Although parameters such as intracranial pressure (ICP) or pupillary reactivity are common targets of neurological intensive care, the ultimate goal is the recovery of brain function. In practice, we spend time and energy in measuring ICP because intracranial hypertension is deleterious. We do that to protect the injured brain, with the goal of recovering full awareness and brain function.
An article in this issue of Anesthesia & Analgesia1 explores a potential link between a mechanistic index, based on signal analysis of ICP and arterial blood pressure (BP), and recovery of consciousness. As such, it is fascinating and worth careful attention.
The attempt to extract as much information as possible from the ICP waveform has a long history. More than 30 yr ago, the main contributors to the ICP waveform were identified in an elegant experimental model in dogs.2 Later, recording from the cisterna magna in cats, the frequency spectrum of ICP pulse and the amplitude transfer function between arterial and cerebrospinal fluid pressures were measured during an induced ICP increase.3 Twenty years ago, those concepts were applied in humans.4 The main idea was that the ICP waveform results from the summation of a large number of sinusoidal waves, each with a specific amplitude and frequency. Using a computer for applying a fast Fourier transformation online, those waves could be traced over time, and changes in the ICP waveform were interpreted as changes in the physical properties of the brain. In this way, the computer helped clinicians identify when the brain became “stiffer,” with a continual (1 determination every 2 min) assessment of intracranial elastance. With the help of bioengineers, ICP waveform analysis became more ambitious and more complex.5 Information was sought on other fundamental functions, such as pressure autoregulation.6 A reevaluation of the topic was published,7 which mentions several promising technologies that unfortunately have not yet demonstrated full clinical value.
The article by Roustan et al. provides fresh enthusiasm in this long line of investigation. In 29 traumatic brain injury (TBI) patients, the authors collected ICP and BP data for 9393 recordings, and end points were studied in 28 of them. The data were processed with specific computer software to derive new information; for each patient, the 6-h results were averaged and correlated with long-term outcome. The authors’ conclusions are extremely positive: some of the derived parameters were able to detect intracranial worsening before ICP increase, and the authors found a correlation between these parameters and the recovery of consciousness. All the parameters investigated were derived from monitoring already in place (ICP and BP), with no additional burden on the patients. Accordingly, the authors demonstrated the potential for signal processing to provide clinically relevant additional information from the signals used for routine monitoring.
Should we, then, apply this approach to the next patients? Generalization is premature until the following 4 points have been clarified.
- Signal analysis can be very interesting, but it is a tricky business because of many technical prerequisites. Any signal analysis is only as good as the signal itself, and it is doubtful that a perfectly clean signal can be guaranteed in the intensive care unit. For instance, the sources (probes, location of the probes, and arterial lines) used both for ICP and BP can be fine for clinical use but may be inadequate for sophisticated analysis, even if the authors believe that using a ratio protects against this bias. Human filtering, moreover, is essential for excluding artifacts and fault data. In addition, as acknowledged by the authors, the model used is extremely simplified and does not take into account many potentially relevant variables, such as cerebrospinal fluid outflow-inflow, venous component, etc.
- ICP and BP in the intensive care unit are not simply analyzed, but also treated. Active treatment for reducing pathological ICP or increasing low BP, for instance, should modify their values and waveforms alike. The relationship between the signal, once modified by therapy, and the outcome should take into account the therapeutic efforts.
- The outcome measure used is not acceptable. Recovery of consciousness is not only extremely important but also very vague. A patient can regain consciousness and enjoy a good recovery or regain consciousness and experience extreme disability. In fact, even the most simplified outcome measure for TBI, the Glasgow Outcome Scale, considers levels of disability: 2 in the classical scale, 5 in the extended version.8
- The most intriguing finding of the article, the link between pressure-related indexes and outcome, is not explained. The pathophysiology of consciousness is complex, and the path leading a comatose patient to regain consciousness shortly after trauma is even more complex. When this problem was investigated using anatomo-pathological correlates or functional imaging studies, the degree of axonal disruption, deep brain structural lesions (thalamic lesions, for instance), and other parameters were identified.9–14 Structural damage demonstrates the most convincing association with persistent loss of consciousness; in general, outcome after TBI has a very strong association with age, initial severity, and computed tomography findings, as proven in the large database of the IMPACT study.15 Therefore, the link between the dynamic indexes proposed in this article and the pathophysiology of “consciousness” needs more work. Because the mechanism is not identified, other explanations should be carefully investigated.
The article by Roustan et al. attempts a deeper analysis of ICP and BP and as such is very welcome. Now that they have our appreciation, the authors have the burden of further proving that this analysis is solid and explaining why it may predict outcome.
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