Quantitative cerebral blood flow and metabolism determination in the first 48 hours after severe head injury with a new dynamic spect device

Corte, Francesco Della; Giordano, Alessandro; Pennisi, Maddalena; Barelli, Alessandro; Caricato, Anselmo; Campioni, Paolo; Galli, G

doi:10.1007/bf01411999

Cited by 24 publications

(2 citation statements)

References 35 publications

(37 reference statements)

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“…Measurement of cerebral blood flow after trauma has been object of several studies in recent years and conflicting results have been reported (11)(12)(13). Since more sophisticated imaging techniques have become available, including Positron Emission Tomography (PET), the pathophysiology of brain hemodynamics is now better understood (4).…”

Section: Discussionmentioning

confidence: 99%

Hyperemia in head injury: can transcranial doppler help to personalize therapies for intracranial hypertension?

Gelormini,

Ioannoni,

Scavone

et al. 2023

Front. Neurol.

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IntroductionAn increase in cerebral blood flow is frequent after traumatic brain injury (TBI) and can lead to brain swelling and refractory intracranial hypertension. We hypothesized that Transcranial EcoDoppler (TCD) monitoring could be useful to detect the cause of intracranial hypertension in these patients. Our main objective was to investigate if the increase of velocity in the middle cerebral artery (MCA) on TCD could be associated with intracranial hypertension.MethodsWe retrospectively studied TBI patients consecutively monitored with TCD. Hyperemia was defined as MCA mean velocity higher than 80 cm/s. Intracranial hypertension was considered when hyperosmolar therapy, hyperventilation, or deep sedation was used.ResultsWe found hyperemia in 40 patients out of 118 (33.9%). On average, it started at day 2.1 ± 0.9 from admission and significantly increased (MCA velocity at day 1: 74 ± 25 cm/s vs. 109 ± 36 cm/s at day 4; p < 0.001). Intracranial hypertension was significantly associated with hyperemia, occurring in 92.5% of hyperemic and 51.3% of non-hyperemic patients (p < 0.001). Moreover, we found that hyperemia preceded severe intracranial hypertension (p < 0.0001). In a logistic regression model, hyperemia was the only variable significantly correlated with intracranial hypertension (OR 10.64; p < 0.001).DiscussionHyperemia was frequent in our population of TBI patients and preceded intracranial hypertension. TCD monitoring, if performed on a daily regular basis, can be a useful method to detect this phenomenon and to guide the therapy. It could be a tool for a cause-oriented therapy of intracranial hypertension.

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Section: Discussionmentioning

confidence: 99%

Hyperemia in head injury: can transcranial doppler help to personalize therapies for intracranial hypertension?

Gelormini,

Ioannoni,

Scavone

et al. 2023

Front. Neurol.

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“…15,31,37 Several studies conclude that there is narrowed microcirculation and persistent vasoconstriction and that posttraumatic vasospasm may occur in as many as 43% of patients who suffer a severe traumatic brain injury. 23 The normal response to hyperventilation was studied by Raichle in a group of healthy volunteers: 40% decrease in CBF 30 min after decreasing the pC02 by 15-20 mm Hg; 4 h later there was an increase in CBF to 90% of baseline; when the original pC02 was restored there was an overshoot in CBF of 31%.41 A study of cerebral blood volume, measured with the 99M-tc-labeled RBC, and simultaneous CBF measurements using carotid duplex scanning found that a reduction of the pC02 to 26 mm/Hg led to a 7.2% decrease in cerebral blood volume, but a 30.7% decrease in CBF.18…”

Section: Processmentioning

confidence: 99%

Hyperventilation

2000

Journal of Neurotrauma

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Chronic prophylactic hyperventilation therapy should be avoided during the first 5 days after severe TBI and particularly during the first 24 h. CBF measurements in patients with severe TBI demonstrate that blood flow early after injury is low and strongly suggest that in the first few hours after injury the absolute values approach those consistent with ischemia. These findings are corroborated by AVdO2 and SjO2 and brain tissue O2 measurements. Hyperventilation will reduce CBF values even further, but will not consistently cause a reduction of ICP and may cause loss of autoregulation. The cerebral vascular response to hypocapnia is reduced in those with the most severe injuries (subdural hematomas and diffuse contusions), and there is substantial local variability in perfusion. While the CBF level at which irreversible ischemia occurs has not been clearly established, ischemic cell change has been demonstrated in 90% of those who die following TBI, and there is PET evidence that such damage is likely to occur when CBF drops below 15-20 cc/100 g/min. A prospective randomized clinical trial has determined that outcomes are worse when TBI patients are treated with chronic prophylactic hyperventilation therapy. Within the standard, guideline, and options, specific paCO2 thresholds have been described that are different for each of the three parameters. These individual thresholds were selected based on the preponderance of literature supporting those thresholds in the contexts of the statements which included them. With the exception of the threshold included for the standard in this guideline, it is emphasized that the paCO2 threshold is not as important as the general concept of hyperventilation. The preponderance of the physiologic literature concludes that hyperventilation during the first few days following severe traumatic brain injury, whatever the threshold, is potentially deleterious in that it can promote cerebral ischemia.

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Acute head injury

Cold

Dahl

2002

Topics in Neuroanaesthesia and Neurointensive Care

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Quantitative cerebral blood flow and metabolism determination in the first 48 hours after severe head injury with a new dynamic spect device

Cited by 24 publications

References 35 publications

Hyperemia in head injury: can transcranial doppler help to personalize therapies for intracranial hypertension?

Hyperemia in head injury: can transcranial doppler help to personalize therapies for intracranial hypertension?

Hyperventilation

Acute head injury

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