Tintinalli Tuesday: Carbon Monoxide Toxicity
Leave a commentAugust 8, 2012 by EmerJencyWEBB
This go around, we learn about carbon monoxide toxicity from TIntinalli’s, but with a question/answer format twist. I’ve also peppered these big ideas with evidence based goodies from the journal stacks, as well as links to posts on CO poisoning from the blogosphere. Enjoy!
Carbon Monoxide Toxicity
How is CO produced outside the body?
Incomplete combustion of carbonaceous material. Possible sources include engine exhaust, heaters (gas/coal), fires, power plant emissions. Smokers also have increased CO levels (5-10% naturally) from inhaling similar material.
How is CO produced inside the body?
Natural byproduct from hemoglobin catabolism into bilirubin. Therefore, there can be increased endogenous CO in hemolytic anemia.
Where does CO bind in the body?
Binds endogenous pigments such as hemoglobin, myoglobin, and cytochrome p450.
How does CO affect oxygen delivery in the body? What is the effect?
Hemoglobin has upwards of 200 x the affinity for CO than O2, and acts as a direct competitor. Also, the O2 that is able to bind to carboxyhemoglobin, is tightly bound and not made available at the tissue level. This can cause end-ischemia at multiple sites in the body, primarily in high O2 consuming organs such as the heart and brain. Because of this, symptoms may be exacerbated by activity/disease processes that cause increased supply/demand mismatch (running, exercise, heart disease, burns, etc…)
In what way does CO cause direct toxicity to tissues?
CO release at the tissue level can cause a breakdown of oxidative phosphorylation as it binds to mitochondrial cytochromes and halts the production of ATP. In this way, aerobic metabolism is prevented and a switch is made to anaerobic energy production. It can also bind cytochrome oxidase and cause lipid peroxidation in the brain.
What organ/tissue specific signs/symptoms are associated with CO toxicity?
Brain: decreased cognition, lethargy, paresthesias, seizures, coma
Heart: chest pain, palpitations, arrythmias, decreased cardiac output (hypotension, poor cap-refill, skin mottling), cardiac arrest
Lungs: Non-cardiogenic Pulmonary Edema
Kidneys: Acute Renal Failure
Muscles: Rhabdomyolysis
How is severity graded?
http://navyemergencymedicine.com/wp-content/uploads/2010/01/CO-poisoning.pdf
What is interval CO syndrome or post interval syndrome?
Delayed neurological sequela seen in a small number of patients. Likely secondary to leukoencephalopathy secondary to mechanisms above.
“Symptoms include cognitive and personality changes, dementia, psychosis, parkinsonism, amnesia, depression, and incontinence.”
Delayed Syndrome in Carbon Monoxide Poisoning. Raj RS, et al. JAPI. Vol 54. (955-956) Dec 2006.
What is the CONSB and what is the key to performing it correctly?
Carbon Monoxide Neuropsychiatric Screening Battery is a test designed to improve neurological assessment of potential CO toxic patients in the emergency setting. The key is to perform this while the patient is breathing room air. Below is a sample of a CONSB used in the literature.
(1) the revised Wechsler Memory Scale for adults, which assesses short-term and long-term semantic and figural memory; (2) digit symbol, which assesses visuomotor coordination; (3) block design, which assesses visuospatial organization and constructional skills; (3) digit span forward and backward, which assess immediate auditory memory, attention, and concentration; (4) Trail-Making Test parts A and B, which assess spatial planing and psychomotor abilities; and (5) the Rey Auditory Verbal Learning Test, which assesses verbal memory and learning ability.
For more click HERE.
What work-up is required for suspected CO toxic patients?
Mild Symptoms: Obtain carboxyhemoglobin level, perform ECG
Moderate Symptoms: Obtain the above, plus search for end-organ damage (i.e. lactate, CK-MB, Troponin assay, CK, Myoglobin, Urine Myoglobin, CXR, etc)
What is the role of brain imaging in acute carbon monoxide poisoning?
Typically not obtained in all cases, but in severe cases, may show evidence of ischemic brain areas for prognostication. Multiple modalities have been studied, but CT and diffusion weighted MRI are probably the only ones (if at all) available for ED use.
For more click HERE, HERE, and HERE.
What populations are at greater risk for complications of CO toxicity?
- Fetus in pregnant patients: fetal-hemoglobin has inc. affinity for CO
- Extremes of age.
- Patients with co-morbid disease.
What is the treatment of CO toxicity?
Mild Symptoms: 100% FIO2 x 4 hours (half life of CO is 60 min on 100% FIO2).
Moderate/Severe Symptoms: Hyperbaric oxygen therapy (HBO)
What is the benefit of HBO?
Controversy exists around this treatment as a whole. Some claim that normobaric oxygen therapy is just as efficacious. On the other hand, there are other reports that claim decreased time to resolution of symptoms and decreased development of delayed neuropsychiatric complications.
Learn more by clicking HERE
At what measured level of COHb should HBO be commenced?
TRICK QUESTION. There is POOR correlation between symptoms, complications, and COHb level. This should NOT guide therapy alone.
Learn more by clicking HERE
What is the disposition for these patients?
Mild Symptoms: If symptoms are improved after 4 hours, discharge home with return precautions. If not improved, refer for HBO therapy.
Moderate/Severe Symptoms: Admission with HBO therapy.
Pregnancy > 20 weeks with suspected toxicity should be admitted with fetal monitoring regardless of symptom severity.
In addition, here are some extra links from the Blogosphere!
http://lifeinthefastlane.com/2011/02/carbon-monoxoide-poisoning/
(This outline is only a reference, and is not all-inclusive of ideas presented in the published chapter. Please refer to the definitive text for details beyond the big ideas above. All credit to the written material above goes to Tintinalli’s Emergency Medicine: A Comprehensive Study Guide 6th Edition)
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