Posthypoxic myoclonus – early and late

We spoke about hypoxic encephalopathy a few times already. The problem of prognosis for early posthypoxic patients is – in my view – quite simple t0 solve:

  1. Make sure that you are dealing with posthypoxia rather than something else (do an exam, imaging [at least CT], perhaps an EEG).
  2. Use as much information as possible.
    • History
      • Time to (any) resuscitation
      • Initial rhythm
      • Time of resuscitation – may use the total epi dose instead
      • Epidemiology: as always, age, CHD and diabetes are bad
    • Exam
      • If he shows any cortical activity, the prognosis cannot be too bad, so don’t bother with additional tests.
      • Especially look out for reaction to (severe) pain, remembering that brainstem activity is necessary but not sufficient to get a meaningful outcome
    • Tests
      • Remember that most of the old tests (say SSEP) have been developed in old age. They didn’t know anything about hypothermia, temperature management and so on. So beware of old data. Always request new studies to be done.
      • Labs: NSE, S100B (I like those; they have been evaluated in recent times)
      • EEG: probably not good for prognosis (except if zero EEG or burst suppression)
      • SSEP, AEP: This is just as good as testing for reactions to pain, but easier to make objective. Never been evaluated for hypothermic patients.
      • MRI: nice to have for rule-out of structural disease (such as stroke), yet not good for (early) prognosis. After 2 weeks it might be fine, but then we all know the outcome.
      • Posthypoxic status: again, this used to portend a bad prognosis, but nowadays the false positive rate is to high (might be about 7-10%).

But really we want to deal with posthypoxic myoclonus – here you have to distinguish the pt with coma + myoclonus vs. the (more or less) awake recovering patient with post-hypoxic (nearly always action induced) myoclonus. The latter used to be taught as rare, but probably is quite common among resuscitation survivors. As for treatment, I recommend

  • Levetiracetam (piracetam is probably no better)
  • Valproate
  • Lacosamid
  • Zonisamid

Nothing is evidence-based, really, but this is the choice you have.

References:

  • There is a good article in Movement Disorders, but I cannot access it’s full text.
  • See this article for the difference of posthypoxic status vs. Lance Adams.
  • Here is a short review on the topic.
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S1-S4

Cardiac auscultation is an art that cardiologists only rarely have to care about, having an echo ready at every corner. For us lowliers, it remains perplexing and difficult to learn. But you should try, as it is quite rewarding and also relevant for patient care (think of endocarditis, pulmonary embolism and so forth).

  • We talk about the basic use of the stethoscope, how much it should cost and where you can put it (both on you and on the patient).
  • Also where and how S1 and S2 sound like.
  • Finally, S3 as a sign of distress – it’s differential.
  • S4 as a more prevalent and probably less important sign.

Cluster headache and the wonders of oxygen

Your patient is not so young anymore and female. Her headache is not perfectly Cluster (now continuous for 3 days), yet it started out fairly typical. Then someone comes by, insufflates some oxygen, she gets better and bang – it has to be Cluster.

Even if you don’t believe in the all primary headaches are spreading depression slogan, you would be surprised if success of oxygen therapy were specific for Cluster headache. Here is a paper that shows some benefit for all primary headaches in an ER.

In today’s session we review Cluster headache and the other trigeminovascular headaches I know (not too many), using

Remember there are some ophthalmologic differentials for cluster:

  • orbital infection/imflammation
  • glaucoma
  • scleritis
  • uveitis.

 

The IST-3 trial

It is the biggest randomized thrombolysis trial for stroke ever and it answers a lot of questions, such as

  • Are we safe with our (quite liberal) indications for tpa in stroke? Is the 4.5h window safe? It is, even 6h would be safe.
  • Do elder patients profit? They do! And even more than the younger ones!

The IST-3 trial is methodologically very advanced, has provided an overview of its statistical evaluation in advance. And it is actually quite readable. So go ahead and view the publication and all slides on their homepage.

Added after the fact: since I am a tpa believer (having done at least 150 thrombolyses for stroke last year) I probably don’t question the statistics enough. Make sure, you don’t fall into any trap and give the tpa agnosticians a try –  such as EM ireland.

Degenerative changes in lumbar spine MRI

Up to 80% of low back pain patients get an acute MRI – despite all guidelines saying otherwise.

We recall the red flags in low back pain and then review possible non-neural degenerative pathology in spinal MRIs, such as

  • disc (protrusion, extrusion, prolaps, sequester, infection)
  • vertebral body (Modic I-III)
  • spondylarthropathy and synovial cysts
  • increased mobility

The easiest way to learn all that is to use an MRI atlas, such as this one. Unfortunately, all the review articles just focus on the indication, not the results of spinal MRI in low back pain…

Intravenous antihypertensives

We have fixed our RR goals and management in our so-called Weissbuch – an internal manual for stroke management. These are our pressure thresholds:

  • 100: Hyperperfusion syndrome
  • 140: ICH, after revascularization
  • 160: during thrombolysis
  • 185: before thrombolysis
  • 180-220 for strokes in general

Here are the drugs we use regularly

  • Urapidil
  • Metoprolol/Esmolol
  • Clonidine
  • Enalaprilate
  • Dihydralazin

We rarely use Nitro or Nitroprusside, so we didn’t talk about that. We aso don’t have Labetalole, Fenoldopam, Nicardipin, because they haven’t been approved in Germany.

 

Catatonia

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.

References: