Kinetics of cerebral blood flow velocities during treatment for delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage

Rouanet, Carolina; Chaddad-Neto, Feres; Freitas, Flávio Geraldo Rezende; Miranda, Munique; Vasconcellos, Natalia; Valiente, Raul Alberto; Muehlschlegel, Susanne; Silva, Gisele Sampaio

doi:10.1007/s12028-021-01288-z

Cited by 7 publications

(4 citation statements)

References 31 publications

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“…Rouanet et al (10) also reported that V mean did not significantly change after the induction of arterial hypertension (in 6-12 patients), but decreased after the initiation of IV milrinone (in 9-15 mostly different patients). Another study, involving 13 patients, reported a decrease in V mean among those receiving IV milrinone.…”

Section: Discussionmentioning

confidence: 92%

Cerebral Vasospasm After Subarachnoid Hemorrhage: Respective Short-Term Effects of Induced Arterial Hypertension and its Combination With IV Milrinone: A Proof-of-Concept Study Using Transcranial Doppler Ultrasound

Lakhal,

Fresco,

Hivert

et al. 2023

Critical Care Explorations

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OBJECTIVES: It is unclear whether IV milrinone relaxes spasmed cerebral arteries and therefore reduces cerebral blood mean velocity (Vmean). In patients treated for cerebral vasospasm, we aimed to assess and delineate the respective impacts of induced hypertension and its combination with IV milrinone on cerebral hemodynamics as assessed with transcranial Doppler. DESIGN: Observational proof-of-concept prospective study. SETTING: ICU in a French tertiary care center. PATIENTS: Patients with aneurysmal subarachnoid hemorrhage who received induced hypertension (mean arterial blood pressure [MBP] of 100–120 mm Hg) and IV milrinone (0.5 µg/kg/min) for moderate-to-severe cerebral vasospasm. We excluded patients who underwent invasive angioplasty or milrinone discontinuation within 12 hours after the diagnosis of vasospasm. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Vmean was measured at vasospasm diagnosis (TDIAGNOSIS), after the induction of hypertension (THTN), and 1 (THTN+MILRINONE_H1) and 12 hours after the adjunction of IV milrinone (THTN+MILRINONE_H12). Thirteen patients were included. Median Vmean was significantly lower (p < 0.01) at THTN+MILRINONE_H1 (99 [interquartile range (IQR) 89; 134] cm.s−1) and THTN+MILRINONE_H12 (85 [IQR 73–127] cm/s) than at TDIAGNOSIS (136 [IQR 115–164] cm/s) and THTN (148 [IQR 115–183] cm/s), whereas TDIAGNOSIS and THTN did not significantly differ. In all patients but one, Vmean at THTN+MILRINONE_H1 was lower than its value at TDIAGNOSIS (p = 0.0005). Vmean-to-MBP and Vmean-to-cardiac output (CO) ratios (an assessment of Vmean regardless of the level of MBP [n = 13] or CO [n = 7], respectively) were, respectively, similar at TDIAGNOSIS and THTN but were significantly lower after the adjunction of milrinone (p < 0.01). CONCLUSIONS: The induction of arterial hypertension was not associated with a significant decrease in Vmean, whereas the adjunction of IV milrinone was, regardless of the level of MBP or CO. This suggests that IV milrinone may succeed in relaxing spasmed arteries.

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Section: Discussionmentioning

confidence: 92%

Cerebral Vasospasm After Subarachnoid Hemorrhage: Respective Short-Term Effects of Induced Arterial Hypertension and its Combination With IV Milrinone: A Proof-of-Concept Study Using Transcranial Doppler Ultrasound

Lakhal,

Fresco,

Hivert

et al. 2023

Critical Care Explorations

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“…While improvement of angiographic vasospasm could be shown after intra-arterial application, the effect following intravenous application remains unclear [ 3 , 10 ]. A few case reports and a small comparative study demonstrated decreasing flow velocities after intravenous milrinone therapy as measured with transcranial Doppler [ 11 , 23 , 25 ]. Clarifying the effect of intravenous milrinone on cerebral perfusion and macroscopic vasospasm was the main aim of the current analysis.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic response and clinical outcome following intravenous milrinone plus norepinephrine–based hyperdynamic hypertensive therapy in patients suffering secondary cerebral ischemia after aneurysmal subarachnoid hemorrhage

et al. 2022

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Purpose Intravenous and intra-arterial milrinone as a rescue measure for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) has been adopted by several groups, but so far, evidence for the clinical benefit is unclear and effect on brain perfusion is unknown. The aim of the actual analysis was to define cerebral hemodynamic effects and outcome of intravenous milrinone plus norepinephrine supplemented by intra-arterial nimodipine as a rescue strategy for DCI following aneurysmal SAH. Methods Of 176 patients with aneurysmal SAH treated at our neurosurgical department between April 2016 and March 2021, 98 suffered from DCI and were submitted to rescue therapy. For the current analysis, characteristics of these patients and clinical response to rescue therapy were correlated with hemodynamic parameters, as assessed by CT angiography (CTA) and perfusion CT. Time to peak (TTP) delay in the ischemic focus and the volume with a TTP delay of more than 4 s (T4 volume) were used as hemodynamic parameters. Results The median delay to neurological deterioration following SAH was 5 days. Perfusion CT at that time showed median T4 volumes of 40 cc and mean focal TTP delays of 2.5 ± 2.1 s in these patients. Following rescue therapy, median T4 volume decreased to 10 cc and mean focal TTP delay to 1.7 ± 1.9 s. Seventeen patients (17% of patients with DCI) underwent additional intra-arterial spasmolysis using nimodipine. Visible resolution of macroscopic vasospasm on CTA was observed in 43% patients with DCI and verified vasospasm on CTA, including those managed with additional intra-arterial spasmolysis. Initial WFNS grade, occurrence of secondary infarction, ischemic volumes and TTP delays at the time of decline, the time to clinical decline, and the necessity for additional intra-arterial spasmolysis were identified as the most important features determining neurological outcome at 6 months. Conclusion The current analysis shows that cerebral perfusion in the setting of secondary cerebral ischemia following SAH is measurably improved by milrinone and norepinephrine–based hyperdynamic therapy. A long-term clinical benefit by the addition of milrinone appears likely. Separation of the direct effect of milrinone from the effect of induced hypertension is not possible based on the present dataset.

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“…Recently, PbtO 2 was utilized to measure tissue oxygenation during CPP adjustments in a study conducted by Kovacs et al [70], which aimed to assess the CPP threshold that correlates with sufficient PbtO 2 levels in brain-injured patients (the target was >20 mmHg). In total, 53 patients with heterogeneous types of ABI (TBI, SAH or ICH) received an infusion of norepinephrine to reach increases in CPP of at least 10 mmHg, 10-15 min each, at two different steps above the baseline, from 73 (70)(71)(72)(73)(74)(75)(76) to 83 (80)(81)(82)(83)(84)(85)(86) and to 92 (90)(91)(92)(93)(94)(95)(96), with a progressive PbtO 2 increase from 20 (17)(18)(19)(20)(21)(22)(23) to 22 (20)(21)(22)(23)(24) and 24 (22-26), respectively. Focusing on CPP, they concluded that PbtO 2 monitoring indicated the need for higher CPP targets than recommended to prevent tissue hypoxia.…”

Section: Cerebral Oxygenation Effectsmentioning

confidence: 99%

“…Several studies have reported a vasodilatory effect on cerebral arteries and arterioles, leading to increased CBF [85,[87][88][89]. The vasodilatory properties of PDE-3 inhibitors have also been demonstrated in several studies involving patients with SAH, showing the potential to attenuate cerebral vasospasm [90][91][92]. Nevertheless, there is still a lack of extensive research on the impact of PDE-3 inhibitors on cerebral oxygenation.…”

Section: Cerebral Oxygenation Effectsmentioning

confidence: 99%

The Impact of Inotropes and Vasopressors on Cerebral Oxygenation in Patients with Traumatic Brain Injury and Subarachnoid Hemorrhage: A Narrative Review

Salvagno,

Geraldini,

Coppalini

et al. 2024

Brain Sciences

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Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are critical neurological conditions that necessitate specialized care in the Intensive Care Unit (ICU). Managing cerebral perfusion pressure (CPP) and mean arterial pressure (MAP) is of primary importance in these patients. To maintain targeted MAP and CPP, vasopressors and/or inotropes are commonly used. However, their effects on cerebral oxygenation are not fully understood. The aim of this review is to provide an up-to date review regarding the current uses and pathophysiological issues related to the use of vasopressors and inotropes in TBI and SAH patients. According to our findings, despite achieving similar hemodynamic parameters and CPP, the effects of various vasopressors and inotropes on cerebral oxygenation, local CBF and metabolism are heterogeneous. Therefore, a more accurate understanding of the cerebral activity of these medications is crucial for optimizing patient management in the ICU setting.

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Kinetics of cerebral blood flow velocities during treatment for delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage

Cited by 7 publications

References 31 publications

Cerebral Vasospasm After Subarachnoid Hemorrhage: Respective Short-Term Effects of Induced Arterial Hypertension and its Combination With IV Milrinone: A Proof-of-Concept Study Using Transcranial Doppler Ultrasound

Cerebral Vasospasm After Subarachnoid Hemorrhage: Respective Short-Term Effects of Induced Arterial Hypertension and its Combination With IV Milrinone: A Proof-of-Concept Study Using Transcranial Doppler Ultrasound

Hemodynamic response and clinical outcome following intravenous milrinone plus norepinephrine–based hyperdynamic hypertensive therapy in patients suffering secondary cerebral ischemia after aneurysmal subarachnoid hemorrhage

The Impact of Inotropes and Vasopressors on Cerebral Oxygenation in Patients with Traumatic Brain Injury and Subarachnoid Hemorrhage: A Narrative Review

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