Does Manipulating Cardiac Output and Blood Pressure Cause Associated Parallel Change in Cerebral Blood Flow in Patients of Traumatic Brain Injury?

✓ Changes in cerebral blood flow (CBF), pial arteriolar diameter, and arterial blood pressure, gases, and pH were examined before and for 3 hours after fluid-percussion brain injury in α-chloralose-anesthetized piglets. The brain injury was induced by a percussion of 2.28 ± 0.06 atm applied for 23.7 ± 0.5 msec to the right parietal cortex. Regional CBF was measured with radiolabeled microspheres, and changes in pial arteriolar diameter were monitored in the left parietal cortex using closed cranial windows. Immediately following brain injury, mean blood pressure transiently (for approximately 10 minutes) either increased or decreased and then exhibited a prolonged decrease in all of the animals. The brains showed changes consistent with traumatic brain injury such as subarachnoid hemorrhage, contusions, or reactive axonal swelling; none showed histological evidence of a global alternative pathogenetic mechanism such as hypoxic ischemic damage. While CBF of uninjured control animals did not change over a 3-hour observation period, after brain injury blood flow decreased 30% ± 1% below the baseline level within 10 minutes and remained there for 2 to 3 hours posttrauma. After adrenergic blockade, CBF did not decrease at any time during the 3-hour period in either the uninjured control or the injured animals. Concomitant with the decreased blood flow after brain injury, pial arteriolar diameter decreased 14% below the preinjury level. However, in piglets treated with adrenoceptor antagonists, uninjured control and brain-injured animals did not show a decrease in pial arteriolar diameter. The present results support the hypothesis that increased sympathetic outflow to the cephalic vasculature following the fluid-percussion brain injury causes cerebral vasoconstriction decreasing pial arteriolar diameter and regional CBF.

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Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response

Journal of Neurosurgery ◽

10.3171/jns.1998.89.6.0983 ◽

1998 ◽

Vol 89 (6) ◽

pp. 983-990 ◽

Cited By ~ 28

Author(s):

Brian J. Zink ◽

Michael A. Sheinberg ◽

Xu Wang ◽

Michelle Mertz ◽

Susan A. Stern ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Blood Flow ◽

Cardiac Output ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Hemorrhagic Shock ◽

Physiological Response ◽

Content Type ◽

Etoh Group ◽

Fine Print

Object. Traumatic brain injury (TBI) is exacerbated by hypotension and hypoventilation. Because previous studies have shown a potentiating effect of ethanol (EtOH) on TBI and hemorrhagic shock (HS), the authors investigated the effects of EtOH on the early physiological response to TBI with and without HS. Methods. Anesthetized swine, weighing approximately 20 kg each, underwent fluid-percussion TBI of 3 atm with or without 30 ml/kg hemorrhage for a period of 30 minutes. The mean arterial blood pressure, intracranial pressure, cerebral perfusion pressure (CPP), cardiac output, cerebral venous oxygen saturation, and metabolic parameters were monitored for 3 hours postinjury. Ventilation and the response to hypercapnia were also measured. Regional cerebral blood flow and renal blood flow were measured using dye-labeled microspheres. Five groups were studied: control, TBI, TBI/EtOH, TBI/HS, and TBI/HS/EtOH. The EtOH (3.5 g) was given intragastrically 100 minutes preinjury. The TBI/HS/EtOH group demonstrated a 3-hour mortality rate of 56% and postinjury apnea requiring ventilation in 44% of animals compared with 0% in all other groups. Minute ventilation and the hypercapnic ventilatory response were significantly reduced in the postinjury period in the TBI/HS/EtOH group. The animals in this group had significantly lower CPP and cardiac output in the first 60 minutes postinjury, as well as lower renal and cerebral blood flow. Postinjury cerebral venous lactate levels were higher, and cerebral venous pH was lower in the TBI/HS/EtOH group. Conclusions. In this model of TBI, acute EtOH intoxication in the presence of HS potentiates the physiological and metabolic alterations that may contribute to secondary brain injury.

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Quantitative cerebral blood flow using xenon-enhanced CT after decompressive craniectomy in traumatic brain injury

Journal of Neurosurgery ◽

10.3171/2017.4.jns163036 ◽

2018 ◽

Vol 129 (1) ◽

pp. 241-246 ◽

Cited By ~ 4

Author(s):

Aditya Vedantam ◽

Claudia S. Robertson ◽

Shankar P. Gopinath

Keyword(s):

Traumatic Brain Injury ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Clinical Outcome ◽

Decompressive Craniectomy ◽

Decompressive Surgery ◽

Hemodynamic Parameters ◽

Enhanced Ct ◽

The Mean

OBJECTIVEFew studies have reported on changes in quantitative cerebral blood flow (CBF) after decompressive craniectomy and the impact of these measures on clinical outcome. The aim of the present study was to evaluate global and regional CBF patterns in relation to cerebral hemodynamic parameters in patients after decompressive craniectomy for traumatic brain injury (TBI).METHODSThe authors studied clinical and imaging data of patients who underwent xenon-enhanced CT (XeCT) CBF studies after decompressive craniectomy for evacuation of a mass lesion and/or to relieve intractable intracranial hypertension. Cerebral hemodynamic parameters prior to decompressive craniectomy and at the time of the XeCT CBF study were recorded. Global and regional CBF after decompressive craniectomy was measured using XeCT. Regional cortical CBF was measured under the craniectomy defect as well as for each cerebral hemisphere. Associations between CBF, cerebral hemodynamics, and early clinical outcome were assessed.RESULTSTwenty-seven patients were included in this study. The majority of patients (88.9%) had an initial Glasgow Coma Scale score ≤ 8. The median time between injury and decompressive surgery was 9 hours. Primary decompressive surgery (within 24 hours) was performed in the majority of patients (n = 18, 66.7%). Six patients had died by the time of discharge. XeCT CBF studies were performed a median of 51 hours after decompressive surgery. The mean global CBF after decompressive craniectomy was 49.9 ± 21.3 ml/100 g/min. The mean cortical CBF under the craniectomy defect was 46.0 ± 21.7 ml/100 g/min. Patients who were dead at discharge had significantly lower postcraniectomy CBF under the craniectomy defect (30.1 ± 22.9 vs 50.6 ± 19.6 ml/100 g/min; p = 0.039). These patients also had lower global CBF (36.7 ± 23.4 vs 53.7 ± 19.7 ml/100 g/min; p = 0.09), as well as lower CBF for the ipsilateral (33.3 ± 27.2 vs 51.8 ± 19.7 ml/100 g/min; p = 0.07) and contralateral (36.7 ± 19.2 vs 55.2 ± 21.9 ml/100 g/min; p = 0.08) hemispheres, but these differences were not statistically significant. The patients who died also had significantly lower cerebral perfusion pressure (52 ± 17.4 vs 75.3 ± 10.9 mm Hg; p = 0.001).CONCLUSIONSIn the presence of global hypoperfusion, regional cerebral hypoperfusion under the craniectomy defect is associated with early mortality in patients with TBI. Further study is needed to determine the value of incorporating CBF studies into clinical decision making for severe traumatic brain injury.

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The Influence of Inhaled Nitric Oxide on Cerebral Blood Flow and Metabolism in a Child with Traumatic Brain Injury

Anesthesia & Analgesia ◽

10.1097/00000539-200108000-00023 ◽

2001 ◽

Vol 93 (2) ◽

pp. 351-353 ◽

Cited By ~ 3

Author(s):

Monica S. Vavilala ◽

Joan S. Roberts ◽

Anne E. Moore ◽

David W. Newell ◽

Arthur M. Lam

Keyword(s):

Nitric Oxide ◽

Traumatic Brain Injury ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Inhaled Nitric Oxide

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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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Cerebral Blood Flow Predicts Recovery in Children with Persistent Post-Concussion Symptoms after Mild Traumatic Brain Injury

Journal of Neurotrauma ◽

10.1089/neu.2020.7566 ◽

2021 ◽

Author(s):

Karen M. Barlow ◽

Kartik Iyer ◽

Tingting Yan ◽

Alex Scurfield ◽

Helen Carlson ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Mild Traumatic Brain Injury

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Transcranial Doppler to Screen on Admission Patients With Mild to Moderate Traumatic Brain Injury

Neurosurgery ◽

10.1227/neu.0b013e31820cd43e ◽

2011 ◽

Vol 68 (6) ◽

pp. 1603-1610 ◽

Cited By ~ 50

Author(s):

Pierre Bouzat ◽

Gilles Francony ◽

Philippe Declety ◽

Céline Genty ◽

Affif Kaddour ◽

...

Keyword(s):

Traumatic Brain Injury ◽

At Risk ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Glasgow Coma Scale ◽

Pulsatility Index ◽

Area Under Curve ◽

Moderate Traumatic Brain Injury ◽

Patients At Risk

Abstract BACKGROUND: Detecting patients at risk for secondary neurological deterioration (SND) after mild to moderate traumatic brain injury is challenging. OBJECTIVE: To assess the diagnostic accuracy of transcranial Doppler (TCD) on admission in screening these patients. METHODS: This prospective, observational cohort study enrolled 98 traumatic brain injury patients with an initial Glasgow Coma Scale score of 9 to 15 whose initial computed tomography (CT) scan showed either absent or mild lesions according to the Trauma Coma Data Bank (TCDB) classification, ie, TCDB I and TCDB II, respectively. TCD measurements of the 2 middle cerebral arteries were obtained on admission under stable conditions in all patients. Neurological outcome was reassessed on day 7. RESULTS: Of the 98 patients, 21 showed SND, ie, a decrease of ≥ 2 points from the initial Glasgow Coma Scale or requiring any treatment for neurological deterioration. Diastolic cerebral blood flow velocities and pulsatility index measurements were different between patients with SND and patients with no SND. Using receiver-operating characteristic analysis, we found the best threshold limits to be 25 cm/s (sensitivity, 92%; specificity, 76%; area under curve, 0.93) for diastolic cerebral blood flow velocity and 1.25 (sensitivity, 90%; specificity, 91%; area under curve, 0.95) for pulsatility index. According to a recursive-partitioning analysis, TCDB classification and TCD measurements were the most discriminative among variables to detect patients at risk for SND. CONCLUSION: In patients with no severe brain lesions on CT after mild to moderate traumatic brain injury, TCD on admission, in complement with brain CT scan, could accurately screen patients at risk for SND.

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