Trial reportCritical care medicine2018
Early Evidence of Sepsis-Associated Hyperperfusion-A Study of Cerebral Blood Flow Measured With MRI Arterial Spin Labeling in Critically Ill Septic Patients and Control Subjects.
Trial report in Critical care medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05202938 (Energy MEtabolism of Septic Heart.), which is not on this map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Energy MEtabolism of Septic Heart.
Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Use of Near-Infrared Spectroscopy and/or Transcranial Doppler as Non-Invasive Markers of Cerebral Perfusion in Adult Sepsis Patients With Delirium: A Systematic Review.Journal of intensive care medicine · 2022Pooled it
- Pathophysiology-driven neuroimaging: decoding brain injury in sepsis.Frontiers in molecular neuroscience · 2026Review
- Severe hypotension but not systemic inflammation or endothelial activation predicts encephalopathy in circulatory shock.Annals of intensive care · 2026Article
- Alterations in Regional Brain Microcirculation in Patients with Sepsis: A Prospective Study Using Contrast-Enhanced Brain Ultrasound.Neurocritical care · 2025Article
- Impact of different blood pressure targets on cerebral hemodynamics in septic shock: A prospective pilot study protocol-SEPSIS-BRAIN.PloS one · 2024Article
- Potential Neuroprotective Role of Melatonin in Sepsis-Associated Encephalopathy Due to Its Scavenging and Anti-Oxidative Properties.Antioxidants (Basel, Switzerland) · 2023Review
- Application of magnetic resonance imaging-related techniques in the diagnosis of sepsis-associated encephalopathy: present status and prospect.Frontiers in neuroscience · 2023Review
- Shock Resuscitation - the Necessity and Priority of Renal Blood Perfusion Assessment.Aging and disease · 2022Article
- Association between neutrophil-to-lymphocyte ratio and major postoperative complications after carotid endarterectomy: A retrospective cohort study.World journal of clinical cases · 2021Article
- Endothelial Dysfunction and Impaired Neurovascular Coupling Responses Precede Cognitive Impairment in a Mouse Model of Geriatric Sepsis.Frontiers in aging neuroscience · 2021Article
- What is a Clinician to Do?Critical care medicine · 2018Article
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesMechanisms underlying sepsis-associated encephalopathy remain unclear, but reduced cerebral blood flow, alone or in conjunction with altered autoregulation, is reported as a potential contributor. We compared cerebral blood flow of control subjects and vasopressor-dependent septic patients.
designRandomized crossover study.
settingMRI with arterial spin labeling. PATIENTS: Ten sedated septic patients on mechanical ventilation (four with controlled chronic hypertension) and 12 control subjects (six with controlled chronic hypertension) were enrolled. Mean ± SD ages were 61.4 ± 10.2 and 44.2 ± 12.8 years, respectively (p = 0.003). Mean Acute Physiology and Chronic Health Evaluation II score of septic patients at ICU admission was 27.7 ± 6.6.
interventionsTo assess the potential confounding effects of sedation and mean arterial pressure, we measured cerebral blood flow with and without sedation with propofol in control subjects and at a target mean arterial pressure of 65 mm Hg and greater than or equal to 75 mm Hg in septic patients. The sequence of sedation versus no sedation and mean arterial pressure targets were randomized. MEASUREMENTS AND MAIN
resultsIn septic patients, cerebral blood flow measured at a mean arterial pressure target of 65 mm Hg (40.4 ± 10.9 mL/100 g/min) was not different from cerebral blood flow measured at a mean arterial pressure target of greater than or equal to 75 mm Hg (41.3 ± 9.8 mL/100 g/min; p = 0.65). In control subjects, we observed no difference in cerebral blood flow measured without and with sedation (24.8 ± 4.2 vs 24.9 ± 5.9 mL/100 g/min; p = 0.93). We found no interaction between chronic hypertension and the effect of sedation or mean arterial pressure targets. Cerebral blood flow measured in sedated septic patients (mean arterial pressure target 65 mm Hg) was 62% higher than in sedated control subjects (p = 0.001).
conclusionsIn septic patients, cerebral blood flow was higher than in sedated control subjects and did not vary with mean arterial pressure targets. Further research is required to understand the clinical significance of cerebral hyperperfusion in septic patients on vasopressors and to reassess the neurologic effects of current mean arterial pressure targets in sepsis.
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