The scope and purpose of this work is 2-fold: to synthesize the available evidence and to translate it into recommendations. This document provides recommendations only when there is evidence to support them. As such, they do not constitute a complete protocol for clinical use. Our intention is that these recommendations be used by others to develop treatment protocols, which necessarily need to incorporate consensus and clinical judgment in areas where current evidence is lacking or insufficient. We think it is important to have evidence-based recommendations to clarify what aspects of practice currently can and cannot be supported by evidence, to encourage use of evidence-based treatments that exist, and to encourage creativity in treatment and research in areas where evidence does not exist. The communities of neurosurgery and neuro-intensive care have been early pioneers and supporters of evidence-based medicine and plan to continue in this endeavor. The complete guideline document, which summarizes and evaluates the literature for each topic, and supplemental appendices (A-I) are available online at https://www.braintrauma.org/coma/guidelines.

Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition

Does age play a role in recovery from sports-related concussion? A comparison of high school and collegiate athletes

Although experimental and pathological studies suggest an important role for ischemia in the majority of fatal cases of traumatic brain injury, ischemia has been a rare finding in most clinical studies of cerebral blood flow (CBF) in head-injured patients. The hypothesis of the present study was that cerebral ischemia occurs in the first few hours after injury, but that CBF measurements have not been performed early enough. Early measurements of CBF (by the 133Xe intravenous method) and arteriovenous oxygen difference (AVDO2) were obtained in 186 adult head-injured patients with a Glasgow Coma Scale score of 8 or less, and were correlated with neurological status and outcome. During the first 6 hours after injury, CBF was low (22.5 +/- 5.2 ml/100 gm/min) but increased significantly during the first 24 hours. The AVDO2 followed the opposite course; the decline of AVDO2 was most profound in patients with low motor scores, suggesting relative hyperemia after 24 hours. A significant correlation between motor score and CBF was found in the first 8 hours after injury (Spearman coefficient = 0.69, p less than 0.001), but as early as 12 hours postinjury this correlation was lost. A similar pattern was found for the relationship between CBF and outcome. Cerebral blood flow below the threshold for infarction (CBF less than or equal to 18 ml/100 gm/min) was found in one-third of the studies obtained within 6 hours, the incidence rapidly decreasing thereafter. A low CBF after 24 hours was not generally associated with a high AVDO2, and was probably a reflection of low oxidative metabolism rather than frank ischemia. In 24 patients, a CBF of 18 ml/100 gm/min or less was found at some point after injury; the mortality rate was significantly higher in this subgroup, and survivors did worse. In some cases, ischemia was successfully treated by reducing hyperventilation or inducing arterial hypertension. These results support the above hypothesis, and suggest that early ischemia after traumatic brain injury may be an important factor determining neurological outcome. Moreover, these data indicate that early hyperventilation or lowering of blood pressure to prevent brain edema may be harmful.

Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia.

Assessment of cerebral autoregulation is an important adjunct to measurement of cerebral blood flow for diagnosis, monitoring or prognosis of cerebrovascular disease. The most common approach tests the effects of changes in mean arterial blood pressure on cerebral blood flow, known as pressure autoregulation. A 'gold standard' for this purpose is not available and the literature shows considerable disparity of methods and criteria. This is understandable because cerebral autoregulation is more a concept rather than a physically measurable entity. Static methods utilize steady-state values to test for changes in cerebral blood flow (or velocity) when mean arterial pressure is changed significantly. This is usually achieved with the use of drugs, shifts in blood volume or by observing spontaneous changes. The long time interval between measurements is a particular concern in many of the studies reviewed. Parallel changes in other critical variables, such as pCO2, haematocrit, brain activation and sympathetic tone, are rarely controlled for. Proposed indices of static autoregulation are based on changes in cerebrovascular resistance, on parameters of the linear regression of flow/velocity versus pressure changes, or only on the absolute changes in flow. The limitations of studies which assess patient groups rather than individual cases are highlighted. Newer methods of dynamic assessment are based on transient changes in cerebral blood flow (or velocity) induced by the deflation of thigh cuffs, Valsalva manoeuvres, tilting and induced or spontaneous oscillations in mean arterial blood pressure. Dynamic testing overcomes several limitations of static methods but it is not clear whether the two approaches are interchangeable. Classification of autoregulation performance using dynamic methods has been based on mathematical modelling, coherent averaging, transfer function analysis, crosscorrelation function or impulse response analysis. More research on reproducibility and inter-method comparisons is urgently needed, particularly involving the assessment of pressure autoregulation in individuals rather than patient groups.

https://iopscience.iop.org/article/10.1088/0967-3334/19/3/001/pdf

Assessment of cerebral pressure autoregulation in humans - a review of measurement methods

The extent and timing of posttraumatic cerebral hemodynamic disturbances have significant implications for the monitoring and treatment of patients with head injury. This prospective study of cerebral blood flow (CBF) (measured using 133Xe clearance) and transcranial Doppler (TCD) measurements in 125 patients with severe head trauma has defined three distinct hemodynamic phases during the first 2 weeks after injury. The phases are further characterized by measurements of cerebral arteriovenous oxygen difference (AVDO[2]) and cerebral metabolic rate of oxygen (CMRO[2]). Phase I (hypoperfusion phase) occurs on the day of injury (Day 0) and is defined by a low CBF calculated from cerebral clearance curves integrated to 15 minutes (mean CBF 32.3 +/- 2 ml/100 g/minute), normal middle cerebral artery (MCA) velocity (mean V[MCA] 56.7 +/- 2.9 cm/second), normal hemispheric index ([HI], mean HI 1.67 +/- 0.11), and normal AVDO(2) (mean AVDO[2] 5.4 +/- 0.5 vol%). The CMRO, is approximately 50% of normal (mean CMRO(2) 1.77 +/- 0.18 ml/100 g/minute) during this phase and remains depressed during the second and third phases. In Phase II (hyperemia phase, Days 1-3), CBF increases (46.8 +/- 3 ml/100 g/minute), AVDO(2) falls (3.8 +/- 0.1 vol%), V(MCA) rises (86 +/- 3.7 cm/second), and the HI remains less than 3 (2.41 +/- 0.1). In Phase III (vasospasm phase, Days 4-15), there is a fall in CBF (35.7 +/- 3.8 ml/100 g/minute), a further increase in V(MCA) (96.7 +/- 6.3 cm/second), and a pronounced rise in the HI (2.87 +/- 0.22). This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma. This research is consistent with and builds on the findings of previous investigations and may provide a useful temporal framework for the organization of existing knowledge regarding posttraumatic cerebrovascular and metabolic pathophysiology.

Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm

Twelve patients who were comatose after head injuries were studied with serial determinations of regional cerebral blood flow, jugular PO2 tension, and intraventricular pressure. These determinations began a few hours after the injury, and were followed throughout the clinical course. Diffuse derangement of cerebral vasomotor regulation is confirmed after severe head trauma, which may contribute to deterioration and poor prognosis, and which indicates a need for therapeutic maintenance of rich oxygenation, hyperventilation with moderate hypocapnia, and steady blood pressure. Continuous recording of IVP (eventually sensitized by fluid infusion or CO2 inhalation tests) may give an early indication of the subsequent clinical state and may suggest the need to submit the patients to further investigative and therapeutic procedures.

https://jnnp.bmj.com/content/jnnp/37/12/1378.full.pdf

Regional cerebral blood flow and intraventricular pressure in acute head injuries

The aims of this paper are (1) to report post-operative angiographic results obtained in a series of 40 patients treated by an extra-intracranial arterial bypass (EIAB) procedure, and (2) to describe the patterns of postoperative regional brain perfusion (rBP), as investigated in a limited series of patients, by a new method.

Angiographic Findings and Cross-Sectional Brain Perfusion Studies after Extra-Intracranial Arterial Bypass

Functional images of brain perfusion can be obtained by a steady-state method which exploits the peculiar physical characteristics of the radioactive gas 81mKr.2 This is a very short half-lived isotope (13 sec half-life), which can be continuously produced either in the gaseous or the solution phase from its parent 81Rb (4.6 hours half-life). It emits 190 keV γ rays, an ideal energy for recording with an Anger γ camera. Because of its short half-life, continuous carotid infusion of 81mKr in solution will never eventually result in the equilibrium of this diffusible tracer within the brain; during continuous infusion continuous recording of the activity over the brain will therefore reflect at any time regional arrival of tracer, which is a linear function of regional perfusion. Thus, when used in conjunction with an ordinary Anger γ camera, it provides images of cerebral perfusion in two dimensions.

Regional Cerebral Perfusion Assessed with 81mKr and Emission Computerized Tomography

Regional Cerebral Blood Flow and Intraventricular Pressure in Acute Brain Injuries

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Regional cerebral blood flow and intraventricular pressure in acute head injuries

Angiographic Findings and Cross-Sectional Brain Perfusion Studies after Extra-Intracranial Arterial Bypass

Regional Cerebral Perfusion Assessed with 81mKr and Emission Computerized Tomography

Regional Cerebral Blood Flow and Intraventricular Pressure in Acute Brain Injuries