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  • Dr Hector Thomson


Updated: Nov 3, 2023

Dr Hector Thomson Emergency Registrar

Peer review: Dr Luke Phillips

Editor: Dr David McCreary

THE CASE A 37-year-old man has been ejected from his car after crashing at high speed. He was initially mildly confused but then rapidly dropped his GCS to 8. The ambulance crew on scene have intubated him and whisk him into your emergency department. During your primary survey you noticed his left pupil is dilated and non-reactive.

WHAT IS HAPPENING INSIDE THIS PATIENT'S HEAD? In this post, we will discuss some concepts of intracerebral pressure regulation and outline some brain herniation syndromes.


You'll have seen this a few times at medical school, in primary exams and on the ATLS/EMST courses, but let's refresh ourselves on it. A couple of 18th century Scottish surgeons Alexander Monro and George Kellie noted that the brain is enclosed in non-expandable bone and is nearly incompressible.

 “ it does not appear very conceivable how any portion of the circulating fluid can ever be withdrawn from the cranium, without its place being simultaneously occupied by some equivalent; or how any thing new or exuberant can be intruded, without an equivalent displacement” – Kellie 1924.

The sum of the volumes of the brain (1400ml), cerebrospinal fluid (150ml) and intracerebral blood (150ml) is constant. An increase in one should cause a reciprocal decrease in either one or both of the remaining two. Aside from being primary examination fodder this principle explains why small changes in volume can have marked changes in intracranial pressure.

The Monro-Kellie model for the contents of the intracranial compartment. 'Brain tissue' includes neurons, glia, extracellular fluid and cerebral microvasculature. 'Venous' and 'Arterial blood' represents the intracranial blood volume in macro-vasculature and cerebral venous sinuses. 'CSF' includes ventricular and cisternal CSF. If into this fixed box we have a haemorrhage such as an extradural haematoma, swelling from an infarct, a tumour or an abscess then CSF and venous blood will be pushed out with an initial small increase in pressure. Extra CSF production or blockage of CSF drainage can also raise the intracranial pressure (ICP). Beyond a certain point, the pressure will rapidly increase. Squeezing brain tissue into another compartment like the last bit of toothpaste in the tube. As the pressure rises the ability of the cerebral vascular to regulate cerebral blood flow reaches a critical point, resulting in decreased compliance as cerebral ischemia.

Image: Pressure Volume Curve for ICP(1)

WHAT ARE THE COMMON EXAMINATION FINDINGS OF RAISED ICP? Initial signs of raised ICP are nonspecific including headache, nausea, vomiting, agitation or conversely increased drowsiness then obtundation. Examination findings of brain herniation can include:

  • Dilated and nonreactive pupils

  • Asymmetric pupils

  • Extensor posturing or not response to painful stimuli

  • Progressive decline in neurologic condition (decrease in GCS > 2 points) that are not associated with non-TBI causes

  • Cushing reflex (hypertension, bradycardia, irregular respirations)