Large Brain Infarction and Intracranial Pressure

At today’s stroke conference, we briefly discussed the question of whether large brain infarcts with mass effect are associated with elevations in intracranial pressure (ICP). Several residents opined that midline shift closely correlates with ICP.

It’s been a while since I looked into the primary literature on this, so I dug up a few articles. This study, from Dr. Jeffrey Frank (neurointensivist then at the Cleveland Clinic, now at University of Chicago) found that in 19 patients with clinical deterioration after large infarction, only 5 had elevated ICP. The mean ICP was 13.4 mm Hg. Similarly, the cerebral perfusion pressure (CPP) was diminished in only 2 subjects, with the mean CPP being 75 mm Hg.

Dr. Frank went on to discuss the question of whether ICP-lowering therapies are likely to be of benefit. After reviewing the theoretical issues and the then-extant literature, his conclusion was that there are not. In the following figure he shows what can happen after various ICP-lowering interventions:

Figure showing effects of ICP-lowering therapy on brain edema


In another study, Stefan Schwab, et al. did find that patients’ ICP rose throughout the monitoring period, but this rise was always preceded by clinical signs (depressed level of arousal, pupillary asymmetry). With regard to the correlation of CT evidence of shift and ICP:

Pressure gradients as indirect evidence of raised ICP, such as midline shift and compressed perimesencephalic cisterns, were seen on CT, and could be approved with ICP monitoring. However, even severe midline shift on CT did not necessarily reflect the actual ICP values. In the group of patients with mild midline shift, six patients showed ICP values above 30 mm Hg at time of CT. On the other hand nine patients with severe midline shift demonstrated ICP values below 30 mm Hg.

Both of these studies are rather old, and the neuro-ICU literature has exploded since then. However, I found these papers referenced in Wijdicks’ The Practice of Emergency and Critical Care Neurology, which was published in 2010. I think this is generally a good little text, especially for our future stroke / neuro-ICU folks. However, despite having referenced the literature above in his discussion of ICP, what does Dr. Wijdicks recommend for malignant brain infarcts? The following sequence of interventions (Table 27.2; p. 396 in my hardcover edition):

  1. Mannitol
  2. 23% saline
  3. Hemicraniectomy
  4. Therapeutic hypothermia

My own take is that there is now excellent evidence in favor of hemicraniectomy, at least when performed within the first 48 hours (we’ll be discussing this further at journal club later this month–any food requests?) and a lot of uncertainty about the value of these other measures. If we’re not going to offer hemicraniectomy, and the family isn’t ready to transition to palliative care, then we and the patient are in a very tough situation.

Khalid, I’m counting on you to sort all of this out during your upcoming fellowship 🙂

About Justin A. Sattin

I'm a vascular neurologist and residency program director. I created this blog in order to share some thoughts with my resident and other colleagues, and to foster my own learning as well.
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2 Responses to Large Brain Infarction and Intracranial Pressure

  1. alsherbini says:

    Thank you Dr. Sattin for this review , it’s really helpful .
    as i know i just came from the neurocritical care conference, and actually one important discussion during the conference was about how they define ICP ? because most studies now and the litriture define ICP as elevation of ICP > 20 mmHG for more than 5 min , some use more than 2 min. but actually they presented severeal cases and many articles in the conference were the ICP absolute value was less than 20 but the patients herniated and had signs of increase ICP. so they went an discuss then the shape of the waveform of the ICP maybe more important , on the other hand they concluded that the value of ICP by itself is meaningless and it has to be within proper clinical encounter and also patient specific . as we all know that we cannot draw a curve that fit every disease and every patient because the physiology and pathology is different. having said that the value of CPP which most studies published considered the normal or the target to be between ” 60-70″ should follow the same role as the ICP which is used to calculate the CPP.
    so to conclude, i think in the patient with large malignant MCA with midline shift and edema in the presence of clinical signs of impaired consciousness or pending herniation indicates elevated ICP regardless of the absolute number. and regarding managment i totally agree that if we are not proceeding with the proven therapy of craniectomy i dont think there is any place for other therapies.

    • Justin A. Sattin says:

      What we have here is a semantic issue. We as a community are having a hard time defining the term “intracranial hypertension”, at least in certain conditions such as cerebral infarction. If we say that midline shift, impaired consciousness, etc. imply the presence of intracranial hypertension by definition, then I think it calls into question why we even use that term. We could just stick with “massive cerebral infarction” or “malignant MCA syndrome” or whatever.

      A reason to favor “intracranial hypertension” is that it implies a treatment approach (pressure-lowering therapies) and a way to monitor treatment response (pressure). But maybe in this context we should be using “edema reducing” therapies and monitoring response clinically, and when the clinical exam is insufficiently informative, radiographically and maybe with the emerging modalities (PjvO2, microdialysis, QEEG, etc.)

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