Encephalopathy due to Alcohol

Does anyone have citations/definitions approved by Medical Staff for the term “METABOLIC or TOXIC encephalopathy due to ETOH”?  How does one distinguish a patient that may be simply be intoxicated with slurred speech and other impairments from what some CDI term “alcoholic encephalopathy”?  Reviewing the literature on our site, I find no author that has published articles or provided education on Encephalopathy that has commented on the existence of “alcoholic encephalopathy”. Is this a valid condition? 

Comments

  • Hi Paul,

    I have always thought of alcoholic encephalopathy as a chronic encephalopathy r/t alcoholism?

    Katy

  • Same here.  I should have clarified my question pertains to ‘acute, toxic (metabolic) encephalopathy.  I see many references to chronic forms of encephalopathy, and ETOH is stated as a cause of chronic encephalopathy in alcoholics.  But, does ETOH also result in acute, metabolic?  Thanks!
  • hmmm... good question. I think it would be hard to discern from intoxication and/or withdrawal unless you have metabolic abnormalities  pointing to a distinct metabolic issue (ex: electrolyte disturbances) beyond simply consumption of ETOH. I would not code 'alcoholic encephalopathy' if the patient is intoxicated.
  • Logical and thoughtful response, Katy!  Certainly agree that mere intoxication is not supportive of 'acute, metabolic or toxic' encephalopathy.  thank you. 
  • If the providers are documenting Acute Toxic Encephalopathy 2/2 to acute intoxication.  There are some who are interpreting the word "toxic" in this statement to Poisoning or Toxic Effect of Alcohol with Toxic Encephalopathy when patient's AMS and brain function appears to be more of just intoxication or drunkenness.  What clinical criteria moves a patient from just being acute intoxicated to toxic.  Blood alcohol level or GCS???? 
  • I have nothing to cite as a point of reference but alcohol-related metabolic encephalopathy could be considered, even in the setting of acute intoxication, when the electrolyte derangement is significant, i.e. magnesium - and the patient's mental status doesn't respond as expected with decreased BAL.  My thoughts.
  • I have nothing to cite as a point of reference but alcohol-related metabolic encephalopathy 
    Update:  Interesting article by Dr. Pinson in ACP.  https://acphospitalist.org/archives/2018/02/coding-alcohol-use-disorders-part-2.htm
  • I saw the question when I came to the forum to look for advise regarding this same issue.  The only information I find is from the 2019 CDI pocket guide that states, “toxic encephalopathy due to alcohol intoxication should be coded as T51.0x1a with G92, not as alcoholic encephalopathy (G31.2).”  Any thoughts on this? 
  • we have had a few denials for coding toxic metabolic encephalopathy in cases of patient coming in with AMS  and then going through withdrawal and the providers say toxic encephalopathy and severe etoh use disorder. They say that the code F10.231 alcohol dependence with withdrawal delirium should be used in  these cases.
  • Regarding this article cited above https://acphospitalist.org/archives/2018/02/coding-alcohol-use-disorders-part-2.htm

    Is Dr Pinson saying that  Providers should  document acute toxic encephalopathy resulting from alcohol intoxication  when intoxication is accompanied by delirium?
    Is he also saying both G92  toxic encephalopathy and alcohol induced delirium would be coded? (  for a patient who has an acute reversible encephalopathic process rather than a nervous system degeneration or cerebral degeneration which represent a chronic encephalopathy)

  • we have had a few denials for coding toxic metabolic encephalopathy in cases of patient coming in with AMS  and then going through withdrawal and the providers say toxic encephalopathy and severe etoh use disorder. They say that the code F10.231 alcohol dependence with withdrawal delirium should be used in  these cases.


    The Insurance companies would look for all reasons not to pay a claim. I would rather argue based on the concise documentation and presentation of the patient at the time of admission. Also, the coding clinic first quarter 2017 page  39 and 40 is clear concerning coding and sequencing of these diagnoses.

    Regards.

  • edited April 30
    If i may jump in with a late response, i would not advise using toxic encephalopathy for alcohol intoxication as the cipro coding clinic was referring to prescribed medicines and clearly the patient did not get a doctors order of "go get drunk tonight".. (or did they??) :smile:

    so we ruled out adverse effect.   I would consider alcohol poisoning but that would have to be supported with a blood alcohol level beyond safe thresholds in a patient who probably required close observation for aspiration, may or may not have been intubated or had their stomach pumped etc.

    You could consider metabolic encephalopathy if they had a multi-factorial presentation where by other unrelated factors such as acid base disruption and electrolyes may have been as much to blame as the alcohol, but that would need to be clearly stated.    Intrestingly, if the drinking CAUSED the metabolic disruptions and you got a poor outcome in a patient, you COULD argue alcohol poisoning on that basis. 

    Even with non alcoholic substances i generally advised against the use of encephalopathy if the drug take was known to directly alter brain chemistry (so you are including benzos, anti psychotics, anti depressants, barbituates, basically any kind of sedative or sleeping pill as well as opoids), i always recommended drug induced delerium.  I reserved toxic encephalopathy for systemic physiology disruption from secondary effects of medicines (over diureses, idiopathic responses, or accurring levels beyond the therapeutic threshold etc.).    Since alcohol directly impacts brain chemistry, i would think you would be out of luck in trying to make a case for acute, non metabolic acute encephalopathy due to alcohol.  

    I don't believe following the advice in 1st quarter 2017  pg 39 is at all appropriate since again, the physician did not prescribe the alcohol, nor do i believe "toxic encephalopathy" is an appropriate diagnosis in a patient who took a substance known to directly effect brain chemisty as the patien'ts body is not "toxic" and they are having no secondary brain "malfunction" induced by metabolites...., they are simply demonstrating known effects of the substances they consumed as the medication impacts cognitive function and brain chemistry in very well know, documented, understood and established ways.  


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