Cerebral vasospasm and delayed cerebral infarctions in 225 patients with non-aneurysmal subarachnoid hemorrhage: the underestimated risk of Fisher 3 blood distribution

Konczalla, Juergen; Kashefiolasl, Sepide; Brawanski, Nina; Lescher, Stephanie; Senft, Christian; Platz, Johannes; Seifert, Volker

doi:10.1136/neurintsurg-2015-012153

Cited by 35 publications

(25 citation statements)

References 31 publications

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“…Only one patient in group D2 had hypotension in this trial, and the differences among the three groups did not reach statistical significance. The incidence of hypotension in group D2 was lower than that of the previous study, which may be attributed to the lower consumption of nimodipine and the synergistic effects of nimodipine and dexmedetomidine (Konczalla et al, 2016). Dexmedetomidine, a new highly selective agonist of α2 adrenergic receptor, is widely used in neurosurgery such as craniotomy, CEA for sedation, analgesia, and low risk of respiratory depression.…”

Section: Discussioncontrasting

confidence: 60%

“…33.7% of patients with SAH have an unfavorable outcome because of cerebral vasospasm caused by an increase of calcium level in the vascular smooth muscle cells. However, the percentage of patients with unfavorable outcome has been underestimated in many studies due to the exclusion of patients who die before treatment (Konczalla et al, 2016). Here, we only recorded the incidence of symptomatic cerebral vasospasm 7 days after surgery since the highest risk period for cerebral vasospasm usually occurs 3–14 days after aSAH and the duration of discharge after surgery was within 8 days for most patients in our center (Oertel et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

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The Nimodipine-Sparing Effect of Perioperative Dexmedetomidine Infusion During Aneurysmal Subarachnoid Hemorrhage: A Prospective, Randomized, Controlled Trial

Ren

Gao

et al. 2019

Front. Pharmacol.

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Background: Nimodipine can block the influx of calcium into the vascular smooth muscle cell and prevent secondary ischemia in patients with aneurysmal subarachnoid hemorrhage. However, the reduction of blood pressure after long-term intravenous administration of nimodipine has been associated with neurological deterioration. Yet, no effective solutions have been suggested to address this phenomenon. The use of neuroprotective drug combinations may reduce the risk of sudden blood pressure loss. This prospective, randomized, controlled trial was performed to evaluate the nimodipine-sparing effect of perioperative dexmedetomidine infusion during aneurysmal subarachnoid hemorrhage. Methods: One hundred nine patients who underwent aneurysm embolization were divided into three groups: group C ( n = 35, infused with 0.9% sodium chloride at the same rate as other two groups), group D1 ( n = 38, dexmedetomidine infusion at 0.5 µg·kg –1 for 10 min, then adjusted to 0.2 µg·kg –1 ·h –1 ), and group D2 ( n = 36, dexmedetomidine infusion at 0.5 µg·kg –1 for 10 min, then adjusted to 0.4 µg·kg –1 ·h –1 ). Patient-controlled analgesia was given for 48 h after surgery. The primary outcome measure was the total consumption of nimodipine during the first 48 h after surgery. The secondary outcome measures were recovery time at post-anesthesia care unit (PACU), postoperative pain intensity scores, dexmedetomidine and sufentanil consumption, hemodynamic, satisfaction of patients and neurosurgeon, neurologic examination (Glasgow Coma Scale, GCS), Bruggemann comfort scale, and adverse effects. Intraoperative hemodynamics were recorded at the following time-points: arrival at the operating room (T1); before intubation (T2); intubation (T3); 5 min (T4), 10 min (T5), and 15 min (T6) after intubation; suturing of femoral artery (T7); end of surgery (T8); extubation (T9); and 5 min (T10), 10 min (T11), and 15 min (T12) after arrival at the PACU. The level of sedation was recorded at 15 min, 30 min, 1 h, and 2 h after extubation. We also recorded the incidence of symptomatic cerebral vasospasm during 7 days after surgery, Glasgow Outcome Score (GOS) at 3 months, and incidence of cerebral infarction 30 days after surgery. Results: The consumption of nimodipine during the first 48 h after surgery was significantly lower in group D2 ( P < 0.05). Compared with group C, HR and MAP were significantly decreased from T2 to T12 in group D1 and D2 ( P < 0.05). Patients in group D2 showed a significantly decreased MAP from T5 to T9 compared with group D1 ( P < 0.05). The consumption of sevoflurane, remifentanil, dexmedetomidine, and nimodipine were all significantly reduced in groups D1 and D2 during surgery ( ...

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Section: Discussioncontrasting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

The Nimodipine-Sparing Effect of Perioperative Dexmedetomidine Infusion During Aneurysmal Subarachnoid Hemorrhage: A Prospective, Randomized, Controlled Trial

Ren

Gao

et al. 2019

Front. Pharmacol.

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“…1). Of these, 19 were prospective [1, 2, 9, 10, 20, 21, 32, 38, 39, 41–44, 47, 48, 50, 51, 53, 54], 37 were retrospective [4, 6–8, 12–15, 17, 24, 25, 27, 28, 30, 31, 34–36, 40, 57, 58, 61, 63, 66–69, 71–76, 78, 80–82] and two studies [11, 52] had both prospective and retrospective data (Table e-1). Quality assessment results are summarised in Fig.…”

Section: Resultsmentioning

confidence: 99%

Subarachnoid haemorrhage with negative initial neurovascular imaging: a systematic review and meta-analysis

et al. 2019

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BackgroundIn patients with spontaneous subarachnoid haemorrhage (SAH), a vascular cause for the bleed is not always found on initial investigations. This study aimed to systematically evaluate the delayed investigation strategies and clinical outcomes in these cases, often described as “non-aneurysmal” SAH (naSAH).MethodsA systematic review was performed in concordance with the PRISMA checklist. Pooled proportions of primary outcome measures were estimated using a random-effects model.ResultsFifty-eight studies were included (4473 patients). The cohort was split into perimesencephalic naSAH (PnaSAH) (49.9%), non-PnaSAH (44.7%) and radiologically negative SAH identified on lumbar puncture (5.4%). The commonest initial vascular imaging modality was digital subtraction angiography. A vascular abnormality was identified during delayed investigation in 3.9% [95% CI 1.9–6.6]. There was no uniform strategy for the timing or modality of delayed investigations. The pooled proportion of a favourable modified Rankin scale outcome (0–2) at 3–6 months following diagnosis was 92.0% [95% CI 86.0–96.5]. Complications included re-bleeding (3.1% [95% CI 1.5–5.2]), hydrocephalus (16.0% [95% CI 11.2–21.4]), vasospasm (9.6% [95% CI 6.5–13.3]) and seizure (3.5% [95% CI 1.7–5.8]). Stratified by bleeding pattern, we demonstrate a higher rate of delayed diagnoses (13.6% [95% CI 7.4–21.3]), lower proportion of favourable functional outcome (87.2% [95% CI 80.1–92.9]) and higher risk of complications for non-PnaSAH patients.ConclusionThis study highlights the heterogeneity in delayed investigations and outcomes for patients with naSAH, which may be influenced by the initial pattern of bleeding. Further multi-centre prospective studies are required to clarify optimal tailored management strategies for this heterogeneous group of patients.Electronic supplementary materialThe online version of this article (10.1007/s00701-019-04025-w) contains supplementary material, which is available to authorized users.

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“…It is a serious complication often experienced by aneurysmal SAH survivors [ 43 , 44 ]. If CV persists, insufficient blood flow reaches affected regions of the brain, causing delayed cerebral ischemia [ 45 ]. CV is characterized by progressive narrowing of cerebral arteries beginning no earlier than day three following hemorrhage and peaking at one week [ 46 ].…”

Section: Secondary Outcomesmentioning

confidence: 99%

Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review

Lucke‐Wold

Logsdon

Manoranjan³

et al. 2016

IJMS

249

181

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Aneurysmal subarachnoid hemorrhage (SAH) can lead to devastating outcomes including vasospasm, cognitive decline, and even death. Currently, treatment options are limited for this potentially life threatening injury. Recent evidence suggests that neuroinflammation plays a critical role in injury expansion and brain damage. Red blood cell breakdown products can lead to the release of inflammatory cytokines that trigger vasospasm and tissue injury. Preclinical models have been used successfully to improve understanding about neuroinflammation following aneurysmal rupture. The focus of this review is to provide an overview of how neuroinflammation relates to secondary outcomes such as vasospasm after aneurysmal rupture and to critically discuss pharmaceutical agents that warrant further investigation for the treatment of subarachnoid hemorrhage. We provide a concise overview of the neuroinflammatory pathways that are upregulated following aneurysmal rupture and how these pathways correlate to long-term outcomes. Treatment of aneurysm rupture is limited and few pharmaceutical drugs are available. Through improved understanding of biochemical mechanisms of injury, novel treatment solutions are being developed that target neuroinflammation. In the final sections of this review, we highlight a few of these novel treatment approaches and emphasize why targeting neuroinflammation following aneurysmal subarachnoid hemorrhage may improve patient care. We encourage ongoing research into the pathophysiology of aneurysmal subarachnoid hemorrhage, especially in regards to neuroinflammatory cascades and the translation to randomized clinical trials.

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Cerebral vasospasm and delayed cerebral infarctions in 225 patients with non-aneurysmal subarachnoid hemorrhage: the underestimated risk of Fisher 3 blood distribution

Cited by 35 publications

References 31 publications

The Nimodipine-Sparing Effect of Perioperative Dexmedetomidine Infusion During Aneurysmal Subarachnoid Hemorrhage: A Prospective, Randomized, Controlled Trial

The Nimodipine-Sparing Effect of Perioperative Dexmedetomidine Infusion During Aneurysmal Subarachnoid Hemorrhage: A Prospective, Randomized, Controlled Trial

Subarachnoid haemorrhage with negative initial neurovascular imaging: a systematic review and meta-analysis

Aneurysmal Subarachnoid Hemorrhage and Neuroinflammation: A Comprehensive Review

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