Delirium tremens

The evidence level at which psychiatric intensive care works is quite depressing. We tried to collect the data on how to treat delirium tremens, but apart from some small case series and review articles such as this recent one, there really is not much to go on.

So here are some of my experiences:

  • Make sure to strictly distinguish delirium from withdrawal. There is a lot of difference in terms of physiology as well as treatment. And delirium is treated in a monitoring unit, withdrawal can be done everywhere. I am not sure whether good withdrawal treatment can actually prevent delirium, but we surely try to…
  • Phenomenologically you can separate a) Agitation b) Vegetative c) Psychotic features. These might be linked to separate neurotransmitters in overdrive (a) GABA b) NA c) dopamine), but again this has not been proven.
  • You can treat agitation by filling those GABA-receptors with benzos, barbiturates or modify them with proposal.
  • Vegetative symptoms are best treated with clonidine or dexmedetomidine.
  • Psychotic features usually respond to dopamine antagonists, where the best (iv available) is haloperidol.¬†
  • As for management, I recommend filling up with diazepam, because of its superb pharmacology, namely it’s accumulation which leads to slow secondary withdrawal symptoms.
  • The problem is that diazepam has different pharmacokinetics every day and in every patient, so that you titrate your loading dose according to some agitation/sedation scale and must not be scared of high doses (such as 100-400mg). Take your time and every opportunity to see your patient should be used to push some more, first in 10 mg steps, then escalating boluses to 20 or even 30 mgs.
  • Once filled, I halve the dose every day in tid-dosing scheme, e.g. 120 mg on the first day leads to 3×20 the second.
  • If properly sedated (drowsy/sleeping, but arousable on command) and still some vegetative action (in particular heart rate), titrate clonidine in steps of 75micg.
  • If, when aroused, the patient hallucinates or speaks with the wall, add haloperidol (3 x 2,5 to 3 x 5mg).
  • Take care of all organ systems during this trip – do prophylaxis as much as you can. Don’t forget ulcer prophylaxis, mobilization, thromboprophylaxis.




All things BPPV

I just wrote up our local SOP BPPV and used the opportunity to collect all current and fancy information of the last 2 years, trying to judge whether they help at all. Apart from the fact that most of the research has been done in Korea and Italy, I found some further interesting things and joined them in a Prezi (in German, though).

Feel free to use that.

Horizontal gaze palsy

I spoke with a colleague recently about the topics for our local stroke convention in the fall and we shrugged shoulders: nothing new really. Really? Quite to the contrary. I stumbled upon a patient last week that had the curious combination of a horizontal gaze palsy to the left with only slight proximal paresis of the left arm, maybe some dysarthria, but you couldn’t quite tell, because his local accent was so thick. And his MRI: shows a microangiopathic lesion only in the right internal capsule, in the posterior crus right behind the genu, perhaps touching the latter a tiny little bit. No thalamic involvement, nothing else.

We reviewed the functional anatomy of the horizontal gaze system and localized the various structures (such as the frontal eye fields, the capsule, the PPRF, MLF, IIIrd and VIth cranial nerve nuclei) in an MRI. I am always surprised how hard this can be, but we use Kretschmann’s atlas to do the main work. The rest can be left to Brazis’ localization book, which – incidentally – has been edited in 2012.