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.





It’s one of those topics, where psychiatry has a century long history of finding the right terminology, establishing their own understanding of a strange syndrome, while neurology has a completely different approach and develops new diseases for an explanation.

We discuss the case of a classic catatonic patient with a breeze of weirdness and a touch of malignancy (fever, tachycardia): mutistic, negativistic, rigorous, yet able to turn away and even walk out of the ER. Here, the differential is not too broad, yet we go through it and then discuss the various investigations you could order. This is what we came up with:

  • Non-convulsive status – EEG
  • Encephalitis – LP, MRI, HSV-PCR
  • Wilson’s – eyes, liver, caeruloplasmin, copper @ urine
  • Hashimoto’s – antibodies
  • NMDAR- and other weird autoimmune/paraneoplastic encephalitides, which may be MRI negative – LP, bands, antibody panel
  • Parkinson crisis
  • Mitochondriopathy
  • Porphyria
  • Septic encephalopathy
  • Toxic encephalopathy
  • Neuroleptic malignan / serotonergic syndrome

The easiest way to deal with it, though, is to get a vial of lorazepam and give it. If he gets better within hours – syndrome away! You still have to find the cause of it. Remember that non-convulsive status resolves in seconds rather than minutes or hours after lorazepam.

Nowadays, neurologists tend to think of NMDAR-encephalitis, before they even consider catatonia and probably they are right in a few percent of the cases, but the ruling is still out there.