Extracellular Brain Ph with or without Hypoxia is a Marker of Profound Metabolic Derangement and Increased Mortality after Traumatic Brain Injury

Cerebral hypoxia and acidosis can follow traumatic brain injury (TBI) and are associated with increased mortality. This study aimed to evaluate a relationship between reduced pHbt and disturbances of cerebral metabolism. Prospective data from 56 patients with TBI, receiving microdialysis and Neurotrend monitoring, were analyzed. Four tissue states were defined based on pHbt and PbtO2: 1—low PbtO2/pHbt, 2—low pHbt/normal PbtO2, 3—normal pHbt/low PbtO2, and 4—normal pHbt/PbtO2). Microdialysis values were compared between the groups. The relationship between PbtO2 and lactate/pyruvate (LP) ratio was evaluated at different pHbt levels. Proportional contribution of each state was evaluated against mortality. As compared with the state 4, the state 3 was not different, the state 2 exhibited higher levels of lactate, LP, and glucose and the state 1—higher LP and reduced glucose ( P < 0.001). A significant negative correlation between LP and PbtO2 (rho = −0.159, P < 0.001) was stronger at low pHbt (rho = −0.201, P < 0.001) and nonsignificant at normal pHbt ( P = 0.993). The state 2 was a significant discriminator of mortality categories ( P = 0.031). Decreased pHbt is associated with impaired metabolism. Measuring pHbt with PbtO2 is a more robust way of detecting metabolic derangements.

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Final Report from the 2000-2003 Traumatic Brain Injury State Planning Grant for the State of Idaho

PsycEXTRA Dataset ◽

10.1037/e691132011-001 ◽

2003 ◽

Author(s):

Beth Hudnall Stamm ◽

Russell C. Spearman

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

The State ◽

Final Report ◽

State Planning

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Faculty Opinions recommendation of Differential influence of arterial blood glucose on cerebral metabolism following severe traumatic brain injury.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1158503.618678 ◽

2009 ◽

Author(s):

Arun Gupta

Keyword(s):

Traumatic Brain Injury ◽

Blood Glucose ◽

Brain Injury ◽

Severe Traumatic Brain Injury ◽

Cerebral Metabolism ◽

Arterial Blood ◽

Arterial Blood Glucose

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Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

10.2310/vasc.2401 ◽

2018 ◽

Author(s):

Ryan Martin ◽

Lara Zimmermann ◽

Marike Zwienenberg ◽

Kee D Kim ◽

Kiarash Shahlaie

Keyword(s):

Traumatic Brain Injury ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Intracranial Pressure ◽

Cerebral Autoregulation ◽

Cerebral Metabolism ◽

Elevated Intracranial Pressure ◽

Metabolic Demand ◽

Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

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Pathophysiology of traumatic brain injury

Oxford Textbook of Neurological Surgery ◽

10.1093/med/9780198746706.003.0041 ◽

2019 ◽

pp. 483-496

Author(s):

Geoffrey T. Manley ◽

John K. Yue ◽

Hansen Deng ◽

Ethan A. Winkler ◽

John F. Burke ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Injury Severity ◽

Cerebral Metabolism ◽

Classification Systems ◽

Reactivity Index ◽

Management Options ◽

Diagnosis And Prognosis ◽

Flow Disturbances

This chapter provides summative information on the biomechanics, classification, and metabolism of traumatic brain injury (TBI). Impact, impulse, static/quasistatic loading, and related biomechanical sequelae following rotational shear and strain are discussed. Morphological classifications across extradural, acute/chronic subdural, subarachnoid, and intraventricular haemorrhages, as well as cerebral contusions and axonal injuries, are characterized and correlated with injury severity. Management options and implications for penetrating TBI and mild TBI/concussion are described. Cerebral metabolism including pressure/viscosity, CO2 reactivity, and autoregulation are explained in detail to provide for in-depth exploration of a spectrum of secondary injury cascades, encompassing glutamatergic excitotoxicity, autoregulatory loss, and the pressure reactivity index, flow disturbances, elevated intracranial pressure, cortical spreading depression and seizures/epilepsy. Beta-amyloid deposition in response to TBI, and genetic susceptibilities to poor recovery are covered. Current developments to standardize TBI classification systems, establish evidentiary benchmarks for quality of care, and accelerate advances in diagnosis and prognosis are highlighted.

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