Monro-Kellie 2.0: The dynamic vascular and venous pathophysiological components of intracranial pressure

Abstract

For 200 years, the 'closed box' analogy of intracranial pressure (ICP) has underpinned neurosurgery and neuro-critical care. Cushing conceptualised the Monro-Kellie doctrine stating that a change in blood, brain or CSF volume resulted in reciprocal changes in one or both of the other two. When not possible, attempts to increase a volume further increase ICP. On this doctrine's "truth or relative untruth" depends many of the critical procedures in the surgery of the central nervous system. However, each volume component may not deserve the equal weighting this static concept implies. The slow production of CSF (0.35 ml/min) is dwarfed by the dynamic blood in and outflow (∼700 ml/min). Neuro-critical care practice focusing on arterial and ICP regulation has been questioned. Failure of venous efferent flow to precisely match arterial afferent flow will yield immediate and dramatic changes in intracranial blood volume and pressure. Interpreting ICP without interrogating its core drivers may be misleading. Multiple clinical conditions and the cerebral effects of altitude and microgravity relate to imbalances in this dynamic rather than ICP per se. This article reviews the Monro-Kellie doctrine, categorises venous outflow limitation conditions, relates physiological mechanisms to clinical conditions and suggests specific management options.

Keywords: Intracranial pressure; Monro-Kellie; cerebral venous outflow; intracranial hypertension; neurotrauma.

Figure 1.

(a) Alexander Monro secundus (1733–1817). Eminent Scottish physician. (b) Adaptation of current explanation of Monro-Kellie doctrine within advanced trauma life support (ATLS) and most critical care teaching demonstrating that additional mass results in a large volume of CSF then venous blood displacement. (c) Demonstrates that once the period of compliance that this displacement affords runs out, there is an exponential rise in pressure. This description fails to explain the importance of volume flow. From ATLS Course Manual 9th edition.

Figure 2.

(a) Schematic representation of the commonest pattern of cerebral venous drainage. Adapted from Wilson et al. (b) Cross-sectional representation of the sagittal sinus. The dural reflections create a triangular lumen with no muscular wall in marked contrast to the arterial circulation. This makes venous structures more vulnerable to compression.

Figure 3.

View of a coronal section through the head, showing the falx cerebri, the tentorium cerebelli, and the associated venous sinuses. The full legend is within the figure.

Figure 4.

(a) Depressed skull fracture and subsequent (superior sagittal sinus) SSS thrombosis caused by a hammer blow – (i) midsagittal reconstruction on day 2 with increasing headaches demonstrating SSS thrombosis, (ii) – midsagittal reconstruction of CTV day 2 post op demonstrating resolution of SSS thrombosis. (b) Occipital extradural from fracture overlying the right transverse sinus. (i) plain axial CT scan, (ii) CT Venogram. The extradural can be seen compressing and narrowing the dominant right transverse sinus. Note the relatively hypoplastic left transverse sinus. (c) The combined conduit score (CCS) adapted from Farb et al. Each transverse sinus is assessed separately and the area with the greatest stenosis graded (0–4) in relation to the superior sagittal sinus (SSS). 0 = discontinuity/aplastic segment; 1 = hypoplasia/severe stenosis with cross-sectional diameter less than 25% of the SSS; 2 = moderate stenosis (25–50% of SSS cross-sectional area); 3 = mild stenosis (50–75% of SSS cross-sectional area), and 4 = no significant stenosis (75–100% of SSS cross-sectional area). Both left and right scores are summed to give a total CCS.

Figure 5.

CT venograms of a male patient aged 48-year-old male with refractory intracranial hypertension. (a) Transverse sinuses severely effaced with raised intracranial pressure. (b) Following bifrontal decompressive craniectomy the transverse sinus calibre increases dramatically.

Figure 6.

Brain herniation occurring at the time of abdominal closure (see text).

Figure 7.

Diagram demonstrating that relative venous outflow restriction can occur intracranially (with compression/obstruction (e.g. with thrombus or fractures) of isolated or diffuse venous structures) and extracranially (from cervical, thoracic and abdominal pressures).