Ann Emerg Med 199424269-76.
• Mocardial Injury and Long-term Mortality
  Following Moderate to Severe Carbon Monoxide
  Poisoning. Henry CR, Satran D, Lindgren B, et
  al. JAMA 2006 295(4)398-402

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Mechanism of Toxicity

• Hypoxia from COHb formation
• Other cellular and molecular mechanisms have been
  postulated
• Lipid peroxidation in the CNS
• Oxidative stress from cellular CO
• Binding to cytochrome c and P450
• Binding to cardiac myoglobin
• Excessive release of excititory amino acid
  neurotransmitters
• Activation of infammatory cascade
• Ginsburg MD Carbon monoxide intoxication
  clinical features, neuropathology and mechanisms
  of injury. Clin Toxicol 198523281-88

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Making the Diagnosis

• An environment containing products of combustion
• Constitutional, GI, neurological, psychiatric or
  cardiovascular signs and symptoms
• Elevated COHb level (not necessary)

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Measuring COHb

• COHb is measured using a co-oximeter
• Arterial or venous blood can be used
• A handheld device measuring exhaled CO may also
  be used as a screening tool
• There is good correlation with exhaled CO values
  and COHb levels
• Non-Invasive handheld co-oximeter also with good
  correlation to venous co-oximeter
• Shenoi R. Stewart G. Rosenberg N. Screening for
  CO in children. Pediatric Emergency Care.
  199814(6)399-402

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Severity of Intoxication
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Severity of Intoxication

• Arbitrary Classification of mild, moderate and
  severe
• Mild constitutional symptoms such as headache,
  dizziness, lightheadedness, nausea and vomiting
• Moderate transient loss of consciousness or
  neuropsychiatric abnormalities
• Severe comatose, gross neurological deficits,
  cardiovascular symptoms, pulmonary edema or
  profound metabolic acidosis

COHb
10-20
20-40
gt40
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Special Populations

• Pregnancy
• Children
• Infants
• Smokers
• Hemolytic Anemia
• Perrone J, Hoffman RS Falsely elevated COHgb
  levels secondary to fetal hemoglobin. Acad Emerg
  Med 19963(3)287-88

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COHb and Pulse Oximetry Gap

• Pulse oximetry overestimates Oxy-Hb by the amount
  of COHb present
• Pulse oximetry is unreliable in estimating Hb
  saturation in CO-exposed patients and should be
  interpreted with caution when used to estimate
  oxygen saturation in smokers
• Buckley RG, Aks SE, Eshom JL, Rhydman R,
  Schaider J, Shayne P The pulse oximetry gap in
  carbon monoxide intoxication. Ann Emerg Med
  August 199424252-255

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COHb and Pulse Oximetry Gap
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Theoretical HBO Benefit

• Faster elimination of CO half-life from 320
  minutes in room air to 24 minutes at 2.8
  atmospheres absolute with 100 oxygen
• Alters the elimination pharmacokinetics of COHb
  from zero order to first order elimination,
  perhaps promoting intracellular compartment
  shifts of CO
• Prevents adverse molecular processes such as
  lipid peroxidation in experimental studies

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Raphael Thom Ducasse Scheinkestel Weaver
N 343 65 26 191 152
Blinded No No No Yes Yes
LOC 0 0 0 53 50
Suicide 0 NR NR 69 31
NP Tests? No Yes No Yes Yes
Treatments 1 1 2 3-6 3
Rx Period (days) 1 1 1 3-6 1
Max P 2 2.8 2.5 2.8 3
Time to Rx lt12 2 lt2 7.1 63
Explicit definitions No No No Yes Yes
Follow up time (mo) 1 1 0.75 1 1.5
F/U rate 90 89 69 38 46 98
HBO Benefit No Yes Yes No Yes
Comments Raw scores not corrected for age EEG and CBF
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ED Screening Study

• SpCO rendered a vital sign.
• Two triage areas at RIH both equipped with
  bedside co-oximeters.
• Measurement of pulse rate, SpO2 and SpCO on every
  patient
• Staff informed what to inquire in review of
  systems for patients found to have high SpCO
  levels incidentally
• ED Charts abstracted for 14 data elements
• IRB approved

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ED Screening Study

• 11-30-05 to 1-7-06
• 6861 patients 4955 (72 ) screened, 52 male

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Mean COHb 5.1 (3.7) for Smokers upto 13 Mean
COHb 2.9 (2.8) for non-Smokers upto 9
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Case Study

• Comatose from house fire
• Intubated emergently
• Initial venous COHb 38.5
• Initial SpCO 36
• Non-invasively monitored to a final SpCO 5
• t1/2 calculated 57 mins
• First order vs Zero order elimination kinetics
• Patient recovered and was discharged days later

ETT 57 Min
NRM 113 Min
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Case Study

• Elderly male complaint of dyspnea. SpCO of 14,
  the patient was a non-smoker.
• After treatment with NRB mask oxygen, SpCO and
  venous COHb decreased to 4.
• Fire department investigated apartment dwelling
  where patient lives. No environmental CO was
  detected.
• 1 month later a second patient was encountered
  from the same apartment building complaining of
  headache with a screening SpCO of 18.
• Fire department environment analysis detected 293
  ppm of CO in the building.
• Boiler 2 was determined to be defective and was
  replaced.

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Case Study

• 25 yo male presents to ED for knee pain which has
  been bothersome for 3 wks. Review of systems
  detects a complaint of headache. SpCO of 11, the
  patient did not smoke.
• Patient lives in a basement which he heats with a
  kerosene space heater.
• Patient advised to find electric heater and vent
  combustible heater properly.
• Patient discharged with discharge instructions
  for CO exposure as well knee sprain.

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Identification of Occult Cases

• Between 12-05 and 03-06
• 8 occult cases identified with non-invasive COHb
  screening (confirmed with venous co-oximetry)
• Chief complaints
• Knee injury
• Toothache
• 0.03 prevalence
• 13 cases of falsely elevated non-invasive COHb

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Benefits of Timely COHb Measurement

• Improve patient outcomes
• Chronic COHb levels gt 10 causes neurological
  problems
• Chronic COHb levels gt 30 can cause death
• Prevent misdiagnosis
• Prioritize which victims need most urgent
  treatment
• Alert to unknown CO exposure affecting others
• Ability to rule out COHb poisoning may also save
  money and valuable emergency care resources

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Can we rely on SpCO alone?

• False positives and negatives for all testing
• We dont know its sensitivity/specificity in
  real world situations yet
• What things might impair its ability to be
  accurate?
• Anything that reduces transmission of light
  through the tissues
• Slow flow through extremities
• More hemoglobin breakdown
• Induction of enzymes that produce CO during
  critical illness
• Hypoperfusion
• Reminder no measure of tissue oxygenation
  exists

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Conclusions

• CO toxicity is prevalent after disasters
• Early detection of CO toxicity may prevent
  morbidity and mortality.
• Screening large number of patients with
  noninvasive device is feasible.
• Smokers have significantly higher CO levels.
• Normal ranges of SpCO may be different from
  textbook values.
• Further studies are required to determine factors
  which effect SpCO levels.

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Collaborators
Gregory Jay MD-PhD
Jennifer Grilo
Andrew Sucov MD
Jonathan Valente MD
Kerlen Chee MD
Ashley Clapprood
Linda Quatrucci
Robert Partridge MD, MPH
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