Ischemic CO Injury
- This is acute toxicity due to tissue hypoxia, often this is cardiac injury and what causes mortality – not really treated by HBOT
- Manifestations include elevated troponin, AMI (including STEMI in pts w/ underlying fixed obstructive lesions), dysrhythmia (afib most commonly), global hypokinesis on echo.
Neurologic Toxicity
- Can present both acutely and/or delayed with broad variety of presentation: dementia, psychosis, apraxias, Parkinsonism, peripheral neuropathies.
- Underlying etiology is neutrophil activation/adhesion and oxidative stress leading to neurologic injury
- HBOT down regulates PMN adherence for ~ 24h – this is where the likely benefit of HBOT lies, preventing long term neurologic sequelae – not mortality
- Probably need at least 2.5-3.0 atm of pressure to get treatment effect
- Benefit seen if used w/in 24 hrs of poisoning, maybe best if w/in 6 hrs
Indications for HBOT:
Any of: Syncope, coma, seizure, AMS, COHb>25%
Softer call: Pregnancy, cardiac ischemia, age > 36, prolonged exposure, persistent symptoms on 100% O2 w/ COHb = 0%.
- Note that there is no good test for predicting who has a serious enough poisoning to get the neuro sequelae. Even the COHb % doesn’t very accurately predict but it’s what we have.
- Animal data supports treating in pregnancy to protect the fetus
- If not treating w/ HBOT, pts should get 100% O2 until asymptomatic then d/c