Imploding head syndrome

What are the contraindications to lumbar puncture? The easy ones are coagulation disorders, infection around the LP site and spinal cord trauma – although to be honest nothing much can be found about the threshold of the three Ps (PT, PTT, platelets) you need for doing an LP; obviously no proper studies have been performed, so there is a project for all those budding research Neurologists or Anesthesists out there; can you do an LP on a patient with Tirofiban? How long after tPA?

Herniation does occur in meningitis

Of course, the most important question is: how much do we have to make sure that herniation will not occur? This has only been studied in bacterial meningits, where LP is felt to be that urgent that the CT cannot be waited for (as an aside: in Germany, our guidelines solved the problem by just requiring ER docs to infuse Ceftriaxone AFTER blood cultures but BEFORE LP) – again without proper evidence base. But meningitis is the most important case, because this is the only disease, where herniation does occur at least rarely (as opposed to never – cf. all other diseases) – the literature estimates about 5-10% of patients. It also can happen without LP.

Intracerebral pressure is not the problem

The first thing to understand is that herniation is usually attributed much more to brain shift than to pressure. Pressure can be very high (see pseudotumor) and still no coning after LP. In fact, most bacterial meningitides do have quite high pressures (30 cm H2O upward). Since papilledema (if at all present) really only signifies raised ICP, a lack of papilledema does not help at all.

Brain shift is the problem

The crux lies in pressure differences, either from left to right (along the falx, from temporal to brainstem), cephalad to caudad or vice versa. These pressure differences stem from space occupying lesions (e.g. abscesses), generalized but locally different edema or even from slight differences in local adhesiveness due to inflamed meninges, leading to reduced mobility of brain tissue. Once the pressure difference is accentuated by LP, brain shift can occur and this then leads to herniation. As an intensive care or emergency neurologist you ought to know your herniation syndromes, if not, you can look them up in any Neurointensive Care Textbook.

Acute brain shifted patients do have neurology

If an acute process such as meningitis or an abscess leads to brain shift, you can expect neurological symptoms. This has been established reasonably well in children and adults (see the NEJM 2001 paper). Here focal neurological symptoms means

  • Severe disorder of consciousness
  • Seizures
  • Pupillary disorders
  • focal deficits

This rule only applies in acute patients and not if your pathology develops slowly (tumors, chronic infections, in particular in immunocompromised patients)!

Normal CT, no neurology – still can herniate

Now this is the downer: not all patients that are going to herniate do have evidence of brain shift in their CT. The Rennick study had 5 of their 14 herniations in children with normal CT. The reasons could be

  • insufficient sensitivity of CT for brain shift (say in comparison to MRI)
  • other pathological processes that lead to herniation without mass effect (see above)

Be prepared for herniation in all cases

Since we cannot rule out herniation even by CT we have to ensure close neurological monitoring in bacterial meningitis after  or even without LP. It is the one reason why meningitis patients do die even nowadays. If herniation does occur – be quick to react: mannitol, tube, CT (is it hydrocephalus, herniation or something else?), OR.

What are CT signs of impending herniation?

  • Evidence of unequal pressure across the falx cerebri (midline shift, one-sided ventricular dilatation, one-sided effaced sulci)
  • Evidence of unequal pressures between supratentorial and infratentorial compartments (loss of suprachiasmatic, pentagon cisterns, cisterna ambiens)
  • Evidence of transforaminal herniation (low standing tonsils, loss of perimedullary space)
  • Evidence of non-communicating hydrocephalus, aqueduct blockade
  • Generalized cerebral edema (effaced sulci anywhere, loss of all cisterns)

What to do if signs of mass effect?

  • Cultivate everything else (blood, sputum, …)
  • In abscess patients try to find the focus or try to get at the content of the abscess surgically, CSF is of little value in this case anyway.
  • Use calculated antibiotics
  • If you really suspect strange bugs (immunocompromised or patient has been to strange places) – get ventricular CSF surgically



So to wrap this all up:

You can forgo CT in neurologically intact acute patients, but they can still herniate



CT versus LP – dawn of the thunderclap headache

As for dogmas to be lysed, no falsity is more resilient than the one that every thunderclap headache (TCH) needs to be tapped to rule out subarachnoid hemorrhage.

Walking through the numbers, our 90,000 pt emergency room probably treats 2,000 headache patients yearly, with 5-10% being thunderclaps, i.e. about 100-200 patients – let’s assume 200. We know from old (Landtbloom 2002) and new (Sayers 2015) series that about 7-15%% of these will be real subarachnoids or about 30 bleeds a year in the worst case. If we tap all of them, we will necessarily induce 10-20% = 40 artificial bleeds, which – according to the best literature we have – is at least hard if not impossible to differentiate from real bleeds:

  •  the red blood cell (RBC) count need not decrease in artificial bleeds
  •  but it can in SAH
  •  Xanthochromia, Ferritin, erythro- and siderophages need time to develop
  • there is no proper threshold for RBCs.

If you look at Sayers 2015 series of LPs in TCH, about 15% were uninterpretable and 13% were inconclusive, while 4% were clearly positive. This amounts to 32% LPs that lead to further workup or 64 patients a year for us. Of these 64 patients between 2% (if you use CTA) or up to 5% (if using DSA) harbour incidental harmless aneurysms, so about 2 patients will have one, which then is coiled or operated on.

On the other hand, at most 1 patient of our 40 real subarachnoids yearly will be CT negative (regardless of the time – see Sayers or Dubosh 2016, but at least in the first 6-24 hours). Unfortunately our LP workup for SAH in Germany (visual inspection for xanthochromia) only has about a third sensitivity. We don’t really know how many SAH do have enough red blood cells in their lumbal CSF and what a proper threshold might be. So it turns out, that we might actually miss the one CT negative patient after all.

In all this discussion I did not even consider other adverse events of lumbar puncture.

Here, then, is my take on the issue:

  •  TCH is way more complex than just ruling out SAHs. Think about the differential (see below) and do a proper history, physical exam and ensure follow-up, if possible with MRI (think of RCVS, SVT and other stuff). A rate of two thirds etiologically unresolved TCHs („primary“) is too much.
  • Always keep in mind that Hunt and Hess I-II may actually have a better prognosis than H&H III-V.
  • Discuss the probabilities with your department and your patient and be reasonable: LP is not the goldstandard test for subarachnoid!
  • If you do an LP to rule out SAH, leave at least 12 hours time (from onset) for xanthrochromia to develop and yes: all this time the patient is in danger, but the probability that he has an SAH is extremely low.


Bedside ultrasound for lumbar puncture

According to this article, bedside ultrasound could be a good idea for difficult lumbar punctures. So today we took the linear transducer to image the anatomy of the spinal canal including transverse and spinous processes. It worked surprisingly well in one of our lean colleagues. Of course, you have to learn the technique in easy patients before you tackle the difficult one, so in our Stroke Unit we will hopefully use the method more often.