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




Monitoring midline shift

While the indication of decompressive craniotomy has become much harder now that everyone has been shown to profit, the prognostication of herniation in probably malignant MCA stroke has always been difficult.

The topic of yesterdays was the ultrasonographic depiction of third ventricle midline shift (mainly used in german centers where ultrasound wizards reside). But there are several steps involved before you can understand what you do there:

  • Depending on the location of the stroke either uncal, posterior transtentorial or anterior-posterior shift can occur – only half of them lead to lateral mass shift.
  • Clinical deterioration not only can come from lateral shift (as determined by the midline shift), but from rostrocaudal shift, compression of the ACA or PCA.
  • Lateral shift can occur at the level of the mesencephalon, the diencephalon or above, thus leading to divergence of CT determination of septal shift and ultrasound determination of third ventricle shift.

Still, if you can spare half of the CTs of an intubated and sedated patient, it should be worth it – so try ultrasound and gain experience.