Hypokalemia

Low pot is by far the most prevalent elyte disturbance in critical care medicine and therefore in stroke medicine. On our wards there is a reflex of ordering K tablets en masse. We want to shed light on the differential diagnosis of hypokalemia, discuss the many reasons why intensive care patients develop it and bring structure into therapy.

There is – of course – no current publication to use as reference, since elyte disorders are mainly good ole medicine. I have Rose’s Clinical Physiology of Acid-Base and Electrolyte Disorders which is wonderful and includes small cases to work on.

The opening phase of the patient interview

Yesterday, we started a small series on communication skills using the best book ever on the subject

We used the first 45 seconds of a student interview with a patient, concentrating on

  • the open-closed cone
  • the 6-tier structure of the patient encounter according to Kurtz/Silverman
  • ways to improve the patient-doctor relationship

In our internal CME repository, I left a copy of a script on communication skills for reference.

Restless legs syndrome

Triggered by a complex patient with myasthenia, polyneuropathy, RLS, organic psychosis and several more we discuss what is to be known about the restless legs syndrome, using

For me the first source provided a fundamental insight into the pathophysiology of RLS (heightened circadianic dopamine variations with consecutive desensitization of dopamine receptors) that finally explains why dopaminergic medication can lead to augmentation.

I still can’t understand why we use long-acting dopamine agonists rather than short-acting or at least SR L-Dopa to cover symptoms and this pathophysiologic view would support the view.

Another brilliant development is transcranial sonography for imaging of the SN, finding hypoechogenicity – as reported in

A neurologist’s guide to propofol

There are two drugs that are not among the usual repertoire of Neurologists unless they are ICU freaks, yet by their unique pharmacological properties can have a special role in acute Neurology, i.e. the emergency room: Ketamine and Propofol. Since Propofol has come to replace barbiturates for status epilepticus, neurointensive care specialists learned to love it. Apart from this we are going to discuss the more exotic applications and also the pharmacology of its designated successor fospropofol (if its ever going to be introduced in Europe – see also fosphenytoin).

Non-anaesthetic applications for Propofol in Neurology:

References for Propofol in general

Dissociative facial paralysis

It is rare when thetraditional  New England Journal of Medicine forgets it’s past. Thus you have to conclude that the appearance of two “Images in Clinical Medicine” on our topic of yesterday within 12 years is intentional rather than careless:

What do you think?
Whatever, we explore the classic phenomenon of dissociative facial paralysis which led old textbooks  to infer a localizing value of volitional facial paralysis (e.g. has to be capsular or higher). Nowadays we know from case reports that emotional facial paralysis can appear in medullary, AICA, capsular and many more lesion locations, leaving the path of emotional facial innervation completely unclear and thus reducing the localizing value of dissociation.
So in my view, it is still one of the most fascinating physiological (and phylogenetic) facts that nature decided to devote so much energy intoproducing  emotional facial expression (also having to come up with quite a lot of machinery to recognize them). But it helps nada in the daily life of a Neurologist.

DVT in stroke

As most of the participants of our daily team rounds are working in the Stroke Center, we return to a typical Stroke Unit topic today – DVTs in stroke patients. Using the (rare) example of a complicated DVT in the stroke unit, we cover the following issues:

  • Epidemiology
  • Clinical picture
  • Investigations
  • Treatment
  • Prophylaxis

With regard to the latter, there are some basic options:

  • Do nothing (when is this allowed?)
  • Give LMWH or Heparin
  • Stockings (we don’t use them anymore since the Lancet 2009 paper)
  • Intermittent pneumatic compression – we currently are trying to buy some of those gadgets
  • Electrical stimulation (this is current research but might become a valuable option in the future)
Here are some further thoughts on the subject:
  • D-Dimer is a problem if you decide to follow-up on each pathological value. Yet it might help to identify cardioembolic strokes and might even increase the probability of pardoxic embolization in young patients. Thus I would not measure D-Dimer in every patient but young patients with small infarcts are a good population to screen.
  • Many strokes have DVT even before their stroke (up to 7% if you believe this recent publication) and develop a few more during their stay
  • Daily clinical examination of the legs are of the utmost importance.
  • If in doubt, you can always grab our small ultrasound device and inspect the popliteal and inguinal veins, see whether they are compressible, if distal compression increases the flow and if respiratory variations persist in order to verify that the proximal and distal veins each are patent.