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

1991 ◽  
Vol 75 (5) ◽  
pp. 685-693 ◽  
Author(s):  
Gerrit J. Bouma ◽  
J. Paul Muizelaar ◽  
Sung C. Choi ◽  
Pauline G. Newlon ◽  
Harold F. Young
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Neurological Status ◽  
Content Type ◽  
Head Injured ◽  
Adult Head ◽  
Injured Patients

✓ 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 < 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 ≤ 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.

Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography

1992 ◽  
Vol 77 (3) ◽  
pp. 360-368 ◽  
Author(s):  
Gerrit J. Bouma ◽  
J. Paul Muizelaar ◽  
Warren A. Stringer ◽  
Sung C. Choi ◽  
Panos Fatouros ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Computerized Tomography ◽  
Regional Ischemia ◽  
Head Injured ◽  
Intracranial Hematomas ◽  
Injured Patients

✓ The role of cerebral ischemia in the pathophysiology of traumatic brain injury is unclear. Cerebral blood flow (CBF) measurements with 133Xe have thus far revealed ischemia in a substantial number of patients only when performed between 4 and 12 hours postinjury. But these studies cannot be performed sooner after injury, they cannot be done in patients with intracranial hematomas still in place, and they cannot detect focal ischemia. Therefore, the authors performed CBF measurements in 35 comatose head-injured patients using stable xenon-enhanced computerized tomography (CT), simultaneously with the initial CT scan (at a mean (± standard error of the mean) interval of 3.1 ± 2.1 hours after injury). Seven patients with diffuse cerebral swelling had significantly lower flows in all brain regions measured as compared to patients without swelling or with focal contusions; in four of the seven, cerebral ischemia (CBF ≤ 18 ml/100 gm · min−1) was present. Acute intracranial hematomas were associated with decreased CBF and regional ischemia in the ipsilateral hemisphere, but did not disproportionately impair brain-stem blood flow. Overall, global or regional ischemia was found in 11 patients (31.4%). There was no correlation between the presence of hypoxia or hypertension before resuscitation and the occurrence of ischemia, neither could ischemia be attributed to low pCO2. Ischemia was significantly associated with early mortality (p < 0.02), whereas normal or high CBF values were not predictive of favorable short-term outcome. These data support the hypothesis that ischemia is an important secondary injury mechanism after traumatic brain injury, and that trauma may share pathophysiological mechanisms with stroke in a large number of cases; this may have important implications for the use of hyperventilation and antihypertensive drugs in the acute management of severely head-injured patients, and may lead to testing of drugs that are effective or have shown promise in the treatment of ischemic stroke.

Ocular pneumoplethysmography in head-injured patients

1983 ◽  
Vol 59 (1) ◽  
pp. 46-50 ◽  
Author(s):  
William Gee ◽  
Michael Rhodes ◽  
Frederick J. Denstman ◽  
Robert M. Jaeger ◽  
David A. Tilly ◽  
...  
Keyword(s):  
Blood Flow ◽  
Life Support ◽  
Diagnostic Procedures ◽  
Neurological Status ◽  
Ocular Blood Flow ◽  
Therapeutic Drug ◽  
Ventilator Support ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients

✓ Severe head injury is frequently associated with multiple trauma. In the comatose patient, endotracheal intubation and ventilator support are often required, if there is associated dyssynchronous spontaneous effort. The latter is managed with therapeutic (drug) paralysis. An elaborate life-support and monitoring system coupled with controlled paralysis limits the mobility of the patient for diagnostic procedures, and a continuing reevaluation of neurological status is difficult. Under these circumstances the ocular pneumoplethysmograph provides a simple rapid noninvasive assessment of ocular blood flow, and this reflects cerebral blood flow and alterations in brain compliance. Alterations in the therapeutic regimen can be based on these observations.

Relation of cerebral blood flow to neurological status and outcome in head-injured patients

1979 ◽  
Vol 51 (3) ◽  
pp. 292-300 ◽  
Author(s):  
Walter D. Obrist ◽  
Thomas A. Gennarelli ◽  
Hiromu Segawa ◽  
Carol A. Dolinskas ◽  
Thomas W. Langfitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vegetative State ◽  
Persistent Vegetative State ◽  
Low Oxygen ◽  
Content Type ◽  
Head Injured ◽  
Luxury Perfusion ◽  
Injured Patients ◽  
Fine Print

✓ Noninvasive studies of regional cerebral blood flow (CBF) were performed on 36 head-injured patients in varying degrees of coma, using the intravenous xenon-133 method. Serial examinations, averaging four per patient, were begun during the acute phase of illness and continued until death or recovery of normal consciousness. Comparison of the initial and final studies revealed that CBF declined to very low levels in all nine patients who died, and remained subnormal in a patient with persistent vegetative state. In contrast, 25 of 26 patients who recovered consciousness showed increases in blood flow. Because of the presence of both reduced and elevated blood flows on the initial study, CBF was not predictive of outcome. Absolute or relative hyperemia, observed in nine acute cases, was associated with either diffuse cerebral swelling (observed on computerized tomography) or recovery from systemic shock. Cerebral metabolic studies in hyperemic patients yielded a very low oxygen uptake and arteriovenous oxygen difference, indicating that the high blood flow was a true “luxury perfusion.” When instances of presumed luxury perfusion were excluded, CBF was positively correlated with level of consciousness, assessed on a four-point coma scale.

Effect of stable xenon inhalation on intracranial pressure during measurement of cerebral blood flow in head injury

1994 ◽  
Vol 81 (6) ◽  
pp. 822-828 ◽  
Author(s):  
Jan Plougmann ◽  
Jens Astrup ◽  
Jens Pedersen ◽  
Carsten Gyldensted
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Stable Xenon ◽  
The Mean ◽  
Injured Patients ◽  
Fine Print

✓ Xenon-enhanced computerized tomography (CT) is well suited for measurements of cerebral blood flow (CBF) in head-injured patients. Previous studies indicated divergent results on whether inhalation of xenon may cause a clinically relevant increase in intracranial pressure (ICP). The authors employed Xe-enhanced CT/CBF measurements to study the effect of 20 minutes of inhalation of 33% xenon in oxygen on ICP, cerebral perfusion pressure (CPP), and arteriovenous oxygen difference (AVDO2) in 13 patients 3 days (mean 1 to 5 days) after severe head injury (Glasgow Coma Scale score ≤ 7). The patients were moderately hyperventilated (mean PaCO2 4.3 kPa or 32.3 mm Hg). Six patients were studied before and during additional hyperventilation. All 13 patients reacted with an increase in ICP and 11 with a decrease in CPP. The mean ICP increment was 6.9 ± 7.7 (range 2 to 17 mm Hg). The mean CPP decrement was −9.7 ± −14.6 (range 17 to 47 mm Hg). The time course of the ICP changes indicated that ICP increased rapidly during the first 5 to 6 minutes, then declined to a plateau (peak-plateau type in four of 13 patients), remained at a plateau (plateau type in six of 13), or continued to increase in three of 13, indicating individual variance in xenon reactivity. Additional hyperventilation had no effect on the xenon-induced increments in ICP but these occurred at lower ICP and higher CPP baseline levels. The AVDO2 values, an index of flow in relation to metabolism, indicated a complex effect of xenon on CBF as well as on metabolism. This study indicates that xenon inhalation for Xe-CT CBF measurements in head-injured patients according to our protocol causes clinically significant increments in ICP and decrements in CPP. It is suggested that the effect of xenon is analogous to anesthesia induction. Individual variations were observed indicating possible individual tolerance, possible influence of type and extent of the cerebral injury, disturbances in cerebrovascular reactivity, and possible influence of medication. These effects of xenon suggest that hyperventilation should be ensured in patients with evidence of reduced compliance or high ICP. On the other hand, inhalation of stable xenon is not believed to pose a risk because no signs of cerebral oligemia or ischemia were indicated in the AVDO2 values.

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

1998 ◽  
Vol 89 (6) ◽  
pp. 983-990 ◽  
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.

Cerebral blood flow, vasoreactivity, and oxygen consumption during barbiturate therapy in severe traumatic brain lesions

1988 ◽  
Vol 68 (3) ◽  
pp. 424-431 ◽  
Author(s):  
Carl-Henrik Nordström ◽  
Kenneth Messeter ◽  
Göran Sundbärg ◽  
Wilhelm Schalén ◽  
Mats Werner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Lesions ◽  
Barbiturate Coma ◽  
Content Type ◽  
Cerebral Metabolic Rate ◽  
Head Injured ◽  
Barbiturate Therapy ◽  
Injured Patients ◽  
Cerebral Vasoreactivity

✓ Mean hemispheric cerebral blood flow (CBF) and intracranial pressure (ICP) were measured in 19 severely head-injured patients treated with barbiturate coma. The CBF was calculated from the clearance of tracer substance monitored by extracranial scintillation detectors after intravenous administration of xenon-133. In 11 of the patients cerebral arteriovenous oxygen differences were measured simultaneously. In all patients the effects of pronounced hyperventilation were recorded prior to initiation of barbiturate treatment. A normal CBF response to hyperventilation (ΔCBF/ΔPaCO2 ≥ 1) was obtained in eight patients. In these patients induction of barbiturate coma was accompanied by physiological decreases in CBF and in the calculated cerebral metabolic rate of oxygen (CMRO2); they also exhibited a rapid and lasting decrease in ICP. A decreased or an abolished CO2 reactivity was recorded (ΔCBF/ΔPaCO2 < 1) in 11 patients. In 10 of these 11 patients the physiological decreases in CBF and CMRO2 were not obtained during barbiturate treatment and the decrease in ICP was transitory. This study demonstrates a correlation between cerebral vasoreactivity, physiological effects of barbiturate therapy, and clinical outcome.

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

2018 ◽  
Vol 129 (1) ◽  
pp. 241-246 ◽  
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.

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

2001 ◽  
Vol 93 (2) ◽  
pp. 351-353 ◽  
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

scholarly journals The Expanding Role of Quantitative Pupillometry in the Evaluation and Management of Traumatic Brain Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Jason H. Boulter ◽  
Margaret M. Shields ◽  
Melissa R. Meister ◽  
Gregory Murtha ◽  
Brian P. Curry ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Injuries ◽  
Ease Of Use ◽  
Brain Injured ◽  
The World ◽  
Injured Patients ◽  
Austere Environments ◽  
Active Investigation

Traumatic brain injury is a rapidly increasing source of morbidity and mortality across the world. As such, the evaluation and management of traumatic brain injuries ranging from mild to severe are under active investigation. Over the last two decades, quantitative pupillometry has been increasingly found to be useful in both the immediate evaluation and ongoing management of traumatic brain injured patients. Given these findings and the portability and ease of use of modern pupillometers, further adoption and deployment of quantitative pupillometers into the preclinical and hospital settings of both resource rich and medically austere environments.

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