Changes in cerebral blood flow during PaCO2 variations in patients with severe closed head injury: comparison between the Fick and transcranial Doppler methods

1998 ◽  
Vol 88 (6) ◽  
pp. 996-1001 ◽  
Author(s):  
Aram Ter Minassian ◽  
Eliane Melon ◽  
Caroline Leguerinel ◽  
Carlo Alberto Lodi ◽  
Françis Bonnet ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Transcranial Doppler ◽  
Closed Head Injury ◽  
High Group ◽  
Content Type ◽  
Closed Head ◽  
Fine Print ◽  
Group 1

Object. The aim of this study was to reassess whether middle cerebral artery blood flow velocity (MCAv) variations measured by transcranial Doppler ultrasonography during acute PaCO2 manipulation adequately reflect cerebral blood flow (CBF) changes in patients with severe closed head injury. Methods. The study was performed by comparing MCAv variations to changes in CBF as assessed by measurements of the difference in the arteriovenous content in oxygen (AVDO2). The authors initiated 35 CO2 challenges in 12 patients with severe closed head injury during the acute stage. By simultaneous recording of systemic and cerebral hemodynamic parameters, 105 AVDO2 measurements were obtained. Patients were stratified into two groups, “high” and “low,” with respect to whether their resting values of MCAv were greater than 100 cm/second during moderate hyperventilation. Four patients displayed an elevated MCAv, which was related to vasospasm in three cases and to hyperemia in one case. The PaCO2 and intracranial pressure levels were not different between the two groups. The slope of the regression line between 1 divided by the change in (Δ)AVDO2 and ΔMCAv was not different from identity in the low group (1/ΔAVDO2 = 1.08 × ΔMCAv − 0.07, r = 0.93, p < 0.001) and significantly differed (p < 0.05) from the slope of the high group (1/ΔAVDO2 = 1.46 × ΔMCAv − 0.4, r = 0.83, p < 0.001). Conclusions. In patients with severe closed head injury, MCAv variations adequately reflect CBF changes as assessed by AVDO2 measurements in the absence of a baseline increase in MCAv. These observations indicate that both moderate variations in PaCO2 and variations in cerebral perfusion pressure do not act noticeably on the diameter of the MCA. The divergence from the expected relationship in the high group seems to be due to the heterogeneity of CO2-induced changes in cerebrovascular resistance between differing arterial territories.

Cerebral blood flow and metabolism in severely head-injured children

1989 ◽  
Vol 71 (1) ◽  
pp. 63-71 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Anthony Marmarou ◽  
Antonio A. F. DeSalles ◽  
John D. Ward ◽  
Richard S. Zimmerman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cerebral Blood Volume ◽  
Closed Head Injury ◽  
Volume Index ◽  
Content Type ◽  
Gcs Score ◽  
Fine Print

✓ The literature suggests that in children with severe head injury, cerebral hyperemia is common and related to high intracranial pressure (ICP). However, there are very few data on cerebral blood flow (CBF) after severe head injury in children. This paper presents 72 measurements of cerebral blood flow (“CBF15”), using the 133Xe inhalation method, with multiple detectors over both hemispheres in 32 children aged 3 to 18 years (mean 13.6 years) with severe closed head injury (average Glasgow Coma Scale (GCS) score 5.4). In 25 of the children, these were combined with measurements of arteriojugular venous oxygen difference (AVDO2) and of cerebral metabolic rate of oxygen (CMRO2). In 30 patients, the first measurement was taken approximately 12 hours postinjury. In 18 patients, an indication of brain stiffness was obtained by withdrawal and injection of ventricular cerebrospinal fluid and calculation of the pressure-volume index (PVI) of Marmarou. The CBF and CMRO2 data were correlated with the GCS score, outcome, ICP, and PVI. Early after injury, CBF tended to be lower with lower GCS scores, but this was not statistically significant. This trend was reversed 24 hours postinjury, as significantly more hyperemic values were recorded the lower the GCS score, with the exception of the most severely injured patients (GCS score 3). In contrast, mean CMRO2 correlated positively with the GCS score and outcome throughout the course, but large standard deviations preclude making predictions based on CMRO2 measurements in individual patients. Early after injury, there was mild uncoupling between CBF and CMRO2 (CBF above metabolic demands, low AVDO2) and, after 24 hours, flow and metabolism were completely uncoupled with an extremely low AVDO2. Consistently reduced flow was found in only four patients; 28 patients (88%) showed hyperemia at some point in their course. This very high percentage of patients with hyperemia, combined with the lowest values of AVDO2 found in the literature, indicates that hyperemia or luxury perfusion is more prevalent in this group of patients. The three patients with consistently the highest CBF had consistently the lowest PVI: thus, the patients with the most severe hyperemia also had the stiffest brains. Nevertheless, and in contrast to previous reports, no correlation could be established between the course of ICP or PVI and the occurrence of hyperemia, nor was there a correlation between the levels of CBF and ICP at the time of the measurements. The authors argue that this lack of correlation is due to: 1) a definition of hyperemia that is too generous, and 2) the lack of a systematic relationship between CBF and cerebral blood volume. The implications of these findings for therapeutic modes of controlling ICP in children, such as hyperventilation and the use of mannitol, are discussed.

Posttraumatic cerebral arterial spasm: transcranial Doppler ultrasound, cerebral blood flow, and angiographic findings

1992 ◽  
Vol 77 (4) ◽  
pp. 575-583 ◽  
Author(s):  
Neil A. Martin ◽  
Curtis Doberstein ◽  
Cynthia Zane ◽  
Michael J. Caron ◽  
Kathleen Thomas ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Doppler Ultrasound ◽  
Transcranial Doppler ◽  
Transcranial Doppler Ultrasound ◽  
Arterial Spasm ◽  
Content Type ◽  
Closed Head ◽  
Extracranial Ica ◽  
Fine Print

✓ Thirty patients admitted after suffering closed head injuries, with Glasgow Coma Scale scores ranging from 3 to 15, were evaluated with transcranial Doppler ultrasound monitoring. Blood flow velocity was determined in the middle cerebral artery (MCA) and the intracranial portion of the internal carotid artery (ICA) in all patients. Because proximal flow in the extracranial ICA declines in velocity when arterial narrowing becomes hemodynamically significant, the extracranial ICA velocity was concurrently monitored in 19 patients. To assess cerebral perfusion, cerebral blood flow (CBF) measurements obtained with the intravenous 113Xe technique were completed in 16 patients. Vasospasm, designated as MCA velocity exceeding 120 cm/sec, was found in eight patients (26.7%). Severe vasospasm, defined as MCA velocity greater than 200 cm/sec, occurred in three patients, and was confirmed by angiography in all three. Subarachnoid hemorrhage (SAH) was documented by computerized tomography in five (62.5%) of the eight patients with vasospasm. All cases of severe vasospasm were associated with subarachnoid blood. The time course of vasospasm in patients with traumatic SAH was similar to that found in patients with aneurysmal SAH; in contrast, arterial spasm not associated with SAH demonstrated an uncharacteristically short duration (mean 1.25 days), suggesting that this may be a different type of spasm. A significant correlation (p < 0.05) was identified between the lowest CBF and highest MCA velocity in patients during the period of vasospasm, indicating that arterial narrowing can lead to impaired CBF. Ischemic brain damage was found in one patient who had evidence of cerebral infarction in the territories supplied by the arteries affected by spasm. These findings demonstrate that delayed cerebral arterial spasm is a frequent complication of closed head injury and that the severity of spasm is, in some cases, comparable to that seen in aneurysmal SAH. This experience suggests that vasospasm is an important secondary posttraumatic insult that is potentially treatable.

Relationship of early cerebral blood flow and metabolism to outcome in acute head injury

1990 ◽  
Vol 72 (2) ◽  
pp. 176-182 ◽  
Author(s):  
Jurg L. Jaggi ◽  
Walter D. Obrist ◽  
Thomas A. Gennarelli ◽  
Thomas W. Langfitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Vegetative State ◽  
Closed Head Injury ◽  
Total Sample ◽  
Prognostic Indicators ◽  
Content Type ◽  
Blood Flows ◽  
Fine Print

✓ Cerebral blood flow (CBF) measurements were obtained acutely in 96 comatose patients with closed head injury, using the intravenous 133Xe technique. Arteriojugular venous oxygen differences and cerebral metabolic rate for oxygen (CMRO2) were determined in a subgroup of 66 patients. The relationship between each of these variables and outcome at 6 months was analyzed, using the Glasgow Outcome Scale. The CMRO2 was significantly depressed in patients who subsequently died or remained in a vegetative state, whereas higher values were obtained in patients who later regained consciousness. Although CBF was not predictive of outcome in the total sample, omission of patients with acute hyperemia resulted in a significant relationship that paralleled the metabolic findings. Follow-up studies in the survivors revealed a correlation between CBF and degree of functional recovery, the lowest blood flows being obtained among patients with severe disability. Age, initial Glasgow Coma Scale score, and occurrence of intracranial hypertension were each found to be predictive of outcome, thus confirming previous reports. When these variables were combined with CMRO2 in a logistic regression analysis, the probability of recovery was correctly predicted in 82% of the cases. The CMRO2 was relatively independent of the other prognostic indicators and, next to age, contributed most to the prediction.

The use of moderate therapeutic hypothermia for patients with severe head injuries: a preliminary report

1993 ◽  
Vol 79 (3) ◽  
pp. 354-362 ◽  
Author(s):  
Donald W. Marion ◽  
Walter D. Obrist ◽  
Patricia M. Earlier ◽  
Louis E. Penrod ◽  
Joseph M. Darby
Keyword(s):  
Head Injury ◽  
Therapeutic Hypothermia ◽  
Closed Head Injury ◽  
Metabolic Effects ◽  
Secondary Brain Injury ◽  
Content Type ◽  
Closed Head ◽  
Hypothermia Group ◽  
Rebound Increase ◽  
Fine Print

✓ Animal research suggests that moderate therapeutic hypothermia may improve outcome after a severe head injury, but its efficacy has not been established in humans. The authors randomly assigned 40 consecutively treated patients with a severe closed head injury (Glasgow Coma Scale score 3 to 7) to either a hypothermia or a normothermia group. Using cooling blankets and cold saline gastric lavage, patients in the hypothermia group were cooled to 32° to 33°C (brain temperature) within a mean of 10 hours after injury, maintained at that temperature for 24 hours, and rewarmed to 37° to 38°C over 12 hours. Patients in the normothermia group were maintained at 37° to 38°C during this time. Deep-brain temperatures were monitored directly and used for all temperature determinations. Intracranial pressure (ICP), cerebral blood flow (CBF), and cerebral metabolic rate for oxygen (CMRO2) were measured serially for all patients. Hypothermia significantly reduced ICP (40%) and CBF (26%) during the cooling period, and neither parameter showed a significant rebound increase after patients were rewarmed. Compared to the normothermia group, the mean CMRO2 in the hypothermia group was lower during cooling and higher 5 days after injury. Three months after injury, 12 of the 20 patients in the hypothermia group had moderate, mild, or no disabilities; eight of the 20 patients in the normothermia group had improved to the same degree. Both groups had a similar incidence of systemic complications, including cardiac arrhythmias, coagulopathies, and pulmonary complications. It is concluded that therapeutic moderate hypothermia is safe and has sustained favorable effects on acute derangements of cerebral physiology and metabolism caused by severe closed head injury. The trend toward better outcome with hypothermia may indicate that its beneficial physiological and metabolic effects limit secondary brain injury.

Demonstration of massive traumatic brain swelling within 20 minutes after injury

1977 ◽  
Vol 46 (2) ◽  
pp. 256-258 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Eugene Timmins ◽  
Rodwan K. Rajjoub ◽  
Hugo V. Rizzoli ◽  
David O. Davis
Keyword(s):  
Head Injury ◽  
Closed Head Injury ◽  
Brain Swelling ◽  
Axial Tomography ◽  
Content Type ◽  
Closed Head ◽  
Vascular Dilatation ◽  
Computerized Axial Tomography ◽  
The Brain ◽  
Fine Print

✓ The authors documented by computerized axial tomography a case of massive brain swelling occurring within 20 minutes of a closed head injury. It is suggested that the cause of the brain swelling is acute vascular dilatation.

Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion

2001 ◽  
Vol 95 (6) ◽  
pp. 1053-1056 ◽  
Author(s):  
Michael L. Cannon ◽  
Steven S. Glazier ◽  
Loren A. Bauman
Keyword(s):  
Metabolic Acidosis ◽  
Head Injury ◽  
Myocardial Dysfunction ◽  
Closed Head Injury ◽  
Pediatric Intensive Care ◽  
Cardiovascular Collapse ◽  
Severe Metabolic Acidosis ◽  
Content Type ◽  
Closed Head ◽  
Fine Print

✓ The authors present the hospital course of a 13-year-old girl with a closed head injury who received a prolonged infusion of propofol for sedation and, subsequently, died as a result of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse. The patient had been treated for 4 days at a referring hospital for a severe closed head injury sustained in a fall from a bicycle. During treatment for elevations of intracranial pressure, she received a continuous propofol infusion (100 µg/kg/min). The patient began to exhibit severe high anion gap/low lactate metabolic acidosis, and was transferred to the pediatric intensive care unit at the authors' institution. On arrival there, the patient's Glasgow Coma Scale score was 3 and this remained unchanged during her brief stay. The severe metabolic acidosis was unresponsive to maximum therapy. Acute renal failure ensued as a result of rhabdomyolysis, and myocardial dysfunction with bizarre, wide QRS complexes developed without hyperkalemia. The patient died of myocardial collapse with severe metabolic acidosis and multisystem organ failure (involving renal, hepatic, and cardiac systems) approximately 15 hours after admission to the authors' institution. This patient represents another case of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse observed after a prolonged propofol infusion in a pediatric patient. The authors suggest selection of other pharmacological agents for long-term sedation in pediatric patients.

Temporal changes in intracranial pressure in a modified experimental model of closed head injury

1998 ◽  
Vol 89 (5) ◽  
pp. 796-806 ◽  
Author(s):  
Koen Engelborghs ◽  
Jan Verlooy ◽  
Jos Van Reempts ◽  
Bruno Van Deuren ◽  
Mies Van de Ven ◽  
...  
Keyword(s):  
Head Injury ◽  
Intracranial Pressure ◽  
Experimental Model ◽  
Closed Head Injury ◽  
Content Type ◽  
Closed Head ◽  
Impact Acceleration ◽  
The Moment ◽  
The Impact ◽  
Fine Print

Object. The authors describe an experimental model of closed head injury in rodents that was modified from one developed by Marmarou and colleagues. This modification allows dual control of the dynamic process of impact compared with impulse loading that occurs at the moment of primary brain injury. The principal element in this weight-drop model is an adjustable table that supports the rat at the moment of impact from weights positioned at different heights (accelerations). The aim was to obtain reproducible pathological intracranial pressure (ICPs) while maximally reducing the incidence of mortality and skull fractures. Methods. Intracranial pressure was investigated in different experimental settings, including two different rat strains and various impact-acceleration conditions and posttrauma survival times. Identical impact-acceleration injuries produced a considerably higher mortality rate in Wistar rats than in Sprague—Dawley rats (50% and 0%, respectively). Gradually increasing severity of impact-acceleration conditions resulted in findings of a significant correlation between the degree of traumatic challenge and increased ICP at 4 hours (p < 0.001, R2 = 0.73). When the impact-acceleration ratio was changed to result in a more severe head injury, the ICP at 4, 24, and 72 hours was significantly elevated in comparison with that seen in sham-injured rats (4 hours: 19.7 ± 2.8 mm Hg, p = 0.004; 24 hours: 21.8 ± 1.1 mm Hg, p = 0.002; 72 hours: 11.9 ± 2.5 mm Hg, p = 0.009). Comparison of the rise in ICP between moderate and severe impact-acceleration injury at 4 and 24 hours revealed a significantly higher value after severe injury (4 hours: p = 0.008; 24 hours: p = 0.004). Continuous recordings showed that ICP mounted very rapidly to peak values, which declined gradually toward a pathological level dependent on the severity of the primary insult. Histological examination after severe trauma revealed evidence of irreversible neuronal necrosis, diffuse axonal injury, petechial bleeding, glial swelling, and perivascular edema. Conclusions. This modified closed head injury model mimics several clinical features of traumatic injury and produces reliable, predictable, and reproducible ICP elevations with concomitant morphological alterations.

Vertebral artery rupture associated with closed head injury

1985 ◽  
Vol 62 (1) ◽  
pp. 135-138 ◽  
Author(s):  
John M. McLean ◽  
Robert M. Wright ◽  
John P. Henderson ◽  
J. Richard Lister
Keyword(s):  
Head Injury ◽  
Vertebral Artery ◽  
Closed Head Injury ◽  
Mechanism Of Injury ◽  
Content Type ◽  
The Third ◽  
Closed Head ◽  
Angiographic Evidence ◽  
Head And Neck Injury ◽  
Fine Print

✓ The authors report two patients with closed head injury who suffered laceration with rupture of the third portion of the vertebral artery. One patient died suddenly, with angiographic evidence of bilateral vertebral artery rupture. The mechanism of injury to the C1–2 segment of the vertebral artery relating to head and neck injury is discussed.

Dissociation of cerebral blood flow, glucose metabolism, and electrical activity in pediatric brain death

1993 ◽  
Vol 79 (5) ◽  
pp. 752-755 ◽  
Author(s):  
Michael D. Medlock ◽  
William C. Hanigan ◽  
Robert P. Cruse
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Brain Death ◽  
Electrical Activity ◽  
Closed Head Injury ◽  
Content Type ◽  
Positron Emission ◽  
Mononuclear Cell Infiltrates ◽  
Fine Print

✓ A 2-month-old infant demonstrated clinical brain death 48 hours after suffering a closed head injury accompanied by cardiac arrest. Two nuclear cerebral blood flow (CBF) studies demonstrated normal perfusion. On the 11th day following injury, cerebral electrical activity ceased and a normal glucose metabolic gradient between gray and white matter was documented on positron emission tomography. Autopsy revealed widespread necrosis with mononuclear cell infiltrates throughout all cerebral cortical layers. Nine children have previously been described with clinical brain death, electrocerebral silence, and evidence of CBF by radionuclide scan. The dissociation between cerebral electrical activity and blood flow may be explained by an increase in cranial volume allowed by the expansile neonatal skull, preventing both intracranial hypertension and a reduction in perfusion pressure. The persistence of glucose metabolism may be associated with the presence of inflammatory microglial cells in the ischemic cortex. The authors conclude that persistence of CBF and glucose metabolism in brain-dead children may not indicate neuronal survival. If repeated neurological examinations with or without electroencephalography support the diagnosis of brain death, the presence of CBF and glucose metabolism should not alter this conclusion.

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