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Carbon Monoxide Poisoning
 

Carbon Monoxide Poisoning

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Carbon Monoxide Poisoning

Carbon Monoxide Poisoning
N Engl J Med 2009;360:1217-25.

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  • The images were obtained with the use of highly sensitive 3-T MRI; typical clinical 1.5-T scans would generally depict less damage. White-matter fiber tracks are revealed on diffusion tensor imaging in a 21-year-old normal volunteer (Panels A and B) and in an age-matched patient with a history of carbon monoxide poisoning (Panels C and D). Each image is a fractional anisotropy map obtained by acquiring data in 32 diffusion directions. The average variances of the fractional anisotropy values and the apparent diffusion coefficient values of the corpus callosum differed significantly more in the patient with carbon monoxide poisoning than in the normal subject. Panels E and F show coronal T2-weighted images of the hippocampus in a normal volunteer and in a patient after carbon monoxide poisoning, respectively. Hippocampal atrophy (Panel F, arrows) was found in the patient.
  • In a patient with carbon monoxide poisoning, abnormally increased T2 signals are revealed on axial T2-weighted images of the globus pallidus (Panel G, arrows) and on spin-echo imaging of subcortical structures (Panel H, arrows). The results of auditory functional MRI after carbon monoxide poisoning in a patient with previously normal auditory acuity shows normal activation after auditory stimulation of the right ear (Panel I, arrows) and no activation after auditory stimulation of the left ear (Panel J). This pattern is consistent with normal auditory processing on one side (the right, in this case) but suppression of processing on the other side, presumably in relation to brain injury from carbon monoxide poisoning.

Carbon Monoxide Poisoning Carbon Monoxide Poisoning Presentation Transcript

  • N Engl J Med. 2009;360:1217-25
  • The Clinical Problem
    Carbon monoxide poisoning resulting in more than50,000 ED visits per year in the US.
    Carbon monoxide's affinity for hemoglobin is more than 200 times that of oxygen.
    Patients commonly have neuropsychological sequelae after CO poisoning.
    In one randomized trial, 46% of poisonedpatients treated with normobaric oxygen had cognitive sequelae6 weeks after poisoning, and 45% had affective sequelae.
  • Short-Term Management
    Non-rebreatherreservoir face mask supplied with high-flow O2, or 100% O2.
    It should be provided until the CO-Hb <5%.
  • Evaluation
    Neurologic examination
    Exposure history (duration, source, and whether others wereexposed)
    ABG, CO-Hb (CO-Hb>3% in nonsmokers or >10% in smokersconfirms exposure to CO)
    ECG and cardiac enzymes
    Intentional poisoning: alcohol, BZD, narcotics, amphetamines...
  • Pathophysiological Mechanisms
    of Carbon Monoxide Poisoning.
  • Hyperbaric Oxygen Therapy
    HBO therapy is defined as the breathing of 100% O2 within hyperbaric chambers compressed to greater than 1.4 atm.
    The role of HBO in the management of CO poisoning remains controversial, although both physiologicaldata and some randomized-trial data suggest a potential benefit.
    Health care providers in the ED should consider HBO for treating poisoned patients.
  • Hyperbaric Oxygen Therapy
    The incidence of cognitive sequelaewas lower among patients who underwent 3 HBO sessions (an initial session of 150 minutes, followed by 2sessions of 120 minutes each, separated by an interval of 6to 12 hours) within 24 hours after acute CO poisoningthan among patients treated with normobaric oxygen (25% vs.46%, P=0.007 and P=0.03).
    HBO reduced the rate of cognitive sequelae at 12 months (18%,vs. 33% with normobaric oxygen; P=0.04).
  • Variability among Patients
    In one study, patients who were 36 years of age or older orwho had been exposed to CO for at least 24 hours,who did not receive HBO, or who had cerebellarabnormalities on presentation had an increased risk of cognitivesequelae at 6 weeks as compared with those without these characteristics.
  • Variability among Patients
    Exposedchildren often become symptomatic earlier, and recover faster because of their lesser bloodvolume and increased minute ventilation per unit of body mass.
    The unborn fetus is highly susceptible to the adverse effectsof CO. The period required to eliminate CO is prolonged for fetal blood, and maternal poisoning and hypoxemia contribute to fetalhypoxia.
    HBO therapy should be considered in pregnant women,and in particular if the fetus shows signs of distress.
  • A
    B
    C
    D
    E
    F
  • G
    H
    I
    J
  • Guidelines
    The Undersea and Hyperbaric Medical Society recommends HBOtherapy for patients with serious CO poisoning (transient or prolonged unconsciousness,abnormal neurologic signs, cardiovascular dysfunction, or severeacidosis) or patients who are >36 years of age,were exposed >24 hours (including intermittent exposures),or have a CO-Hb level >25%.
  • Guidelines
    A Clinical Policies Subcommittee of the American College ofEmergency Physicians states that hyperbaric oxygen "is a therapeuticoption for CO poisoned patients; however, its use cannot be mandated....
  • Conclusions and Recommendations
    Patients who have had CO poisoning should be treated immediately withnormobaric oxygen (with a fraction of inspired oxygen as highas possible).
    Clinicians evaluating patients with acute poisoning should considerHBO therapy.
    Patientsshould be informed that they may not fully recover after poisoning, and they should be given referrals as appropriate for theirsequelae.
  • Conclusions and Recommendations
    Patientsshould be informed that they may not fully recover after poisoning.
    In one randomized trial, 46% of poisonedpatients treated with normobaric oxygen had cognitive sequelae6 weeks after poisoning, and 45% had affective sequelae.