Early and Severe Symptomatic Cerebral Vasospasm After Mild Traumatic Brain Injury

Ogami, Kyle; Dofredo, Melissa; Moheet, Asma M.; Lahiri, Shouri

doi:10.1016/j.wneu.2017.03.039

Cited by 12 publications

(8 citation statements)

References 8 publications

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“…Studies have also shown that the prevalence of cerebral vasospasm may be >50% during EITs, which can result in intracranial hypertension and cerebral ischemia. Eventually, cerebral vasospasm could increase the risk of postoperative complications and shorten the survival time of patients (Andereggen et al, ; Ogami et al, ). Hence, several methods have been adopted to reduce the risk of this complication.…”

Section: Discussionmentioning

confidence: 99%

“…We also recorded the requirement of narcotic and vasoactive drugs, prevalence of complications and symptomatic cerebral vasospasm (the positive findings on transcranial Doppler (TCD) examination as a maximum flow velocity >200 cm/s or a mean flow velocity >120 cm/s at M1) (Ogami, Dofredo, Moheet, & Lahiri, ), duration of PACU stay and hospitalization, patients and surgeon satisfaction scores (on a 10‐point scale where 0 = poor, and 10 = excellent), (Berkhemer et al, ; McDonagh et al, ) GOS at 3 months, and prevalence of cerebral infarction 30 days after surgery.…”

Section: Methodsmentioning

confidence: 99%

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Effect of intraoperative infusion of dexmedetomidine on postoperative recovery in patients undergoing endovascular interventional therapies: A prospective, randomized, controlled trial

Ren

et al. 2019

Brain and Behavior

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Background Rapid emergence from general anesthesia during endovascular interventional therapies (EITs) is important. However, the solution that improved quality of both analepsia and postoperative recovery after EITs has not been specifically addressed. We conducted this prospective, randomized, controlled trial to evaluate the intraoperative infusion of dexmedetomidine on quality of analepsia and postoperative recovery in patients undergoing EITs. Methods Eighty‐six patients undergoing EITs were divided into three groups: RD1 (dexmedetomidine at an initial dose of 0.5 μg/kg for 10 min adjusted to 0.2 μg kg−1 hr−1 throughout EIT), RD2 (dexmedetomidine at an initial dose of 0.5 μg/kg for 10 min adjusted to 0.4 μg kg−1 hr−1 throughout EIT), and RD3 (dexmedetomidine at an initial dose of 0.5 μg/kg for 10 min adjusted to 0.6 μg kg−1 hr−1 throughout EIT). An analgesia system delivered sufentanil only. The primary outcome measure was the total consumption of nimodipine during the first 48 hr after surgery. The secondary outcome measures were sufentanil consumption, pain intensity, hemodynamics, functional activity score (FAS), neurologic examination, level of sedation (LOS), and Bruggrmann comfort scale (BCS). We also recorded the intraoperative hemodynamic data, requirement of narcotic and vasoactive drugs, prevalence of complications and symptomatic cerebral vasospasm, duration of postanesthesia care unit (PACU) stay, Glasgow Outcome Score (GOS) at 3 months, and prevalence of cerebral infarction 30 days after surgery. Results Dexmedetomidine application in the regimen RD3 reduced the consumption of the total dose of nimodipine and sufentanil 48 hr after surgery, prevalence of symptomatic cerebral vasospasm, consumption of narcotic drugs and nimodipine during surgery, pain intensity during the first 8 hr after surgery, and increased both BCS during the first 4 hr after surgery and hemodynamic stability. However, the LOS was increased at the 0.5 hr after surgery and surgeon satisfaction score was lower. There were no significant differences among the groups for consumption of vasoactive drugs except urapidil, Glasgow coma scale (GCS) and FAS during the first 48 hr after surgery, GOS at 3 months, and cerebral infarction after 30 days. Conclusions Dexmedetomidine (an initial dose of 0.5 μg/kg for 10 min adjusted to 0.6 μg kg−1 hr−1 throughout EIT) could reduce the total consumption of nimodipine and opioid during the first 48 hr after surgery, the concerning adverse effects, and improve pain scores. The optimal dosage of dexmedetomidine during EITs merits further investigation.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Effect of intraoperative infusion of dexmedetomidine on postoperative recovery in patients undergoing endovascular interventional therapies: A prospective, randomized, controlled trial

Ren

et al. 2019

Brain and Behavior

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“…The acute management of traumatic brain injury is usually focused on preventing hematoma expansion and reducing intracranial pressure. However, there have been many reports of delayed cerebral hypoperfusion leading to ischemic damage [10][11][12][13] . Previous studies have reported that cerebral vasospasm occurs frequently after T-SAH [1][2][3]5,14) .…”

Section: Discussionmentioning

confidence: 99%

Cerebral Vasospasm After Traumatic Subarachnoid Hemorrhage and Its Risk Factor: Combined Periodic Follow Up of Transcranial Doppler and CT Angiography

Lee

Kim

et al. 2023

J Neurointensive Care

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Background: Cerebral vasospasm is a prevalent complication in traumatic brain injury (TBI), particularly in cases of traumatic subarachnoid hemorrhage (T-SAH), for which monitoring and treatment policies remain undefined.Methods: A study was conducted on 49 T-SAH patients with multiple traumas to investigate cerebral vasospasm following T-SAH. Participants underwent transcranial doppler (TCD) and brain CT angiography (CTA) upon hospitalization and subsequent follow-up within seven days. Vasospasm was diagnosed through a comprehensive evaluation of TCD, CTA, and symptoms, with risk factors analyzed accordingly. The initial clinical status was assessed using the Glasgow Coma Scale (GCS), modified Fisher scale (mFS), and Hunt-Hess grade (HHG), while examining various factors to identify underlying risks and evaluating overall body damage via the Injury Severity Score (ISS).Results: Cerebral vasospasm was confirmed in 19 out of the total 49 patients, which is 38.8%. Furthermore, the characteristics that had a statistically significant correlation with the vasospasm group were low GCS (p=0.03, odd ratio=0.592) and high ISS (p=0.022, odd ratio=1.124). Moreover, patients with vasospasm exhibited worse prognoses based on the Glasgow Outcome Scale (GOS) and modified Rankin Scale (mRS).Conclusion: These findings suggest that T-SAH patients with severe initial brain and systemic damage or neurological deficits should undergo active monitoring using modalities such as TCD and CTA, followed by treatment to prevent and manage vasospasm.

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“…The mechanism of mTBI-induced decrease in cerebral blood flow may involve vasospasm, edema, and neuroinflammation. A body of studies have reported post-TBI vasospasm (Kramer et al, 2013;Fehnel et al, 2014;Perrein et al, 2015;Ogami et al, 2017). In severe TBI, post-traumatic vasospasm is detected in 30-40% of patients (Perrein et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

In vivo Two-Photon Imaging Reveals Acute Cerebral Vascular Spasm and Microthrombosis After Mild Traumatic Brain Injury in Mice

et al. 2020

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Mild traumatic brain injury (mTBI), or concussion, is reported to interfere with cerebral blood flow and microcirculation in patients, but our current understanding is quite limited and the results are often controversial. Here we used longitudinal in vivo twophoton imaging to investigate dynamic changes in cerebral vessels and velocities of red blood cells (RBC) following mTBI. Closed-head mTBI induced using a controlled cortical impact device resulted in a significant reduction of dwell time in a Rotarod test but no significant change in water maze test. Cerebral blood vessels were repeatedly imaged through a thinned skull window at baseline, 0.5, 1, 6 h, and 1 day following mTBI. In both arterioles and capillaries, their diameters and RBC velocities were significantly decreased at 0.5, 1, and 6 h after injury, and recovered in 1 day post-mTBI. In contrast, decreases in the diameter and RBC velocity of venules occurred only in 0.5-1 h after mTBI. We also observed formation and clearance of transient microthrombi in capillaries within 1 h post-mTBI. We concluded that in vivo two-photon imaging is useful for studying earlier alteration of vascular dynamics after mTBI and that mTBI induced reduction of cerebral blood flow, vasospasm, and formation of microthrombi in the acute stage following injury. These changes may contribute to early brain functional deficits of mTBI.

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Early and Severe Symptomatic Cerebral Vasospasm After Mild Traumatic Brain Injury

Cited by 12 publications

References 8 publications

Effect of intraoperative infusion of dexmedetomidine on postoperative recovery in patients undergoing endovascular interventional therapies: A prospective, randomized, controlled trial

Effect of intraoperative infusion of dexmedetomidine on postoperative recovery in patients undergoing endovascular interventional therapies: A prospective, randomized, controlled trial

Cerebral Vasospasm After Traumatic Subarachnoid Hemorrhage and Its Risk Factor: Combined Periodic Follow Up of Transcranial Doppler and CT Angiography

In vivo Two-Photon Imaging Reveals Acute Cerebral Vascular Spasm and Microthrombosis After Mild Traumatic Brain Injury in Mice

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