CIWA, valium, thiamine, oh my: approaches to treating alcohol withdrawal

I ask myself three questions about patients needing treatment for alcohol withdrawal:
Is it uncomplicated or complicated? (Complicated=delirium tremens, active seizing, cardiovascular compromise)
Are the symptoms relatively under control right now, or is the patient soaking through their sheets/intractably vomiting/having bad hallucinations?
Is the patient willing to stay for treatment of withdrawal, or are they ripping out their IV and promising to avoid withdrawal by getting a post-hospitalization discount from their favorite liquor store?
(True story.)

On CIWA: every medical nurse out there has had a patient try to win the CIWA game. MINDS is an alternative scale that correlates strongly with CIWA and can be used in the ICU setting. However, RASS is thought to be a more objective, simpler scale than CIWA. I prefer to use RASS when thinking about who needs more/faster doses of IV benzos, drug loading, more aggressive care.

Medical floor:

  • Uncomplicated withdrawal: these patients will probably be fine with a light dose of PRN benzo of your choice on a CIWA score.
  • Complicated withdrawal: these patients should be treated more aggressively, and if they have underlying medical problems, bad electrolyte problems, rhabdo, or other issues, warrant consideration for ICU-level care.

On withdrawal seizures: around 15% of patients will have seizures around withdrawal. Of these patients, about 50% have seizures for non-withdrawal reasons like SDH, trauma, electrolyte derangements, infection, etc. So work it up! A patient who just seized (or who has DTs) should be treated more aggressively, and definitely with IV benzos.

Choices of medications:

  • Valium (diazepam): I was taught that patients with cirrhosis should get Ativan instead (L.O.T.!) This review argues that (1) that is not true based on studies of cirrhotics from the 70s and 80s (2) Valium has a shorter acting half-life (more rapid onset of action) but longer elimination half-life (tapers down more easily), which means it can be titrated to symptoms more safely and is a better taper. The review also cites studies reporting better outcomes with “Valium loading.”
  • Ativan (lorazepam): everyone’s favorite.
  • Librium (chlordiazepoxide): there’s older pro-Librium data. Librium, like Valium, is a longer-acting benzo. If you have less familiarity with it, though, prescribe it with guidance.
  • Antipsychotics: studied, and may be useful for acute, howling, punch-throwing agitation but known to lower the seizure threshold so…may not be the best choice.

On scheduled benzos for prophylaxis: UptoDate recommends giving patients who are minimally symptomatic with history of complicated withdrawal prophylactic scheduled benzos to prevent worsening symptoms, but also: “A fixed dose schedule strategy is most useful for preventing withdrawal in patients who are at risk but asymptomatic or minimally symptomatic. The only advantage of this strategy is for the provider, as frequent reassessment is not required.” There are no studies cited for either of these statements. I could only find a couple of studies on giving scheduled benzos (in the surgical literature) which didn’t show improved outcomes with prophylactic benzos. In addition, I’ve had the experience of patients whose real problem was benzo addiction pretend to have alcohol withdrawal and specifically demand scheduled benzos for “history of withdrawal seizures.” I only start scheduled benzos on the floor if a patient had a seizure in the last few weeks-months or has had multiple ICU stays for withdrawal.

On thiamine: given to prevent Wernicke’s. It will feel futile, but there is some evidence that IV/IM thiamine does prevent Wernicke’s in patients who are at risk of thiamine deficiency. If the patient has been on a bender bad enough to make them withdraw, they are probably at risk of malnutrition and thiamine deficiency. Just do it! If your hospital has a shortage of IV thiamine, you can give doses of oral thiamine like 300 mg TID x3 days, but I’m not sure if these higher oral doses have been studied or if it’s just hopeful thinking.

Medical ICU:

  • Benzo drip: I don’t know what the record for an Ativan drip is, but I’ve had patients running at 25 ml/hr (so…600 mg of IV Ativan in a day?). The stalwart of ICU withdrawal treatment. Coming down from the drip can be prolonged if patients develop signs of benzo withdrawal, though.
  • Phenobarbital: Research from my old hospital shows it’s effective, self-tapering, and easy to administer, with shorter length of stay and no adverse outcomes–as long as the nurses and ED docs agree on giving it up front. This PulmCrit piece by Josh Farkas provides an excellent overview. If a patient is going to leave AMA and already got a dose of phenobarb, I don’t worry about it, because the half-life is very long.
  • Ketamine?

The bleeding heart in me reminds you: whenever you have the opportunity to care for someone with ETOH withdrawal, you also have the opportunity to prescribe a medication to assist with sobriety, or encourage the patient to think about an intensive substance abuse program.

“Why does potassium have to be repleted to 4?”

There is general agreement–but not an official statement that I could find–that in all comers, K <3.0 should be repleted. In patients with a history of past cardiac surgery, heart disease, and definitely in the post-MI population, K<3.5 should be repleted for a goal of 4.0. When there is acute concern for torsades or other arrhythmia, there is again general agreement but no official consensus that the goal is raised to >4.5.

Remember action potentials? The ins and the outs with K, Na, and Ca with the alphabet soup of channels? (Brief review in the first section of this editorial.) In the short-term, having a low serum K affects repolarization and has a chain effect on the action potential, causing increased automaticity, excitability, and QT prolongation, potentially triggering fatal arrhythmia. In the long-term, hypokalemia is associated with cardiovascular mortality in patients with underlying heart disease, arrhythmias like RBBB, and heart failure.

NB: Kind of supporting this are findings that higher doses of thiazide diuretic are linked to sudden cardiac death. Some argue that the mortality benefit of ACE inhibitors and beta-blockers in heart failure comes in part from an ability to better stabilize potassium levels. (Beta-blockers keep potassium extracellular through beta-2 receptors.)

Many studies linking hypokalemia to arrhythmia were relatively smaller studies (it seems like anything fewer than n=5,000 is not impressive in general cardiology) done in the 1980s, with mixed patient populations of mostly acute MI, hypertension (looking specifically at thiazide diuretics), or heart failure. These studies implied that the higher the potassium (K>4.5) the better:


A more recent population-based cohort study of post-MI patients in JAMA (n>38,000), on the other hand, showed the following:

Because the lowest rate of mortality was found in the group with K 3.5-4.5, a goal of 4.0 is generally set for post-MI patients, which was extrapolated to any patient with heart disease. A similar distribution was found in patients who also had renal disease, and this study based on data from MERLIN-TIMI 36. This is a good reminder that hyperkalemia is linked to increased cardiovascular mortality, too.