The effect of the volemic and cardiac status on brain oxygenation in patients with subarachnoid hemorrhage: a bi-center cohort study

Abstract Background Fluid management in patients after subarachnoid hemorrhage (SAH) aims at the optimization of cerebral blood flow and brain oxygenation. In this study, we investigated the effects of hemodynamic management on brain oxygenation by integrating advanced hemodynamic and invasive neuromonitoring. Methods This observational cohort bi-center study included data of consecutive poor-grade SAH patients who underwent pulse contour cardiac output (PiCCO) monitoring and invasive neuromonitoring. Fluid management was guided by the transpulmonary thermodilution system and aimed at euvolemia (cardiac index, CI ≥ 3.0 L/min/m2; global end-diastolic index, GEDI 680–800 mL/m2; stroke volume variation, SVV < 10%). Patients were managed using a brain tissue oxygenation (PbtO2) targeted protocol to prevent brain tissue hypoxia (BTH, PbtO2 < 20 mmHg). To assess the association between CI and PbtO2 and the effect of fluid challenges on CI and PbtO2, we used generalized estimating equations to account for repeated measurements. Results Among a total of 60 included patients (median age 56 [IQRs 47–65] years), BTH occurred in 23% of the monitoring time during the first 10 days since admission. Overall, mean CI was within normal ranges (ranging from 3.1 ± 1.3 on day 0 to 4.1 ± 1.1 L/min/m2 on day 4). Higher CI levels were associated with higher PbtO2 levels (Wald = 14.2; p < 0.001). Neither daily fluid input nor fluid balance was associated with absolute PbtO2 levels (p = 0.94 and p = 0.85, respectively) or the occurrence of BTH (p = 0.68 and p = 0.71, respectively). PbtO2 levels were not significantly different in preload dependent patients compared to episodes of euvolemia. PbtO2 increased as a response to fluid boluses only if BTH was present at baseline (from 13 ± 6 to 16 ± 11 mmHg, OR = 13.3 [95% CI 2.6–67.4], p = 0.002), but not when all boluses were considered (p = 0.154). Conclusions In this study a moderate association between increased cardiac output and brain oxygenation was observed. Fluid challenges may improve PbtO2 only in the presence of baseline BTH. Individualized hemodynamic management requires advanced cardiac and brain monitoring in critically ill SAH patients.

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Monitoring of HHH-therapy using brain tissue oxygenation after subarachnoid hemorrhage

Clinical Neurology and Neurosurgery ◽

10.1016/s0303-8467(97)81734-9 ◽

1997 ◽

Vol 99 ◽

pp. S104

Author(s):

J. Meixensberger ◽

A. Jäger ◽

J. Dings ◽

S. Baunach ◽

K. Roosen

Keyword(s):

Subarachnoid Hemorrhage ◽

Brain Tissue ◽

Tissue Oxygenation ◽

Brain Tissue Oxygenation ◽

Hhh Therapy

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Cardiac output augmentation with fluid resuscitation improves brain tissue oxygenation after severe brain injury

Critical Care ◽

10.1186/cc8579 ◽

2010 ◽

Vol 14 (Suppl 1) ◽

pp. P347

Author(s):

R Helbok ◽

P Kurtz ◽

J Claassen ◽

J Schmidt ◽

L Fernadez ◽

...

Keyword(s):

Cardiac Output ◽

Brain Injury ◽

Brain Tissue ◽

Fluid Resuscitation ◽

Tissue Oxygenation ◽

Severe Brain Injury ◽

Brain Tissue Oxygenation

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Effects of cardiac output-guided hemodynamic management on fluid administration after aneurysmal subarachnoid hemorrhage

Critical Care ◽

10.1186/cc13645 ◽

2014 ◽

Vol 18 (Suppl 1) ◽

pp. P455 ◽

Cited By ~ 1

Author(s):

B Bergmans ◽

M Egal ◽

J Van Bommel ◽

J Bakker ◽

M Van der Jagt

Keyword(s):

Cardiac Output ◽

Subarachnoid Hemorrhage ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Fluid Administration ◽

Hemodynamic Management

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Relative importance of hypertension compared with hypervolemia for increasing cerebral oxygenation in patients with cerebral vasospasm after subarachnoid hemorrhage

Journal of Neurosurgery ◽

10.3171/jns.2005.103.6.0974 ◽

2005 ◽

Vol 103 (6) ◽

pp. 974-981 ◽

Cited By ~ 104

Author(s):

Andreas Raabe ◽

Jügen Beck ◽

Mike Keller ◽

Hartmuth Vatter ◽

Michael Zimmermann ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Brain Tissue ◽

Cerebral Vasospasm ◽

Moderate Hypertension ◽

Cerebral Oxygenation ◽

Brain Oxygenation ◽

Content Type ◽

Arterial Blood ◽

Hypertension Therapy ◽

Fine Print

Object. Hypervolemia and hypertension therapy is routinely used for prophylaxis and treatment of symptomatic cerebral vasospasm at many institutions. Nevertheless, there is an ongoing debate about the preferred modality (hypervolemia, hypertension, or both), the degree of therapy (moderate or aggressive), and the risk or benefit of hypervolemia, moderate hypertension, and aggressive hypertension in patients following subarachnoid hemorrhage. Methods. Monitoring data and patient charts for 45 patients were retrospectively searched to identify periods of hypervolemia, moderate hypertension, or aggressive hypertension. Measurements of central venous pressure, fluid input, urine output, arterial blood pressure, intracranial pressure, and oxygen partial pressure (PO2) in the brain tissue were extracted from periods ranging from 1 hour to 24 hours. For these periods, the change in brain tissue PO2 and the incidence of complications were analyzed. During the 55 periods of moderate hypertension, an increase in brain tissue PO2 was found in 50 cases (90%), with complications occurring in three patients (8%). During the 25 periods of hypervolemia, an increase in brain oxygenation was found during three intervals (12%), with complications occurring in nine patients (53%). During the 10 periods of aggressive hypervolemic hypertension, an increase in brain oxygenation was found during six of the intervals (60%), with complications in five patients (50%). Conclusions. When hypervolemia treatment is applied as in this study, it may be associated with increased risks. Note, however, that further studies are needed to determine the role of this therapeutic modality in the care of patients with cerebral vasospasm. In poor-grade patients, moderate hypertension (cerebral perfusion pressure 80–120 mm Hg) in a normovolemic, hemodiluted patient is an effective method of improving cerebral oxygenation and is associated with a lower complication rate compared with hypervolemia or aggressive hypertension therapy.

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The effect of nimodipine on cerebral oxygenation in patients with poor-grade subarachnoid hemorrhage

Journal of Neurosurgery ◽

10.3171/jns.2004.101.4.0594 ◽

2004 ◽

Vol 101 (4) ◽

pp. 594-599 ◽

Cited By ~ 33

Author(s):

Michael F. Stiefel ◽

Gregory G. Heuer ◽

John M. Abrahams ◽

Stephanie Bloom ◽

Michelle J. Smith ◽

...

Keyword(s):

Blood Pressure ◽

Subarachnoid Hemorrhage ◽

Brain Tissue ◽

Cerebral Oxygenation ◽

Content Type ◽

Poor Grade ◽

Physiological Variables ◽

Arterial Blood ◽

End Tidal ◽

Fine Print

Object. Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2. Methods. Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4 ± 10.9 mm Hg. The baseline MABP and CPP were 90 ± 20 and 84 ± 19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9 ± 7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5 ± 7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7 ± 11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2. Conclusions. Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.

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Brain tissue oxygenation guided therapy and outcome in non-traumatic subarachnoid hemorrhage

Scientific Reports ◽

10.1038/s41598-021-95602-6 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Elisa Gouvea Bogossian ◽

Daniela Diaferia ◽

Narcisse Ndieugnou Djangang ◽

Marco Menozzi ◽

Jean-Louis Vincent ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Brain Tissue ◽

Neurological Outcome ◽

Tissue Oxygenation ◽

Secondary Outcome ◽

Brain Tissue Oxygenation ◽

Brain Hypoxia ◽

Traumatic Subarachnoid Hemorrhage ◽

The Impact ◽

Guided Therapy

AbstractBrain hypoxia can occur after non-traumatic subarachnoid hemorrhage (SAH), even when levels of intracranial pressure (ICP) remain normal. Brain tissue oxygenation (PbtO2) can be measured as a part of a neurological multimodal neuromonitoring. Low PbtO2 has been associated with poor neurologic recovery. There is scarce data on the impact of PbtO2 guided-therapy on patients’ outcome. This single-center cohort study (June 2014–March 2020) included all patients admitted to the ICU after SAH who required multimodal monitoring. Patients with imminent brain death were excluded. Our primary goal was to assess the impact of PbtO2-guided therapy on neurological outcome. Secondary outcome included the association of brain hypoxia with outcome. Of the 163 patients that underwent ICP monitoring, 62 were monitored with PbtO2 and 54 (87%) had at least one episode of brain hypoxia. In patients that required treatment based on neuromonitoring strategies, PbtO2-guided therapy (OR 0.33 [CI 95% 0.12–0.89]) compared to ICP-guided therapy had a protective effect on neurological outcome at 6 months. In this cohort of SAH patients, PbtO2-guided therapy might be associated with improved long-term neurological outcome, only when compared to ICP-guided therapy.

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Faculty Opinions recommendation of Effects of hypervolemia and hypertension on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation after subarachnoid hemorrhage.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1090296.567123 ◽

2008 ◽

Author(s):

Andreas Kramer

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Subarachnoid Hemorrhage ◽

Intracranial Pressure ◽

Brain Tissue ◽

Regional Cerebral Blood Flow ◽

Tissue Oxygenation ◽

Regional Cerebral Blood ◽

Brain Tissue Oxygenation

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Controlled Hypercapnia Enhances Cerebral Blood Flow and Brain Tissue Oxygenation After Aneurysmal Subarachnoid Hemorrhage: Results of a Phase 1 Study

Neurocritical Care ◽

10.1007/s12028-016-0246-x ◽

2016 ◽

Vol 25 (2) ◽

pp. 205-214 ◽

Cited By ~ 15

Author(s):

Thomas Westermaier ◽

Christian Stetter ◽

Ekkehard Kunze ◽

Nadine Willner ◽

Judith Holzmeier ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Subarachnoid Hemorrhage ◽

Brain Tissue ◽

Tissue Oxygenation ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Phase 1 ◽

Phase 1 Study ◽

Brain Tissue Oxygenation

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Brain Tissue Oxygenation Guided Therapy and Outcome in Non-Traumatic Subarachnoid Hemorrhage

10.21203/rs.3.rs-228515/v1 ◽

2021 ◽

Author(s):

Elisa GOUVEA BOGOSSIAN ◽

Daniela DIAFERIA ◽

Narcisse NDIEUGNOU DJANGANG ◽

Marco MENOZZI ◽

Jean-Louis VINCENT ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Brain Tissue ◽

Neurological Outcome ◽

Tissue Oxygenation ◽

Secondary Outcome ◽

Normal Brain ◽

Brain Tissue Oxygenation ◽

Brain Hypoxia ◽

The Impact ◽

Guided Therapy

Abstract Background Brain hypoxia can occur after spontaneous subarachnoid hemorrhage (SAH), even when levels of intracranial pressure (ICP) remain normal. Brain tissue oxygenation (PbtO2) can be measured as a part of a neurological multimodal neuromonitoring Low PbtO2 has been associated with poor neurologic recovery. There is scarce data on the impact of PbtO2 guided-therapy on patients’ outcome. Methods This single-center cohort study (June 2014-March 2020) included all patients admitted to the ICU after SAH who required multimodal monitoring. Patients with imminent brain death were excluded. Our primary goal was to assess the impact of PbtO2-guided therapy on neurological outcome. Secondary outcome included the association of brain hypoxia with outcome. Results Of the 163 patients that underwent ICP monitoring, 62 were monitored with PbtO2 and 54 (87%) had at least one episode of brain hypoxia. In patients that required treatment based on neuromonitoring strategies, PbtO2-guided therapy (OR 0.33 [CI 95% 0.12–0.90]) compared to ICP-guided therapy had a protective effect on neurological outcome at 6 months. Brain hypoxia was associated with unfavorable neurological (OR 4.51 [95% CI 1.17–17.45]). Conclusions In this cohort of SAH patients, PbtO2-guided therapy when compared to ICP guided therapy may be associated with improved long-term neurological outcome.

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