32 F – presents with AMS. EMS reports neighbors smelled gas and called 911. They found patient unresponsive (? Sleeping) initially in the apt.  Patient doesn’t remember these events  but does recall that she is staying at a friends and had a few drinks earlier in the night mixed with 1 Xanax. nd isn’t sure how the gas got turned on. Vitals stable. Physical exam aside from being confused about events unremarkable.

Labs: alcohol (271), ASA (wnl), Tylenol (wnl)

Initial VBG: pH 7.34, PCO2 55, PO2 40 lactate 1.5

Carboxyhemoglobin 0.9

EKG- NSR 79, no STT changes. Incomplete RBBB. Flattening T waves laterally

CO poisoning

CO – colorless, odorless gas formed from hydrocarbon combustion that binds to Hgb at much higher affinity (240x) than O2 forming COHb à results in impaired oxygen transportation and utilization

–          Once it binds to the heme moiety it changes the heme so that it cant unload the three oxygen binding sites to the peripheral tissue and also interferes with cytochrome oxidase

Symptoms depend on duration of exposure and CO levels.

–          Cardiac: myocardial ischemia, MI , dysrhythmias, cardiac arrest

–          Brain: Stroke like symtpoms , Seizures Syncope,  Leukoencephalopathy, DNS

  • DNS (delayed neuro sequlea)– not well understood  – theorized that involved lipid peroxidation by toxic oxygen species- when you recover from CO exposure you have a similar phenomenom to ischemia-reperfusion injury and exposure to hyperoxia may exacerbate oxidvative damage

–          Skin- cherry red skin – usually only present in excessive exposure (fatal levels)- also can see cutaneous bullae but uncommon as well

Workup

A+B – hypoventilation, high flow O2 via NRB With resevor – remember SPO2 wont change much

ECG (MI, dysrhythmia), cardiac monitor, volume resuscitation

Mental status / mini mental

Get an exposure history—duration, soursc, other exposures, other people exposed…

VBG- Initial respiratory alkalosis (compensation for reduced delivery); later anion gap metabolic acidosis  due to elevated lactate

CO-oximetry – levels correlate poorly with degree of poisoning and do not predict DNS (normal CO levels in a non-smoker up to 3%; smoker 10-15%)

–          Children are more likely to be affected cause they have a higher RR so they get higher doses of the poison;

Treatment: supplemental oxygen (NRB) or hyperbaric oxygen (JACOBI hospital)

–          Hyperbaric oxygen – 100% oxygen pressurized –not used to expedite removal of blood CO but to stop tissue level destruction

–           Indications for HBO (recommendations, not criteria): Syncope, Coma, Sz, AMS/confusion, COHb > 25% (even if asymptomatic), pregnant woman and children, abnormal cerebellar exam

–          Should be considered up to 24 hours after exposure

 

Hyperbaric fellow consulted on this patient but determined due to other causes of AMS (alcohol) and low levels not a candidate for hyperbaric at that time.

Thanks to Dr. Hernandez for this case!