Early neurological deterioration – a new mnemonic

So I love mnemonics. Sue me.

We really tend to have problems with the myriad of possibilities for a stroke patient to deteriorate in the first – say – 72 hours. Even worse and more problematic if he chooses to decline in the first hours after thrombolysis, where everyone only thinks hemorrhage.

After a decade of juggling the options in my head, I came up with a reasonably simple mnemonic for the etiology of END – HEMODYNAMICS:

  • H emorrhage – need a CT for this
  • E mbolism from a proximal stenosis – need ultrasound or CTA for this
  • M icroangiopathic: these tend to fluctuate a lot, but there is no proof. Think of it, if the same symptoms tend to progress or fluctuate from 100% to 0% and back
  • O edema: early edema can pose problems in large strokes or if a microangiopathic lesion occurs near the capsule and swells; need a CT for this, better even: MRI
  • D islocation: this is important in tPA patients – a well collateralized proximal embolus can shrink through thrombolysis and occlude a distal arterial segment where collateralization is not so good, thus increasing symptoms or even leading to new symptoms – need a CTA
  • Y namics: both occlusions and high grade stenoses can lead to fluctuations along with blood pressure instability. Need an ultrasound or CTA for that, but a better proof is orthostatic increase of symptoms. What I really like is: raising the blood pressure by 50 mmHg to see whether the patient improves.
  • M imics: think of migraine or encephalitis as the original cause of the stroke symptoms. As for diagnostics, probatory treatment with Metamizol+MCP and a spinal tap can help.
  • I ctal: another mimic, requiring EEG to rule out or – if not possible – 1g of Levetiracetam
  • C sf circulation problems – CT is enough
  • S preading depression: after ruling out everything else, this is what remains. No proper diagnostics for that, but try Topiramate.

So here is our diagnostic algorithm:

  • History – timecourse of deterioration, headache, other symptoms
  • Examination – vital signs, neurological and internal
  • Labs: routine labs + cTnI + EtOH
  • Imaging: preferrably MRI, but if that is not acutely available: CT + CTA
  • Ultrasound for hemodynamics
  • EEG to rule out status, or 1g LEV
  • Novalgin + MCP for Migraine
  • Spinal tap to rule out encephalitis

The exquisitely neurological pharmacology of Ketamine

Ketamine is just getting 50 years old and it seems to me that it is underused. Not only is it an excellent anaesthetic, it is also of great use for some very special neurological diseases. The problem, of course, is the lack of data for any of them, for no one will study a drug that you can buy for 15€ an ampule (500 mg!) and that is produced really cheaply by every second drug company. So don’t expect more data about the following applications:

  1. Status epilepticus – from animal experiments it is clear that NMDA receptors play a special role that changes over the development of status. Currently, I use ketamine as adjunct for burst suppression anesthesia (say with midazolam or propofol), but we might come to use it early, maybe even before starting to intubate people.
  2. Chronic pain – the analgesic properties are really not well understood, but Vitamin K seems to be an excellent add-on for complex regimens, in particular for neuropathic pain, say radicular avulsion, trigeminal neuralgia and so on.
  3. Migraine aura – while we have a great list of weapons against migraine headache, there is absolutely nothing known about the aura phase, which becomes relevant in the ED in the case of prolonged aura. I happily apply one-time anaesthetic ketamine infusions (0,5-07 mg S-Ketamine or about ~ 1-1,4 mg Ketamine) together with a topping of 2 mg midazolam and have very good experience. An alternative is proposal, but that needs more monitoring.
  4. Sedation for neurointerventional stroke therapy – the combination of ketamine with propofol (so-called ketofol) is perfect for keeping patient quiet and more or less still, without needing a tube or pressors and that is really important for the RR-sensitive proximal artery occlusion in stroke.
  5. RSI – this is, of course, the standard situation, where ketamine comes more handy than any other induction drug.

Literature