Thread by @IM_Crit_

Alcohol withdrawal syndrome: I don’t know if u have a similar experience in other countries (or other places in the States) but I've recently seen a big spike in alcohol abuse-related disorders, especially alcohol withdrawal syndrome (AWS). I'm obviously referring to severe AWS

that eventually will need to come to the ICU (if we have a bed available!). There are many fantastic, well-searched reviews on this topic but it may be hopefully interesting for some if I put “my way” out there & also for me to learn from your experience. Even though the focus

will be on the neuropsychiatric component, I believe it is quite important to highlight other parts of AWS management. To this end, I will use the assessment/plan “per organ” approach which is commonly used when we write progress notes here in US. Here it goes:

Neuro/Psych:
The common scenarios when I get a call for a case of AWS is either 1) from a hospitalist regarding a pt who was admitted 1 day ago & is getting worse despite “large doses” of lora-/dia-zepam or 2) from an ED attending for a very tremulous pt that is “not responding

to treatment. Admittedly for scenario #1 it is not easy to predict who is going to progress to severe AWS, but my rule of thumb is that (besides the usual risk factors, like hx of AWS or AW-related seizures) if a pt is already withdrawing with a detectable blood etoh level, he is

gonna be tough to manage. We've been taught that someone withdraws when etoh level falls to 0 but if you see someone in withdrawal w an etoh level of 150 mg/dl, then you should treat aggressively from the start. Here is where scenario #2 also comes into play. IMHO, every AW case

which is more severe than mild, needs phenobarbital. Alcohol binds to GABA receptors and, in its absence, we need a GABA-philic drug: benzos or barbiturates or propofol. Propofol is a no-no for non-intubated pts, so we are left w the other two options. Everybody old enough in

Critical Care can recall pts that did not respond to benzos but did fine with phenobarbital. I don't know if it's just difficult to find the right benzo dose (some pts have received 100s of mg of lorazepam without control) but it seems that phenobarbital’s pluripotency (working

on other receptors besides GABA) is partially responsible for doing the trick. Phenobarbital has also interesting pharmacokinetics; its half-life is > 4 days while lorazepam’s is 0.5 days. To be practical, if an AWS pt comes to the ICU, I do not fool around w benzos; I give

phenobarbital. I am not a big fan of fixed doses like 10 or 20 mg/kg ideal body weight because some pts have already benzos and/or opiates on board and I have to go slowly and others may be in such a bad (and "late in the game") AWS that will eventually need higher doses

Some other management points:
1. It feels like everybody is fixated on use of dexmedetomidine; in fact in many US hospitals this is the reason for ICU transfer. I still use it as “add-on” but w the caveat that there is nothing magical about it since it is not addressing

the primary problem, which is @ GABA not @ a-2 receptor. If u want to see a pt seizing, just treat the AW w dexmed and not benzos/phenob.
2. I often keep prn lorazepam in the orders in case of “breakthrough agitation” since it works bit faster than phenob & it’s usually available

in the ICU while phenob has to come from pharmacy. For me: lorazepam = regular insulin & phenobarbital = long-acting insulin
3. In very bad AW, I may use ketamine since AWS is not just a disease of GABA receptors; others, like NMDA-Rs, play a role
4. I try to keep an open mind &

avoid treating psychiatric dz & personality disorders w phenob. These are cases where, for example, you may need antipsychotics
4. When the pt is in the ICU, I ask the nurses to NOT use any of the AW scoring scales. They don't make me wise & they just add to the nurses’ workload

Pulm:
I keep the pt in aspiration precautions w the head of bed elevated. Usually there is no need for any supplemental O2

Cv:
One of my pet peeves is seeing pts in AWS on diuretics/hydralazine/ace inh etc & their healthcare providers spending energy on how to control the BP/HR

If the AWS is adequately treated w phenobarbital (+/- a sprinkle of dexmed), the hemodynamics will be fine

Renal/Fluids etc:
I NEVER use “banana bag”. Makes no sense to me to take a lt of ivf, add some laughable doses of Mg (2g), thiamine (100mg) etc & infuse it over 12-24h. If

the pt is in severe AWS, will need decent amount of ivf (see below what type!) as well as a lot of K & Mg (I give easily >6-8 g the 1st day). Even if K/Mg levels are within “normal range”, the body stores are depleted. Also, the thiamine dose should be several hundred mg the 1st

few days (Wernicke’s encephalopathy is not fun; and neither is Marchiafava-Bignami!)

GI:
I keep all severe AW pts npo the first day or two. I don’t want them to vomit & create another problem to deal with. I also add PPI or H2B under the assumption that most have a degree of

of alcoholic gastritis. Finally, I check liver enzymes - functio as, not infrequently, these pts have either alcoholic hepatitis & may be candidates for steroid treatment or have cirrhosis & need to come under the RADAR of the GI service

Hem:
It’s probably a good time to give

some hematopoiesis-promoting vitamins. I always check coagulation profile on admission. A prolonged INR may be a marker of severe etoh hepatitis. I usually give 3 days of vitamin K to determine if there is a nutritional component

Endo:
This is an underemphasized issue. I ask for

Accuchecks q4h in all these pts. Alcohol-induced ketoacidosis is a real thing & can be associated w normal blood glucose, since alcohol inhibits gluconeogenesis. For this reason, I use dextrose-containing iv fluids

ID:
Not a bad idea to keep an eye on signs/symptoms of

infection (aspiration, cellulitis etc) but no need for empiric antibiotics

Other issues:
Many of these pts have low platelet count. If it is not <30-50k, I use pharmacologic DVT proph as they will be probably in an ICU/hospital bed for several ds

Very important point & another

pet peeve of mine: every severe AWS needs at least 2 peripheral ivs. A poor 22g catheter in the thumb is not a winning strategy. In fact, it is quite risky... I can guarantee you that the pt will pull it at 3:00 am.

When a patient w severe AWS loses his iv access, it’s a nightmare. If I enjoyed wrestling, I would have pursued a different path in my life...

Thanks for reading!

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