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Carbon Monoxide

Carbon Monoxide. Gavin Greenfield Mark Yarema March 21, 2002. Carbon Monoxide - Overview. Sources Pathophysiology (3 effects) Acute Presentation Delayed Neurological Sequelae presentation Co-oximeter – what is it? Treatment – NBO vs HBO. CO – What is it?. colourless poisonous gas

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Carbon Monoxide

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  1. Carbon Monoxide Gavin Greenfield Mark Yarema March 21, 2002

  2. Carbon Monoxide - Overview • Sources • Pathophysiology (3 effects) • Acute Presentation • Delayed Neurological Sequelae presentation • Co-oximeter – what is it? • Treatment – NBO vs HBO

  3. CO – What is it? • colourless poisonous gas • generated through incomplete combustion of carbon containing products – anything that contains carbon and is burned • most common cause of fire related death • responsible for more morbidity and mortality than any other toxin (in industrialized countries); leading cause of poisonous deaths in the U.S.

  4. Examples of Exposurenote • smoke from fires • smoke from cigarettes • indoor burning of charcoal (bbq’s) • fossil fuel engine exhaust • gas or coal heater emissions • formaldehyde producing plants • CO also produced from hepatic metabolism of methylene chloride vapour (paint removers and other solvents)

  5. Pathophysiology – Carboxyhemoglobinnote • CO binds to hemoglobin 240 times as strongly as oxygen • amount of oxygen that can be carried by the hemoglobin is inversely related to the number of binding sites occupied by CO

  6. Oxygen Dissociation Curve

  7. Pathophysiology – Oxygen Dissociation Curvenote • Shifted to the left (as does low body temperature and alkalosis) • caused by change in structure of the Hb molecule after CO binds it – results in Hb more tightly holding on to remaining oxygen molecules • results in hemoglobin being unable to release its bound oxygen to tissues

  8. Pathophysiologynote • Binding of hemoglobin by CO (with induction of carboxyhemoglobin and shifting of curve to left) does not account for all of the consequences observed • animals transfused blood with highly saturated carboxyhemoglobin but minimal free CO do not get symptoms • the small free portion that is dissolved in plasma likely has a major role

  9. Quick Review of Kreb’s Cycle

  10. Pathophysiology – Toxic effects of CO on respiratory pigments and mitochondrial cytochromesnote • CO results in the cessation of cytochrome oxidative phosphorylation • at a cellular level get a switch to anaerobic metabolism (pyruvate utilization switches from aerobic Kreb’s cycle to being metabolized to lactate) • CO pathologically activates neutrophils leading to vascular adherence and a reperfusion injury manifested by lipid peroxidation • CO also binds myoglobin and disrupts its activity • decreased myocardial contractility

  11. Summary of Pathophysiologynote • 1. Carboxyhemoglobin + Shift of Oxygen Dissociation Curve to left results in decreased tissue oxygen delivery • 2. Cellular toxin – impairment of oxidative phosphorylation resulting in anaerobic metabolism and impairment of myoglobin • 3. Lipid peroxidation

  12. Typical Presentationsnote • benign headache syndrome or viral illness • particularly if group of people have similar symptoms or if it improves after leaving an exposure site • seizures, coma, myocardial ischemia • everywhere in between

  13. Clinical Featuresnote • Tissues that have high oxygen utilization are more severely affected (heart and brain) • severe CO toxicity • brain: altered mental status, coma, seizures • heart: hypotension, cardiac arrest • mild CO toxicity • headache, nausea, vomiting, dizziness, confusion, emotional ability, weakness • chest pain, palpitations, mottled skin from decreased cardiac output • symptoms exacerbated during times of increased neurologic or myocardial oxygen demand

  14. Clinical Features – Delayed Neurological Sequelae • typically develop 2 to 40 days post exposure • may include headache, difficulty concentrating, lethargy, emotional lability, amnestic syndromes, dementia, psychosis, parkinsonism, chorea, apraxia, agnosia, peripheral neuropathy, urinary incontinence

  15. Diagnosis (in addition to history and physical examination) • Pulse oximetry not useful – why? • oxygen saturation displayed is the ratio of oxyhemoglobin to total (oxy + deoxy) hemoglobin • pulse oximeters use only two wavelengths of light therefore each hemoglobin molecule is classified as oxyhemoglobin or deoxyhemoglobin • carboxyhemoglobin absorbs approximately the same light as does oxyhemoglobin therefore the pulse oximeter misinterprets carboxyhemoglobin as oxyhemoglobin

  16. Diagnosisnote • Arterial Blood Gas – what do you expect? • P02 should be normal or high if on O2 • is useful for demonstrating metabolic (lactic) acidosis • can do venous COHb level as it correlates well with arterial • CBC • give hemoglobin level so can estimate arterial oxygen content

  17. Diagnosis – Co-oximetry • Co-oximetry is the investigation • co-oximeters use four rather than two wavelengths of light • detect oxyhemoglobin, deoxyhemoglobin, carboxyhemoglobin, methemoglobin • co-oximeters require a sample of whole arterial blood

  18. Co-oximetry • signs and symptoms of CO injury correlate with on-scene co-oximeter determination of COHb • very little correlation with emerg carboxyhemoglobin levels • healthy non-smokers have baseline level of 1-3% • smokers commonly have levels of 10% and in some cases may exceed 15%

  19. Other Investigationsnote • EKG to detect myocardial ischemia • If clinically indicated • cardiac enzymes • serum CK, serum myoglobin, urine myoglobin to detect rhabdo • CXR • CT / MRI modestly sensitive for CNS ischemic injury 6 h after exposure • Other routine investigations to exclude alternative diagnoses

  20. Treatment – 100% Oxygennote • nonrebreather with reservoir • PO2 increases resulting in increased total oxygen content of blood and increased oxygen delivery • half life of carboxyhemoglobin is inversely related to P02 – the higher the PO2 the shorter the half life of carboxyhemoglobin • 320 min breathing room air • 60 -130 min breathing 100% oxygen at normal atmospheric pressure • 23 min breathing 100% oxygen at 2.8 atmospheres of pressure (hyperbaric)

  21. 100% Oxygen • Tintinalli recommends treating for 4 hours • Rosen recommends treating until resolution of symptoms or substantial fall of COHb levels and then changing to low-flow oxygen (<50%)

  22. Treatment – Hyperbaric Oxygen (HBO) note • dramatic improvement in symptoms and signs but +++ debate with regard to HBO resulting in improved short and long term outcomes compared with NBO (normobaric oxygen) • Carboxyhemoglobin levels are not used to determine eligibility for HBO (Tintinalli) • some institutions use arbitrary COHb levels as one determinant of referral for HBO therapy (Edmonton) regardless of presence of symptoms (Rosen) • consider costs and risks of transport

  23. HBO – MOA and Complicationsnote • shortens half life of carboxyhemoglobin • improves oxygen delivery to ischemic tissue (by increasing PO2) • may regenerate cytochrome oxidase • lessens CO induced reperfusion injury • complications rare and include oxygen induced seizures (1 in 1000), ear and sinus barotrauma, pulmonary barotrauma, vascular gas embolism • possible higher seizure risk with higher pressure • only absolute contraindication is untreated pneumothorax

  24. HBO • standard HBO treatment uses 100% oxygen at 2.4-2.8 atmospheres of pressure for 90 min • most respond to one treatment although some may require more • efficacy may decrease if delayed more than 6 hours after exposure

  25. HBO – History and Research“Carbon monoxide” and “Hyperbaric” • Pre-1989 • multiple studies claimed benefit • all uncontrolled or retrospective • 1989 – first randomized study • Trial of Normobaric and Hyperbaric Oxygen for Acute Carbon Monoxide Intoxication. The Lancet, August 19, 1989 • Prospective, randomized nonblinded clinical trial in 629 patients • no benefit of HBO over NBO in pt’s with no history of LOC (therefore likely less severe poisoning) • reported incidence of delayed neurological sequelae in more than 40% of both treatment groups • outcome measured was recovery (self assessment questionnaire and physical examination) at one month (delayed neurological sequelae diagnosed when pt’s reported any of a variety of complaints on the questionnaire) • pt’s randomized for treatment at a mean time of almost 6 hours

  26. HBO - Literature • 1995 • Delayed Neurological Sequelae After Carbon Monoxide Poisoning: Prevention by Treatment With Hyperbaric Oxygen. Annals of Emergency Medicine, 25(4), April 1995 • prospective, randomized, nonblinded study of 65 pt’s with mild to moderate (no history of LOC or cardiac instability) CO poisoning who presented within 6 hours • outcome was delayed neurological sequelae tested by a neuropsychologic screening battery (not defined), and simply asking for the presence of symptoms • no difference between groups immediately after treatment • 7 patients in the ambient pressure group had DNS diagnosed • 0 patients in the HBO group had DNS diagnosed (p<0.05, 95% CI on the difference between the proportion of pt’s in whom DNS developed in the two groups (23% vs. 0%) was 8.2% to 38.4% • pt’s treatment begun at a mean time of 2.0 hours

  27. HBO – Literaturenote • 1995 (cont’d) • Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea & Hyperbaric Medicine, Vol. 22, No. 1, 1995 • 26 patients randomized to either 6h 100% NBO + 6h 50% NBO or 2h HBO + 4h 100% NBO + 6h 50% NBO • no patient blinding; ?investigators blinded • clinical signs and symptoms assessed at 2h and at 12h • less clinical abnormalities at both 2h and 12h in HBO group • no clinical abnormalities in any pt at hospital discharge • mean time to treatment 53 minutes

  28. HBO - Literature • 1999 • Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial. Medical Journal of Australia, 170:203-210, 1999 • randomized controlled double-blind trial of 191 patients • included all pt’s (minus pregnant women, children and burn victims) irrespective of severity of poisoning • daily 100 minute treatments with 100% oxygen in a hyperbaric chamber (either at 2.8 atm for 60 min or 1.0 atm) for 3 days • main outcome was neuropsychologic performance (tests) at completion of treatment and at one month (where possible) • no benefit and possible harm in HBO group

  29. HBO - Literature • 1999 (cont’d) • Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial. Medical Journal of Australia, 170:203-210, 1999 • criticisms: cluster randomization, more intense and higher pressure oxygen therapy may have resulted in oxygen toxicity, some authors questioned the appropriateness of the neuropsychological testing, 54% of pt’s lost to follow up, another author subsequently reviewed their statistics and using the exact same data found a benefit to HBO therapy

  30. HBO – Literaturenote • 2000 • Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database of Systematic Reviews, Jan 01, 2000. • included all randomized controlled trials (6) involving non-pregnant adults acutely poisoned with carbon monoxide, regardless of severity. Trials with a score of 3 out of 5 or higher on the validity instrument of Jadad were included • no evidence that unselected use of HBO is helpful; however, evidence is insufficient to provide clear guidelines for practice

  31. HBO - Literature • 2000 (cont’d) • Hawkins et al. – another retrospective review that did show benefit to HBO

  32. HBO - Literature • 2002 • Hyperbaric Oxygen Does Not Prevent Neurologic Sequelae after Carbon Monoxide Poisoning. Academic Emergency Medicine. 9(1), January 2002 • mice study • no benefit to HBO

  33. HBO – Literature Summary • all reported non-randomized studies have suggested benefit from HBO • of the 4 published randomized studies, two report benefit (the two from 1995) and two report no benefit (1989, 1999) • So what the heck do we do?

  34. HBO - Tintinalli Recommendations For Usenote • If mild CO Toxicity then treat with NBO for 4 hours and only consider HBO if symptoms persist • mild toxicity listed as weakness, nausea, dizziness, headache, mildly abnormal CONSB • If severe toxicity than HBO 90 minute treatment, if symptoms persist repeat treatment in 3-6 h • severe toxicity listed as LOC or near syncope, confusion (moderately normal CONSB), focal neuro changes, myocardial ischemia, persisting hypotension, persisting acidosis, pregnant mother with COHb > 15%, concurrent injury or intoxication

  35. HBO – Calgary vs. Edmonton • Calgary • monoplace chamber in Calgary (HBOT clinics) but can only take stable pediatric or pregnant patients, not intubated patients • Edmonton • HBO located at Misericordia Hospital • Senior Therapist for The Chamber told me that it is used regularly (maybe one patient q 2 months) • ER Doc consults Doc on call for the chamber who has final decision as to the use of the chamber

  36. HBO - Edmonton • No specific guidelines as to who gets the HBO • the ones mentioned include COHb>20% (controversial and dependent on the MD on call), severity of presentation (syncope, seizures, metabolic acidosis, etc.) • Pt gets 3.0 atm pressure x 90 min – up to tid in first 24 hours then prn at 2.0 atm x 90 min up to bid

  37. HBO - Calgary • HBOT Clinic in south Calgary has monoplace chambers • deals more with patients with DCS, diabetic wounds, osteonecrosis of mandible • will dive stable pregnant and pediatric patients with CO poisoning but cannot take intubated patients • can call HBOT clinic --> will be referred to MD on call to discuss case • will usually treat at 2.5 ATA for 3-4 treatments, depending on patient

  38. Bottom Line re: HBO in Alberta • Can call HBOT if patient is pregnant or a child, but if patient is unstable/intubated, must discuss with Misericordia MD on call as HBOT cannot take unstable patients

  39. Special Patients • very young and very old more severely affected • pregnant patients • fetus at greater risk due to greater affinity of fetal hemoglobin than adult hemoglobin for CO • pt’s with chronic exposures have greater risk of sequelae independent of COHb levels

  40. Pregnancy • CO is known teratogen • fetal hemoglobin binds CO more tightly than maternal hemoglobin • longer elimination half life of carboxyhemoglobin in fetus • lower threshold for HBO

  41. Dispositionnote • Discharge (ensure not to same environment) • Mild symptoms with full resolution after 4 h of 100% O2 • Mild symptoms with full resolution after one HBO treatment • Admit • mild symptoms but persist • severe symptoms regardless of improvement with treatment • pregnant pt’s for fetal monitoring • All patients need follow up to evaluate for delayed sequelae

  42. CONSB (from Tintinalli) Weaver LK should be publishing data on a randomized double blind study comparing HBO to NBO note

  43. CASE 1 • 28 year old female • fight with significant other • depressed • locks self in garage with car running • found in garage by friend • no LOC or syncope reported • transported on 100% 02 NRB by EMS

  44. CASE 1 • Vitals stable in ED, c/o headache only • exam normal • ABG normal, no acidosis • COHb level 31% • What would you do?

  45. CASE 2 • 42 year old male • lives alone in Airdrie • girlfriend comes over to visit nightly for a 7 day period - reports feeling nauseated, dizzy, and having a headache after leaving house each morning • day 8 - arrives to find him unconscious in house

  46. CASE 2 • Intubated/ventilated by EMS. No CPR necessary. • Fire department confirms presence of CO in home from furnace • transferred to FMC • COHb level 14% at FMC • What would you do?

  47. CASE 3 • paramedic calls in stating there has been an outbreak of CO poisoning at a local skating rink because of a problem with the refrigeration mechanisms • up to 25 people symptomatic, reporting headaches, nausea, vomiting • 4 paramedics on scene, can treat 8 people at once with 02 • wants to know how to manage patients and whether they should all come to your emerg

  48. OUTCOMES

  49. CASE 1 • treated with 100% 02 NRB for 4 hours • symptoms resolved • no longer suicidal • discharged to f/u with GP

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