Thromboelastometry as a Comprehensive Assessment of Hypercoagulation After Aneurysmal Subarachnoid Hemorrhage: A Case Report and Literature Review

Баранич, А И; Полупан, А. А.; Сычев, А А; Савин, И А; Tabasaranskiy, T F; Kurdumova, Natalia; Eliava, Shalva

doi:10.1007/978-3-030-04615-6_25

Cited by 6 publications

(5 citation statements)

References 24 publications

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Section: Delayed Platelet Activationmentioning

confidence: 99%

“…In the days following aneurysm securement, aSAH patients remain hypercoagulable which contributes to DCI. 8 More specifically, platelet reactivity is increased in aSAH patients who go on to develop DCI compared to aSAH patients who did not develop DCI. 9 Platelets coursing through the vasculature are subject to numerous activation signals released during in response to SAH (Figure 2).…”

Section: Delayed Platelet Activationmentioning

confidence: 99%

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Role of platelets in the pathogenesis of delayed injury after subarachnoid hemorrhage

Dienel

Blackburn

et al. 2021

J Cereb Blood Flow Metab

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Aneurysmal subarachnoid hemorrhage (aSAH) patients develop delayed cerebral ischemia and delayed deficits (DCI) within 2 weeks of aneurysm rupture at a rate of approximately 30%. DCI is a major contributor to morbidity and mortality after SAH. The cause of DCI is multi-factorial with contributions from microthrombi, blood vessel constriction, inflammation, and cortical spreading depolarizations. Platelets play central roles in hemostasis, inflammation, and vascular function. Within this review, we examine the potential roles of platelets in microthrombi formation, large artery vasospasm, microvessel constriction, inflammation, and cortical spreading depolarization. Evidence from experimental and clinical studies is provided to support the role(s) of platelets in each pathophysiology which contributes to DCI. The review concludes with a suggestion for future therapeutic targets to prevent DCI after aSAH.

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Section: Delayed Platelet Activationmentioning

confidence: 99%

Section: Delayed Platelet Activationmentioning

confidence: 99%

Role of platelets in the pathogenesis of delayed injury after subarachnoid hemorrhage

Dienel

Blackburn

et al. 2021

J Cereb Blood Flow Metab

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“…Platelets within the subarachnoid space are activated by numerous factors, including reactive microglia, dysfunctional endothelium, and other activated platelets [ 78 , 79 ] (See Figure 5 ). Activated platelets promote the endothelial release of von Willebrand factor and P-selectin expression, as well as the further release of inflammatory cytokines, creating a self-reinforcing inflammatory and procoagulant state [ 80 ].…”

Section: The Interplay Between Cortical Spreading Depolarization and ...mentioning

confidence: 99%

“…Thus, microthrombi formation plays an increasingly recognized role in DCI via both vascular compromise and amplification of inflammatory response and glutamate release [ 2 , 9 , 81 ]. A procoagulant state has been noted to precede DCI, correlating with higher thromboxane levels [ 78 ]. In one small study including 12 aneurysmal SAH patients, a persistent increase in platelet reactivity was described [ 82 ].…”

Section: The Interplay Between Cortical Spreading Depolarization and ...mentioning

confidence: 99%

Cortical Spreading Depolarization and Delayed Cerebral Ischemia; Rethinking Secondary Neurological Injury in Subarachnoid Hemorrhage

Mehra

Gomez

Bischof

et al. 2023

IJMS

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Poor outcomes in Subarachnoid Hemorrhage (SAH) are in part due to a unique form of secondary neurological injury known as Delayed Cerebral Ischemia (DCI). DCI is characterized by new neurological insults that continue to occur beyond 72 h after the onset of the hemorrhage. Historically, it was thought to be a consequence of hypoperfusion in the setting of vasospasm. However, DCI was found to occur even in the absence of radiographic evidence of vasospasm. More recent evidence indicates that catastrophic ionic disruptions known as Cortical Spreading Depolarizations (CSD) may be the culprits of DCI. CSDs occur in otherwise healthy brain tissue even without demonstrable vasospasm. Furthermore, CSDs often trigger a complex interplay of neuroinflammation, microthrombi formation, and vasoconstriction. CSDs may therefore represent measurable and modifiable prognostic factors in the prevention and treatment of DCI. Although Ketamine and Nimodipine have shown promise in the treatment and prevention of CSDs in SAH, further research is needed to determine the therapeutic potential of these as well as other agents.

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“…13 Studies have shown a hypercoagulable ROTEM-profile in aSAH patients compared to controls, already present early after ictus and worsening over time. [14][15][16][17][18][19] To date, two studies have evaluated ROTEM in DCI patients and showed hypercoagulability within 72 hours following SAH. 14,18,20 These studies evaluated group differences of a few ROTEM-parameters only, and were limited by small sample sizes, hampering determination of cut-off values.…”

Section: Introductionmentioning

confidence: 99%

The discriminative ability of ROTEM for Delayed Cerebral Ischemia and Poor Clinical Outcome following Aneurysmal Subarachnoid Haemorrhage

Tjerkstra,

Labib,

Coert

et al. 2023

Preprint

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IntroductionAneurysmal subarachnoid haemorrhage (aSAH) and delayed cerebral ischemia (DCI) have been associated with hypercoagulability as detected by viscoelastic testing. In this study, we evaluate temporal alterations in rotational thromboelastography (ROTEM-) coagulation profiles and the discriminative ability of ROTEM-parameters for DCI and poor clinical outcome following aSAH.Materials and MethodsROTEM-parameters were measured on days 0, 3-5 and 9-11 after aSAH and compared between patients with and without DCI, radiological DCI and 6-months’ poor clinical outcome (modified Rankin Scale 4-6). ROC-curve analyses were used to calculate areas-under-the-curve (AUC) and to determine optimal cut-off values with a sensitivity of >90% and highest possible specificity for DCI and radiological DCI. For poor outcome, a specificity >90% with highest possible sensitivity was used.ResultsOf 160 aSAH patients, 31 (19%) had DCI, 16 (10%) radiological DCI and 68 (44%) had poor outcome at six months. DCI, radiological DCI and poor clinical outcome were associated with hypercoagulability. The ROTEM-parameter with the best discriminative ability for radiological DCI was INTEM CT (AUC: 0.75), with optimal cut-off value <153 seconds (sensitivity 94%, specificity 59%). For poor outcome, this was FIBTEM A10, (AUC: 0.85), with optimal cut-off value >27 mm (specificity 94%, sensitivity 49%).ConclusionsHypercoagulability, as detected by ROTEM-parameters, is an excellent marker of poor clinical outcome after aSAH and might be useful for stratifying patients for inclusion in future trials on therapeutic interventions. Conversely, the absence of hypercoagulability on ROTEM may be used to identify patients at low risk of DCI for early hospital discharge.

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Thromboelastometry as a Comprehensive Assessment of Hypercoagulation After Aneurysmal Subarachnoid Hemorrhage: A Case Report and Literature Review

Cited by 6 publications

References 24 publications

Role of platelets in the pathogenesis of delayed injury after subarachnoid hemorrhage

Role of platelets in the pathogenesis of delayed injury after subarachnoid hemorrhage

Cortical Spreading Depolarization and Delayed Cerebral Ischemia; Rethinking Secondary Neurological Injury in Subarachnoid Hemorrhage

The discriminative ability of ROTEM for Delayed Cerebral Ischemia and Poor Clinical Outcome following Aneurysmal Subarachnoid Haemorrhage

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