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Carbon Monoxide Poisoning

Carbon Monoxide Poisoning. Maria Rica P. Patawaran M.D. Resident Grand Rounds May 1, 2008. Objectives. To discuss the clinical features, diagnosis, complications and treatment of CO poisoning Hyperbaric Oxygen Treatment. Case Presentation. B.A. 26 yo female Single Roman Catholic

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Carbon Monoxide Poisoning

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  1. Carbon Monoxide Poisoning Maria Rica P. Patawaran M.D. Resident Grand Rounds May 1, 2008

  2. Objectives • To discuss the clinical features, diagnosis, complications and treatment of CO poisoning • Hyperbaric Oxygen Treatment

  3. Case Presentation • B.A. • 26 yo female • Single • Roman Catholic • Right-handed • No known co-morbidities

  4. Case Presentation CHIEF COMPLAINT: Unresponsiveness

  5. 4 mos PTA 2 weeks PTA Voiced out relational problems at work Noted to be indecisive; difficulty concentrating; more withdrawn, quiet and had negative thoughts More withdrawn and quiet Still had negative thoughts Evasive when asked about reason for being depressed Case Presentation

  6. 1 week PTA 2 weeks PTA Went to a motel alone and drank 1/8 bottle of whiskey Advised psychiatric consult but declined Seen inside a their car gasping with drooling of the saliva. Also found unburnt charcoals with thinner and chinese herbal medications for insomnia Case Presentation MMC ER

  7. REVIEW OF SYSTEMS: No fever, no pallor No cough or colds, dyspnea No chestpain, orthopnea, PND No abdominal pain, vomiting, no bowel changes No dysuria, hematuria, oliguria No bleeding diathesis No polyuria, polydipsia, polyphagia No edema, cyanosis Case Presentation

  8. Case Presentation • Past Medical History: Unremarkable • Family History: (+) Hypertension; Diabetes; and Heart Disease • Social History: Non-smoker and Non-alcoholic beverage drinker; Denies Illicit drug use

  9. Case Presentation PE: • Unconscious, GCS 5 (E1V2M2) • BP:90/60 CR : 125 bpm, regular RR: 16 cpm, regular T: 36.5C O2 sat 84% • Pink palpebral conjucnctivae, anicteric sclerae, (+) soot inside anterior nares • Supple neck, no palpable cervical, supraclavicular nor axillary LNs, neck veins not distended, no carotid bruit

  10. SCE, no retractions, clear BS, no rales, no wheezes • Adynamic precordium, tachycardic, regular rhythm, AB 6th LICS, MCL, no murmurs • Flabby abdomen, normoactive bowel sounds, soft, nontender, no hepatojugular reflux • No edema, no cyanosis, full and equal pulses, (+) soot stained fingertips

  11. Case Presentation Neurologic Examination: • Mental Status: very drowsy; opens eyes to vigorous stimuli; does not follow command • Cranial Nerves: CN: I – cannot be assessed II – pupils 3-4mm ERTL III,IV,VI – horizontal eye movements V – not done VII - grimaces to pain VIII – XII – cannot be assessed

  12. Case Presentation Neurologic Examination: • Sensory: LUE localizes to pain RUE withdraws to pain Both LE withdraws to pain • Motor: moves all extremities against resistance • Pathologic Reflexes: Bilateral babinski; (+) ankle clonus (L) • Meninges: supple neck

  13. Case Presentation Neurologic Examination • Deep Tendon Reflexes L R ++ ++ +++ +++ ++ +++ ++ +++ ++ +++

  14. Case Presentation • Salient Features: • 26 yo female • No known Co-morbidities • (+) Behavioral Changes • unresponsive • charcoals, thinner and chinese herbal medications • (+) soot in the nares and fingertips • GCS 5 (E1V2M2) • (+) Babinski sign

  15. Admitting Impression • Inhalational Injury 2 to Carbon Monoxide Poisoning • Adjustment Disorder with Depressed Features

  16. Course in the Wards At the ER • Intubated with the ff MV settings: FiO2 100% vT 400 RR 20 PEEP 5 Peakflow 40L/min • Referred to the ff services: Medico-legal and Pulmonary Medicine • Labs Requested: ABGs with CO Hb and Met Hb, CBC, PT, PTT, CXR, 12L ECG, Spec 19, CBG • IVF Started • Immediately transferred to ICU

  17. Course in the Wards At the ICU • Pulmonary Medicine: • Antibiotics started: Co-amoxyclav 1.2 gms IV q8 • Piracetam 1gm IV q8 hrs • Referred to Neurology service • Following tests requested: • CT Scan - Normal • EEG - Normal • Drug Tests • Started Citicholine 1gm IV q12

  18. Course in the Wards 6 - 8 hours post-admission • Repeat labs requested: • Electrolytes • BUN and Creatinine • Total CPK, CK-MB • Repeat ABGs with COHb and MetHb • FiO2 decreased to 60%

  19. Course in the Wards 2nd Hospital Day: • Patient noted to be more awake and follows commands • Feeding started • Repeat CXR • Patient shifted to CPAP with PS 10, PEEP 5, FiO2 30% • Repeat labs: • Electrolytes • Total CPK and CK-MB • Repeat ABGs • Started on CoQ10 1 tab 3x a day, Abixa 1 tab daily and Clexane • Referred to Psychiatry Service

  20. Course in the Wards 3rd Hospital day • Babinski sign now absent • Mech vent settings adjusted: CPAP, PS 5, PEEP 3, FiO2 28%  in-line neb via T-piece • Repeat ABGs done

  21. Course in the Wards 4th Hospital Day • Patient extubated and shifted to nasal cannula • Feeding per orem started • Allowed to move around with assist • Started on Serraline (Zoloft) ½ tab OD

  22. Course in the Wards 5th Hospital Day • O2 and clexane discontinued • Regular diet given

  23. Course in the Wards 6th Hospital Day • Transferred out of the ICU to NP ward The rest of the hospital stay was unremarkable

  24. DISCUSSION

  25. Pathophysiology • CO is a colorless, odorless, nonirritant gas • Known as the “Silent Killer” • CO is diffusion-limited. Amount of CO absorbed is dependent on: • Level of CO in the environment • Minute ventilation • Duration of exposure

  26. Pathophysiology • Rapidly absorbed across alveolar-capillary membrane • Hemoglobin’s affinity for CO is 200 to 250 times its affinity for oxygen

  27. O2 Dissociation Curve • CO binding to hemoglobin causes allosteric modifications increasing its affinity for oxygen • Shift of O2 dissociation curve to the left • Decreased tension at which O2 is released from hemoglobin • Less O2 delivery to the cells

  28. Pathophysiology • CO exerts toxic effects by combination of tissue hypoxia and inflammatory activity • 3 mechanisms of hypoxia: • Decrease O2 capacity of Hgb • Decrease uptake of bound oxygen into tissues • Impairs mechanism of cellular respiration

  29. Pathophysiology • Other mechanisms of toxicity: • Binding to cytochrome oxidase • Lipid peroxygenation • Reperfusion injury • Binding to myoglobin

  30. Pathophysiology • CO poisoning in pregnancy • endogenous fetal production • fetal hemoglobin has a higher affinity for CO • longer elimination half-life in fetus • fetal hypoxia worsened by maternal shift of O2 dissociation curve to the left

  31. Epidemiology • Incidence is underestimated • Most common cause of poisoning death • Death rates higher in males, blacks, ages 15 to 24 and the elderly • Higher in northern and midwestern states • North Carolina 18th (‘79 to ‘88) • More common in winter months

  32. Sources of Carbon Monoxide • Tobacco smoke is the largest source of inhaled CO • independent of nicotine levels • HbCO levels chronically elevated • 0.5% for nonsmokers • 1.9% for one ppd • 3% for two ppd • other sources - 3% to 8% for “heavy smokers”

  33. Sources of Carbon Monoxide • Endogenous production • Motor vehicles produce approximately 250 million tons per year, much is converted to CO2 in the upper atmosphere • “Clean” fuels such as propane, butane, etc. can also be culprits

  34. Sources of Carbon Monoxide • Methylene chloride (CH2-Cl2) found in paint removers • absorbed through the skin or inhaled • metabolized in the liver to CO • longer half-life

  35. Diagnosis - Symptoms • Symptoms are numerous and nonspecific • Acute CO toxicity often misdiagnosed as an acute viral syndrome, in part because of increased frequency in winter months

  36. Diagnosis - Symptoms • Most common Sx from 3 case series: • headache 91% • dizziness 77% • weakness 53% • nausea 47% • difficulty conc./confusion 43% • shortness of breath 40%

  37. Diagnosis - Symptoms • Common symptoms cont. • visual changes 25% • chest pain 9% • loss of consciousness 6% • abdominal pain 5% • muscle cramping 5%

  38. Diagnosis - Symptoms • The Delayed Neuropsychiatric Syndrome • Subacute manifestation (days to months) • Occurs in spite of normal HbCO levels • Broad variety of symptoms including cognitive defects, personality changes, psychic akinesia, parkinsonism, psychotic encephalopathy, amnesia, incontinence, gait disturbances, etc.

  39. Diagnosis - Symptoms • The Delayed Neuropsychiatric Syndrome • reported incidence varies widely, est. 10-30% • can occur in initially asymptomatic patients • symptoms can be subtle, often missed • the Carbon Monoxide Neuropsychologic Screening Battery consists of six subtests, valuable for pre and post treatment and to assess for later occurring Sx.

  40. Diagnosis - Signs • Physical exam signs are also generally nonspecific • tachypnea, tachycardia, vestibular signs common • cerebral edema if poisoning severe • retinal hemorrhages uncommon but more specific

  41. Diagnosis - Signs • Signs of smoke inhalation such as singed nasal hairs, injured mucous membranes, carbonaceous mucus discharge • “Classic” findings of cherry-red lips, skin, and mucus membranes are very rare

  42. Diagnosis - Labs • Carboxyhemoglobin • measured with a co-oximeter • arterial or venous blood sampling • chronically elevated in smokers • consider time of exposure to time of sampling • Expired Carbon Monoxide • monitor that measures CO in parts per million then converts value to estimate HbCO • gives rapid results and can be used at the scene of suspected exposure

  43. Diagnosis - Other • Pulse Oximetry • notoriously poor at detecting HbCO • HbCO and HbO2 similar light absorbance, are read as the same • study of 25 CO exposed pts with measured HbCO from 2.2-44% (mean of 16.1%), all had simultaneous pulse-ox readings of 96-100%

  44. Diagnosis - Labs • Arterial Blood Gas • may show metabolic acidosis • normal to low normal PaO2 • HbO2 saturation is calculated from PaO2 • CK Levels

  45. CPK and CK-MB Levels CPK Levels CK-MB Levels

  46. Diagnosis - Other • Other labs: • CBC • Electrolytes • BUN, Creatinine • Met-Hb • Toxicology screening

  47. Diagnosis - Other • Chest X-ray abnormalities in up to 30%, all nonspecific and often related to associated exposures or conditions • Neuroimaging • typically normal after acute exposure, used to rule-out other pathology • abnormalities in DNS sometimes seen on CT, MRI, and SPECT, most often in deep white matter and / or globus pallidus

  48. Treatment • First step is to remove victim from the source of carbon monoxide • High-flow 100% FiO2 continued until HbCO levels have normalized • Admission for underlying medical conditions (cardiac pts) and assoc. injuries • Screening of other possible victims at scene

  49. Treatment • Elimination of carbon monoxide is related to minute ventilation, duration of exposure to O2, and FiO2 • Half-life of HbCO: • 4 to 6 hours breathing room air • 40 to 80 minutes breathing 100% O2 • 15 to 30 minutes breathing hyperbaric O2

  50. Tx – Hyperbaric Oxygen • Defined as a treatment in which a patient intermittently breathes 100% oxygen • Expressed in Atmospheres (ATM) • Treatment chamber is pressurized to a pressure greater than sealevel • Multiplace chambers - pressurized with air; O2 given via face mask, hood tent, or ET tube • Monoplace chambers – pressurized with O2

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