Sonoencephalography

We concentrate on the non-classical neurocritical applications of transcranial b-picture sonography, i.e., everything apart from investigating the vessels for their own sake. Starting with a female patient with ICH due to sinus thrombosis, we discuss the neuroanatomy of the mesencephalic and diencephalic slices and consider

  • quantification of midline shift
  • screening for temporal or deep ICH
  • monitoring of ICP (using the pulsatility)

References

  • The Widder (in its recent new edition)
  • This article on using transcranial midline shift assessment in deep ICH

Cerebral hyponatremia: salt wasting syndrome vs SIADH

The story of neurological hyponatremia is probably as interesting as the management is complicated. While early reports (where side effects of therapy cannot have played a role) clearly depicted salt wasting, the discovery of SIADH left the salt wasting syndrome forgotten until rediscovered in the 80ies, not the least by Wijdicks, who then saw it everywhere.

Start out with any patient on your neurocritical ward, say a subarachnoid hemorrhage patient, who develops hyponatremia. Before you think, grab all data you can get, such as

  • history (fluid balance, speed of development, drugs, …)
  • examination (hypovolemia vs. eu- or hypervolemia)
  • osmolality, Na, K, Cl, uric acid, urea/BUN, creatinine, TSH, (cortisol level if in doubt)
  • urine osmo, Na, K, Cl, uric acid, urea/BUN, creatinine

Then open your favorite textbook, review article or any proper neurocritical care reference (such as those below) to arrive at a categorical diagnosis. Most of the time, it will be diuretic-induced, but in your Neuro patient it could also be neurological hyponatremia, meaning

  • we don’t know where it comes from,
  • it has to do with the patient’s disease (rather than our treatment) and
  • it looks like SIADH, but could also be CSWS.

The problem is that both diagnoses might be unstable over time (what looks like SIADH today, can waste salt tomorrow) and that the volume status is the arbiter between them, while clinical assessment of volume status is difficult at best – we all know how bad CVP is for deciding the volume status and all other physical signs fare even worse. And how do you judge the volume status of your septic right heart failed hypalbuminic swollen post-SAH patient?

In these difficult cases  I recommend  to just give some saline, say 500-1000 cc. Then give the patient some time (say 1 hour) and remeasure sodium – if it is not worse, your strategy was fine. Otherwise try the management of SIADH (which includes vaptans nowadays). By the way – fludrocortisone can be helpful in either case.

Of course, you have to remember the 0,5 mmol/h maximum rule – if Na rises more quickly, counter that with D5.

With this strategy I am not as tough as Sterns his in his block-diuresis-and-fill-up-the-sodium-slowly approach, as recently studied in this series (which has not been tried in Neuro patients).

References

Fulminant demyelination – Marburg variant, ADEM, tumefactive MS and the differential

Think of a young 26 yo female patient with a bit of optic neuritis in her past and now a rapidly progressing aphasic and encephalopathic picture. MRI reveals a huge left sided frontal demyelinating lesion with open-ring enhancement. What is the differential? How do you separate abscess from lymphoma and astrocytoma and proper demyelinating lesions, such as in tumefactive MS, ADEM/Hurst? What is the role of CSF and MR spectroscopy?

Given, then, a real (but huge) demyelinating lesion, how do you proceed? You apply the neurologic step ladder:

  • Steroids
  • Plasma exchange
  • Cyclophosphamide or Rituximab

But before you give cytotoxic agents, I would require a proper biopsy. There are plenty of reasons for this – choice of the right agent, making sure you aren’t treating lymphoma or astrocytoma. There are also many case reports that justify this approach, such as this one.

There is a wonderful book called “Tough Calls in Acute Neurology”, which covers this topic better than any review article (in fact, ther are no proper reviews on this subject).

Status therapy

As with many neurocritical care topics, there is no big evidence for status therapy, which is why the various guidelines differ dramatically, if only in the dose of drugs to be used. Since the german guidelines have just been released (though not online yet – hate them for it), it is time to review the basic steps (all the following is for Germany, only):

  • Status is when seizures take longer than 5 minutes (all guidelines agree on this, all original papers use different definitions)
  • If in doubt, give Thiamine 100 mg, Glucose (say 2-4 ampules of 40% dextrose) and (this is my personal recommendation and not really the guidelines) an ampule of Mg.
  • Monitor and ensure monitoring.
  • Make sure that an adequate dose of benzoshas been given
    • Lorazepam is preferred (0,05 mg/kg, at most twice)
    • Diazepam is mostly used by the Notarzt, because it needn’t be cooled – 0,15 mg/kg < 10 mg, at most twice
    • Midazolam 0,2 mg/kg can be given im or buccaly or any other way
  • If this fails, hit them with a non-sedating antiepileptic
    • Valproate 20-30 mg/kg (may be repeated with 10 mg/kg after 10 min) with 10mg/kg/min (an ampule of 300 mg a minute is ok)
    • Phenytoin 20 mg/kg (may be repeated with 10 mg/kg) with only 50 mg/min (which is why we rarely use it – takes over half an hour to be completed)
    • Levetiracetam 30-60 mg/kg (may be repeated full dose after 10 min)
    • Lacosamid is offered as an option with 5 mg/kg over 15 mins (too slow for my taste)
  • Next step, narcotic anticonvulsants(intubate, EEG controlled – Burst suppression)
    • Midazolam bolus 0,2 mg/kg, continuous infusion with 0,1-0,5 mg/kg/h
    • Disoprivan bolus 2 mg/kg, continuous infusion with 4-10 mg/kg/h
    • Thiopental bolus 5 mg/kg, continuous infusion with 3-7 mg/kg/h

All this should happen in less than an hour in the case of generalized or complex partial convulsive status epilepticus.
For non-convulsive, things go a bit slower, preferably with less sedating agents and without intubation, if possible.
Personally I often omit step 1 if the beginning of status lies back more than 15 mins (as usually is the case in the ER) as benzos probably don’t work so well then (due to internalization of GABA_A-receptors).

As last resort, our guidelines offer the following

  • Ketamine (good idea because of Glutamate antagonism) bolus of about 1 mg/kg, then 0,3-5,8 mg/kg/h
  • Magnesium
  • Lidocaine bolus 1-2 mg/kg, 1-4 mg/kg/h
  • Dexamethasone (how much?)
  • Sevoflurane and other inhalational anaesthetics

References