Hydrocephalus and the neuro-intensivist: CSF hydrodynamics at the bedside

Abstract

Hydrocephalus (HCP) is far more complicated than a simple disorder of cerebrospinal fluid (CSF) circulation. HCP is a common complication in patients with subarachnoid hemorrhage (SAH) and after craniectomy. Clinical measurement in HCP is mainly related to intracranial pressure (ICP) and cerebral blood flow. The ability to obtain quantitative variables that describe CSF dynamics at the bedside before potential shunting may support clinical intuition with a description of CSF dysfunction and differentiation between normal pressure hydrocephalus and brain atrophy. This review discusses the advanced research on HCP and how CSF is generated, stored and absorbed within the context of a mathematical model developed by Marmarou. Then, we proceed to explain the main quantification analysis of CSF dynamics using infusion techniques for deciding on definitive treatment. We consider that such descriptions of multiple parameters of measurements need to be significantly appreciated by the caring neuro-intensivist, for better understanding of the complex pathophysiology and clinical management and finally, improve of the prognosis of these patients with HCP.

Keywords: Cerebrospinal fluid; Craniectomy; Cranioplasty; Hydrocephalus; Hydrodynamics; Shunt.

Fig. 1

CSF circulation. Overview of the ventricular system. CSF is produced and flows from the choroid plexuses in the lateral ventricles into the third and then fourth ventricle via the foramina of Monro and the cerebral aqueduct, respectively. From the IVth ventricle, CSF empties into the cisterns of the skull base through the foramen of Magendie and foramina of Luschka and subsequently into the lumbar CSF space and the subarachnoid space at the sagittal sinus. Cardiac contraction induces an arterial distension during systole and a subsequent recoiling during diastole. A portion of this energy is transferred to the brain in the form of brain pulsation and to the CSF in the form of CSF pulsation. This dissipation of arterial blood flow energy by the CSF pulsation energy provides for the maintenance of low intracranial pressure (ICP) according to the Windkessel effect on CSF flow

Fig. 2

Example of normal CSF circulation during a constant rate infusion study. Infusion test of a patient with normal CSF circulation. Opening (before starting the infusion) intracranial pressure (ICP) is around 6 mmHg and estimated R = 8 mmHg × min/ml. The blue arrows indicate the beginning and the end of the infusion test. HR refers to heart rate and AMP to the amplitude of ICP (pulse pressure). A parallel increase in AMP with ICP is noticed

Fig. 3

Example of a constant rate infusion test in a post-SAH patient with HCP. HCP with normal baseline ICP. The dark red area depicts infusion period. Although baseline ICP was normal (4.75 mmHg), it rises until 36.5 mmHg until the end of the infusion study (plateau pressure), whereas the R to CSF outflow (Rcsf) is increased (18.59 mmHg × ml⁻¹ × min⁻¹). There are also a lot of spikes in both ICP and AMP (amplitude) tracings reflecting strong vasogenic B waves. Changes in AMP are well correlated with changes in ICP. The RAP index that is the correlation coefficient between the pulse amplitude AMP and the mean value of ICP is close to + 1, signifying poor compensatory reserve. This is a case of post-SAH communicating HCP

Fig. 4

Example of a constant rate infusion test in post-SAH HCP with B (slow) waves. The same patient as in Fig. 3 where a RAP index close to + 1 is associated with an increased power of B (slow) waves during infusion test. A fast Fourier transformation (FFT) was performed to evaluate the energy (power) of B waves within the ICP signal

Fig. 5

Example of a constant rate infusion test in a post-SAH patient with brain atrophy. ICP during the infusion study (gray area) remains low, increasing from 5.24 mmHg to 10.36 mmHg (plateau values). There is no increase in either RAP index or AMP (amplitude), whereas there is a lack of B waves during infusion (absence of significant spikes in ICP and AMP signals). Elasticity and resistance R to CSF outflow are 0.04 ml⁻¹ and 3, 4 mmHg × ml⁻¹ × min⁻¹, respectively. Such low values indicate brain atrophy rather than hydrocephalus

Fig. 6

Example of a constant rate infusion test in a patient with craniectomy and brain atrophy. In this post-craniectomy, post-SAH patient, baseline and plateau pressures during infusion test (gray area) are normal (5.33 and 15.45 mmHg, respectively). Resistance R to CSF outflow is low (7.61 mmHg × ml⁻¹ × min⁻¹) but there are some B waves in the tracings of both ICP and AMP (pulse amplitude). Nevertheless, their energy and duration are lower in relation with cases of disturbed CSF circulation. This patient does not need any shunt. RAP index is close to + 1 during infusion test, signifying poor pressure–volume reserve

Fig. 7

Example of a constant rate infusion test in a post-SAH and post-cranioplasty patient. The same patient as in Fig. 6 upon cranioplasty 6 months later during an infusion study. The patient exhibits a high plateau ICP during infusion (35 mmHg), a high RAP index close to + 1 with elevated elasticity (0.25 ml⁻¹), indicating poor compensatory reserve and increased resistance R to CSF outflow (15 mmHg × ml⁻¹ × min⁻¹). This case illustrates disturbed CSF circulation and the need for a limited period without a bone flap, something that only an infusion study might confirm