A Point-of-Care Noninvasive Technique for Surrogate ICP Waveforms Application in Neurocritical Care

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.

Intracranial pressure (ICP) monitoring is a staple of neurocritical care. The most commonly used current methods of monitoring in the acute setting include fluid-based systems, implantable transducers and Doppler ultrasonography. It is well established that management of elevated ICP is critical for clinical outcomes. However, numerous studies show that current methods of ICP monitoring cannot reliably define the limit of the brain’s intrinsic compensatory capacity to manage increases in pressure, which would allow for proactive ICP management. Current work in the field hopes to address this gap by harnessing live-streaming ICP pressure-wave data and a multimodal integration with other physiologic measures. Additionally, there is continued development of non-invasive ICP monitoring methods for use in specific clinical scenarios.

The configuration of the intracranial pressure (ICP) pulse wave represents a complex sum of various components. Amplitude variations of an isolated component might reflect changes in a specific intracranial structure. Fifteen awake patients suffering from hydrocephalus, benign intracranial hypertension, or head injury underwent ICP monitoring through a ventricular catheter and were subjected to three standardized maneuvers to alter the intracranial dynamics: head elevation, voluntary hyperventilation, and cerebrospinal fluid (CSF) withdrawal. A 12 degrees head elevation and fractionated CSF withdrawal caused a mild ICP drop and a proportionate amplitude reduction of all the wave components. Voluntary hyperventilation caused a comparable fall in ICP, and a disproportionate reduction in the amplitude of the wave components, especially the P2 component. It is postulated that the decrease in amplitude of the P2 component reflects the reduction of the cerebral bulk caused by hyperventilation. Head elevation and CSF withdrawal caused a decrease of global ICP but no specific changes in any intracranial structure, and consequently the configuration of the pulse wave remained unchanged. The establishment of relationships between anatomical substrate and particular wave components is promising since potentially it could be useful for monitoring conditions such as vasoparalysis, impaired cerebrovascular reactivity, and cerebral edema.