This review on multimodality monitoring for severe traumatic brain injury management aims to act as a comprehensive reference document for the field of neurocritical care. Particularly, the integration of intracranial pressure, brain tissue oxygenation, and cerebral microdialysis into clinical decision making is contextualized, ensuring clarification of subtleties that have crucial implications in terms of safety and maximizing the benefit of neuromonitoring. The future directions and capabilities of multimodality monitoring are explored. Relevance to point-of-care is highlighted, with actionable suggestions and potential risks presented.
Key points
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Multimodality monitoring confers advantages for informing treatment decisions over relying on a single parameter alone.
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Technological and infostructural advancements are increasing the practicality of multimodality monitoring for real-time clinical guidance.
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Multimodality monitoring informed research into deranged physiology may usher in less intense yet more effective, individualized therapy.
| BTF | Brain Trauma Foundation |
| CA | cerebral autoregulation |
| CAD | cranial access device |
| CBF | cerebral blood flow |
| CMD | cerebral microdialysis |
| CPP | cerebral perfusion pressure |
| CPP opt | optimal CPP |
| ETC | electron transport chain |
| ICP | intracranial pressure |
| LPR | lactate-to-pyruvate ratio |
| MAP | mean arterial pressure |
| MD | mitochondrial dysfunction |
| MMM | multimodality monitoring |
| PbtO 2 | pressure of brain tissue oxygen |
| PRx | pressure reactivity index |
| sTBI | severe TBI |
| TBI | traumatic brain injury |
Introduction
Severe Traumatic Brain Injury
Traumatic brain injury (TBI) is incurred when sufficiently critical forces originating externally from the brain are transferred to and through the brain. Severe TBI (sTBI) is essentially defined by a score of 8 or less on the Glasgow Coma Scale, a staple metric for impaired consciousness. Intensive care for sTBI aims to maintain brain physiology within acceptable bounds and prevent secondary injury, which encompasses systemic and intracranial processes following initial injury that cause neuronal damage through means such as inflammation and oxidative stress. A selection of current best practices for sTBI management may be seen in Box 1 .
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Maintaining normothermia
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Managing seizures
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Employing mechanical ventilation
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Regulating cerebral perfusion pressure
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Regulating intravascular volume
Multimodality Monitoring
Multimodality monitoring (MMM) may be employed for guidance from multiple vital signals and biomarkers to inform clinical decisions in accordance with management goals, often met by a multidisciplinary team of intensivists, anesthetists, and surgeons. Many modalities and parameters have been trialed in sTBI research, but the most recent edition of the Brain Trauma Foundation’s (BTF) Guidelines for the Management of Severe Traumatic Brain Injury only recommends targets for 4 monitored parameters, as seen in Table 1 . A potential MMM setup for monitoring intracranial pressure, brain oxygenation, and cerebral microdialysis is displayed in Fig. 1 A–D. The present review aims to elucidate the current state of MMM for sTBI primarily in relation to these key modalities.
| Parameter | Target Recommendation |
|---|---|
| Systolic blood pressure | ≥100 mm Hg a , d or ≥110 mm Hg b , d |
| Intracranial pressure | ≤22 mm Hg c |
| Cerebral perfusion pressure | 60–70 mm Hg c , e |
| Jugular venous oxygen saturation | ≥50% d |
a If patient age is 50 to 69 years
b If patient age is 15 to 49 years or over 70 years
c Level IIB recommendation (based on low-quality body of evidence)
d Level III recommendation (based on low-quality body of evidence)
e Level III recommendation for avoiding aggressive attempts to maintain CPP above 70 mm Hg
Methods
Materials
A cranial access device (CAD) allowing insertion of multiple probes is beneficial for intraparenchymal monitoring. For this purpose, we devised a triple-lumen Cambridge CAD which is capable of being inserted in the neurocritical care unit outside of the operating theater, does not interfere with brain imaging, and has divergent probe trajectories to prevent probe interference and artifact. Evidence shows that the safety of such multi-lumen CADs is comparable to well-established single lumen bolts. Box 2 highlights certain checks for the safety and quality of CAD and probe use for MMM.
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Confirm CAD/probes’ safe placement in desired location of the brain with a computed tomographic scan.
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Ensure zero-point reference of the external pressure transducer for intracranial pressure (ICP) is properly accounted for (level with highest external point of the head is suggested; associated underestimation can be simply corrected for).
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Verify detectable pulsatile waveform of ICP.
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Test PbtO2 probe’s responsiveness with a fraction of inspired oxygen (Fi o 2 ) challenge (eg, Fi o 2 at 100% for 5 min). ,
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Regularly test cerebral microdialysis (CMD) probe by running known concentrations, including after each reagent change.
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Denote inaccuracy of first-hour CMD measurements due to insertion trauma and pump flush.
Data Handling
In order to aid in the interpretation of multimodality signals over time, software ( Box 3 ) can help with signal integration, processing, and index calculation, some even offering streamlined support for incorporating pre-trained machine learning models at the patient’s bedside in real-time. , The large amount of data required for optimal MMM-guided management requires innovative solutions in terms of integration, processing, and storage. These requirements are often overlooked, despite their time-intensive nature and regularly costing up to 20% of clinical research study budgets. However, advances may soon afford automation of consuming data-processing steps like annotating and rejecting artifacts in MMM signals, and developments in multidimensional data formatting such as HDF5 are already enhancing large-scale data mobility for collaborative projects.
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BedMasterEx (Excel Medical Electronics, Inc; Jupiter, FL, USA)
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CNS Monitor (Moberg Solutions, Inc; Ambler, PA, USA)
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ICM+ (Cambridge Enterprise, Ltd; UK)
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Sickbay (Medical informatics Corp.; Houston, TX, USA)
Key modalities
Intracranial Pressure and Cerebral Perfusion Pressure
An increased intracranial pressure (ICP) may result from mass lesions, intracranial edema, or an increase in cerebral blood volume. , In the case of high ICP with deficient compliance of the intracranial compartment, fatal brain herniation and brainstem compression may occur. Cerebral perfusion pressure (CPP) is equal to ICP subtracted from mean arterial pressure (MAP). Deficient CPP will bring about ischemia, entailing an inadequate perfusion of blood and its nutrients. Ultimately, management is aimed at mitigating detrimental pressure on brain tissue and avoiding ischemia. Table 2 outlines treatments, alongside their goals, for lowering ICP and thus increasing CPP.
| Treatment | Goal |
|---|---|
| Sedation a | Reduce the metabolic load |
| Hyperventilation | Cause cerebral vasoconstriction by expelling CO 2 , a vasodilator |
| Hyperosmotic solutions b | Draw water out of brain tissue |
| Hypothermia c | Counteract inflammation |
| Craniectomy | Allow brain expansion |
| External ventricular drain | Displace cerebrospinal fluid |
a The Seattle International severe Traumatic Brain Injury Consensus Conference (SIBICC) consensus advises against high doses of propofol to induce burst suppression when only ICP is monitored.
b SIBICC consensus stipulates avoidance of specific continuous and scheduled hyperosmotic infusions when only ICP is monitored.
c SIBICC consensus does not recommend routine hypothermia below 35 ˚C when only ICP is monitored.
Higher ICP has been heavily associated with mortality in patients with sTBI. Upholding clinical relevance, it is recognized that complications or lack of benefit , associated with monitoring ICP (and adjunctly, monitoring CPP) may result from issues of study validity. , , Indeed, evidence , demonstrates advantages for a refined selection of patients who might benefit from therapy informed by ICP monitoring. , Importantly, rather than ICP monitoring negatively impacting outcome, associations with worse outcome could be due to increased use of adverse treatments for intracranial hypertension. In accord is the recent Seattle International Severe Traumatic Brain Injury Consensus Conference’s delphi-based consensus on specific treatments that are not recommended to be employed for patients with sTBI when only ICP is guiding their use; however, MMM systems may better direct these therapies (see footnotes in Table 2 ). Indiscriminate and adverse treatment lacking nuanced and holistic guidance from MMM may explain why the BTF’s most recent threshold recommendations for ICP and CPP could only be made based on a low-quality body of evidence (see Table 1 ).
Optimizing cerebral perfusion pressure
A concise, universal threshold for CPP has been a long-abandoned gray area, with initial enthusiasm around maintaining a CPP above 70 mm Hg curbed by the complex requirements of each patient throughout their care. , Generally, higher CPP values have been shown to reduce ischemia and unfavorable outcomes, but this is offset by the risk of hyperemia and intracranial hypertension for CPP values above 70 mm Hg. Solving issues of harmfully intense treatment accompanying standardized CPP thresholds, neurocritical care (NCC) is converging on a patient-personalized approach to determining the optimal CPP (CPP opt ). Much of this personalization focuses on cerebral autoregulation (CA), for which patients can have different levels of regardless of similar ICP or CPP values.
CA dictates the ability of the brain to adjust to CPP changes, maintain stable cerebral blood flow (CBF), and avoid ischemia. Perhaps the most vetted measure of CA monitored in NCC is the pressure reactivity index (PRx), with lower values indicating less disturbed CA. It follows that the CPP opt can be found for a patient at their minimum PRx value for a range of CPP values, as seen in Fig. 2 .
For over 20 years, the field has been aware of a positive association between the proximity of patients’ mean CPP to their CPP opt and more favorable outcomes. An asymmetrical association of outcome and deviation from CPP opt has become more apparent with investigation of acceptable bounds around CPP opt ; the percent of time spent below the lower CPP limit is associated with unfavorable outcome and mortality. Regardless of direction, CPP deviations from CPP opt are more robustly correlated with outcome than deviations from traditional, fixed CPP thresholds of 60 mm Hg or 70 mm Hg.
In terms of clinical applicability, the recent COGiTATE study shows that targeting CPP opt is feasible and safe. Nonetheless, typical PRx values have not decreased over the past few decades despite much technological advancement. Thus, rather than solely optimizing conditions like CPP for patients with disturbed CA, although important, research leveraging MMM will likely be needed to remediate CA itself. ,
Brain Tissue Oxygenation
Measuring the partial pressure of brain tissue oxygen (PbtO 2 ) became entrenched in NCC for sTBI ever since its initial, and still employed, use in monitoring the development of ischemia during hyperventilation therapy for intracranial hypertension. Monitoring PbtO 2 may also inform the minimum therapeutic increase in MAP that mitigates hypoxia while avoiding complications, seeing as PbtO 2 and MAP are correlated (particularly under a MAP of 80 mm Hg). , The usual PbtO 2 target is above 20 mm Hg, , despite the most recent BTF guidelines not recommending a threshold for measures of brain oxygenation other than for jugular venous oxygen saturation based on low-quality evidence (see Table 1 ). Notwithstanding, the clinical significance of hypoxia is well established; low PbtO 2 in combination with other deranged brain physiology parameters has been associated with poor outcome, but detrimental hypoxia may still occur in the absence of concerning ICP, CPP, or PRx values. , Common treatments for hypoxia are outlined in Box 4 .
Related posts:
Fundamentals of Acute Care for Patients with Traumatic Spinal Cord Injury
Special Pediatric Considerations in the Management of Severe Traumatic Brain Injury and Spinal Cord Injury
Challenges in Pulmonary Management after Traumatic Brain and Spinal Cord Injury
Fever in the Neurocritically Ill Patient
Thrombosis and Coagulopathy
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