Fine Tuning of Traumatic Brain Injury Management in Neurointensive Care-Indicative Observations and Future Perspectives

Abstract

Neurointensive care (NIC) has contributed to great improvements in clinical outcomes for patients with severe traumatic brain injury (TBI) by preventing, detecting, and treating secondary insults and thereby reducing secondary brain injury. Traditional NIC management has mainly focused on generally applicable escalated treatment protocols to avoid high intracranial pressure (ICP) and to keep the cerebral perfusion pressure (CPP) at sufficiently high levels. However, TBI is a very heterogeneous disease regarding the type of injury, age, comorbidity, secondary injury mechanisms, etc. In recent years, the introduction of multimodality monitoring, including, e.g., pressure autoregulation, brain tissue oxygenation, and cerebral energy metabolism, in addition to ICP and CPP, has increased the understanding of the complex pathophysiology and the physiological effects of treatments in this condition. In this article, we will present some potential future approaches for more individualized patient management and fine-tuning of NIC, taking advantage of multimodal monitoring to further improve outcome after severe TBI.

Keywords: multimodality monitoring; neurointensive care; secondary brain injury; secondary insults; traumatic brain injury.

Figure 1

Five critical steps in the pathway to cerebral energy metabolism in relation to multimodality monitoring. By monitoring all the steps in this pathway to achieve sufficient cerebral energy metabolism, energy failure may be detected in time and the correct diagnosis can be made. Treatments should aim at counteracting the specific mechanism that causes cerebral energy metabolic disturbances.

Figure 2

The Uppsala standardized traumatic brain injury (TBI) management protocol as an example of a local escalated intracranial pressure (ICP)-oriented management protocol with a focus on avoiding secondary insults. The figure demonstrates an example of a local ICP-oriented management protocol (2). The therapeutic intensity is gradually increased by starting with ICP-lowering treatments that carry a lower risk of complications and escalating to treatments with greater risks if the ICP target cannot otherwise be controlled. Decompressive craniectomy may be performed both on a primary indication (first surgical procedure, i.e., the fourth step is used as the first step) in the case of severe brain edema in the early course, but chiefly on a secondary indication (when all other treatments are exhausted).

Figure 3

Optimal cerebral perfusion pressure (CPPopt)—differences in curve shape. The CPPopt curves may vary over time and between patients, as illustrated in these three different curves. There are questions on how the curve shape and the absolute pressure reactivity index (PRx) are relevant in CPPopt management. Patients with a steeper CPPopt curve may, in theory, be more vulnerable to changes in CPP.

Figure 4

Illustrative patient case with multimodal monitoring. The figure demonstrates the temporal evolution of cerebral physiology over ~2 days. Although intracranial pressure (ICP), cerebral perfusion pressure (CPP), pressure reactivity index (PRx), and oxygen saturation (SpO₂) were within adequate intervals, the patient developed brain tissue hypoxia and cerebral energy failure (high lactate/pyruvate ratio). The pathophysiology may include microvascular thrombosis and/or increased diffusion limitations from cerebral edema.