Morning Report: 5/14/2013

Here’s Dr. Aherne with today’s Morning Report!

Carbon Monoxide Poisoning

– CO: Odorless, tasteless, non-irritating

– Formed by the incomplete combustion of hydrocarbons, or endogenously from the metabolism of methylene chloride (paint stripper, aerosol propellants)

– Impairs oxygen delivery and peripheral utilization –> cellular hypoxia

– Binds to hemoglobin with >200 times affinity to that of oxygen –> COHg

– Leads to leftward shift of oxygen dissociation curve –> reduces O₂ delivery

– CO generates reactive oxygen species (–>cellular apoptosis), interferes with cytochrome oxidase pathway (–>impairs oxidative metabolism)

Cellular hypoxia leads to acute CNS effects
- Hippocampus and basal ganglia are most sensitive

– CO displaces NO from platelets –> smooth muscle relaxation –> decrease in SVR

Can lead to ACS, cardiogenic shock, pulmonary edema, dysrhythmia
- Those with underlying CV disease are at high risk

– Up to 46% of patients develop neurologic sequelae, including cognitive and affective changes, gait and motor disturbances, peripheral and cranial neuropathies, psychosis, and eventually dementia, which can arise days to weeks after apparent recovery (Likely due to reactive oxygen species, lipid peroxidation in the CNS, and apoptosis).

– Most common complaint is headache

May present with flu-like symptoms

– History is very important to recognizing CO poisoning

All carbon-containing fuel can produce CO (wood, coal, gas, diesel, oil)
Be thoughtful of any co-toxin exposures (cyanide)

– Stabilization includes IV access to address CV collapse, removal of contaminants, airway security, high flow oxygen

– Frequent vital signs and neuro/mental status checks are necessary

Gait evaluation is necessary to identify neurotoxicity

– COHb level should be collected (ABG if concern for acidosis)

Correlation between COHb levels and poisoning severity is poor
Arterial & venous samples are approximately equivalent
Levels greater than 3% in non-smokers and 10% in smokers is abnormal
Lactate level does not correlate with degree of poisoning

– EKG if AMS or CV symptoms are present

Ventricular dysrhythmia or ST changes may be present
- Cardiac markers should be sent

– Standard co-oximetry will not be able to distinguish between O₂ and CO

– Newer, non-invasive pulse co-oximetry can differential between oxyhemoglobin, deoxyhemoglobin, carboxyhemoglobin, and occasionally methemoglobin.

– Women of child-bearing age should undergo pregnancy tests

CO clearance from fetal Hg takes three times as long (sheep model)

– CXR in patients with persistent hypoxia or respiratory failure

– CT head is necessary if trauma may be present, or in case of undifferentiated AMS, especially if the patient will be undergoing hyperbaric therapy and cannot be reevaluated frequently

Changes due to CO poisoning may take up to 12 hours. These include hypodense lesions in the globus pallidus, caudate, and putamen

– Treatment is oxygen therapy

300+ minutes (5-6 hours) on room air
90 minutes on 100% NRB
30 minutes breathing hyperbaric oxygen (100% at 1.4atm)
- Hastens clearance of CO
- Removes CO from cytochrome oxidase, and prevents effects of lipid peroxidation
  - Any patient with LOC, seizure, acidosis (<7.1), neuropsych abnormalities, fetal distress, or evidence of myocardial ischemia should undergo HBO
  - 20-25% CO or greater requires HBO
  - Data supporting these guidelines are sparse
    - A Cochrane review of 6 RCTs did not find evidence that HBO reduced incidence of delayed neurologic sequelae

– Individuals who did not have LOC, have complete recovery of symptoms, whose COHB level is normal, and who has no evidence of cardiac ischemia can be safely discharged home.