Abstract T P355: Dobutamine versus Mirlinone for Intensive Hemodynamic Augmentation to Relieve Clinical Delayed Cerebral Ischemia after Subarachnoid Hemorrhage

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Tatsushi Mutoh ◽  
Tatsuya Ishikawa ◽  
Ken Kazumata ◽  
Keigo Matsumoto ◽  
Yasuyuki Taki ◽  
...  

Intensive hemodynamic augmentation by increasing cardiac output (CO) is a valuable method of elevating cerebral blood flow and oxygenation in the dysautoregulated vascular territories after subarachnoid hemorrhage (SAH). We prospectively assessed the effect of hyperdynamic therapy with dobutamine (DOB) or milrinone (MIL) on regional cerebral oxygenation (rSO 2 ) for reversing clinical deterioration induced by delayed cerebral ischemia, using an integrative monitoring with uncalibrated pulse contour CO analysis and multi-channel near-infrared spectroscopy. One-hundred ten SAH patients diagnosed to have clinical deterioration due to delayed cerebral ischemia were assigned to receive hemodynamic augmentation with DOB or MIL (n=56 per each group). For hyperdynamic therapy, each inotrope was initiated at low dose (DOB: 3μg/kg/min; MIL 0.15μg/kg/min) and then increased in each dose increment until resolution of the symptoms unless any adverse effects occur during the therapy, based on our predefined hemodynamic regimen to induce similar dose-related increase in CO. Real-time CO and rSO 2 changes in conjunction with the assessment of neurological improvements were compared. A total of 425 dose increment challenges (DOB, n=197; MIL, n=228) were performed. In spasm-affected territories, decreased and/or fluctuating rSO 2 was detected compared with recordings in other brain region. Patients who exhibited rapid elevation of CO by each challenge had subsequent uptake and stabilization of rSO 2 . The responses (total number and degree of neurological improvements) were more significant in patients treated with DOB than those treated with MIL ( P < 0.05), although tachycardia that may affect stroke volume depression during the DOB therapy was more evident (DOB 28% vs. MIL 9%). Area under the ROC curve to predict rSO 2 elevation or neurological improvement for both drug groups were significant ( P < 0.0001) and the values were significantly greater in DOB than in MIL ( P < 0.05). In conclusion, DOB can provide more effective hemodynamic augmentation in relieving focal cerebral ischemia in patients after SAH. MIL is also effective in the hyperdynamic therapy but may be used as a second line in a patient subgroup when DOB was contraindicated.

Stroke ◽  
2009 ◽  
Vol 40 (11) ◽  
pp. 3493-3498 ◽  
Author(s):  
Jan Willem Dankbaar ◽  
Nicolien K. de Rooij ◽  
Birgitta K. Velthuis ◽  
Catharina J.M. Frijns ◽  
Gabriel J.E. Rinkel ◽  
...  

2020 ◽  
Vol 9 (5) ◽  
pp. 1595
Author(s):  
Jeong Jin Park ◽  
Chulho Kim ◽  
Jin Pyeong Jeon

We investigated the role of near infrared spectroscopy (NIRS) in identifying delayed cerebral ischemia (DCI) in patients with subarachnoid hemorrhage (SAH). We measured the cerebral regional oxygen saturation (rSO2) continuously for 14 days. The differences in rSO2 according to DCI were analyzed. We also compared the diagnostic accuracy of NIRS and transcranial Doppler ultrasonography (TCD) for DCI detection using the area under receiver operator characteristic (ROC) curve. Fifty-two patients treated with coil embolization were enrolled, including 18 with DCI (34.6%) and 34 without DCI (65.4%). Significant differences in rSO2 levels were observed from days 7 to 9. The rSO2 level was 60.95 (58.10–62.30) at day 7 in the DCI vs. 63.90 (62.50–67.10) in the non-DCI patients. By day 8, it was 59.50 (56.90–64.50) in the DCI vs. 63.30 (59.70–68.70) in the non-DCI cases. By day 9, it was 61.85 (59.40–65.20) in the DCI vs. 66.00 (62.70–68.30) in the non-DCI. A decline of >12.7% in SO2 rate yielded a sensitivity of 94.44% (95% CI: 72.7–99.9%) and a specificity of 70.59% (95% CI: 52.5–84.9%) for identifying DCI. Changes in NIRS tended to yield better diagnostic accuracy than TCD, but were not statistically significant. NIRS is a feasible method for real-time detection of DCI.


Neurosurgery ◽  
2009 ◽  
Vol 65 (2) ◽  
pp. 316-324 ◽  
Author(s):  
Emmanuel Carrera ◽  
J. Michael Schmidt ◽  
Mauro Oddo ◽  
Luis Fernandez ◽  
Jan Claassen ◽  
...  

Abstract OBJECTIVE Transcranial Doppler (TCD) is widely used to monitor the temporal course of vasospasm after subarachnoid hemorrhage (SAH), but its ability to predict clinical deterioration or infarction from delayed cerebral ischemia (DCI) remains controversial. We sought to determine the prognostic utility of serial TCD examination after SAH. METHODS We analyzed 1877 TCD examinations in 441 aneurysmal SAH patients within 14 days of onset. The highest mean blood flow velocity (mBFV) value in any vessel before DCI onset was recorded. DCI was defined as clinical deterioration or computed tomographic evidence of infarction caused by vasospasm, with adjudication by consensus of the study team. Logistic regression was used to calculate adjusted odds ratios for DCI risk after controlling for other risk factors. RESULTS DCI occurred in 21% of patients (n = 92). Multivariate predictors of DCI included modified Fisher computed tomographic score (P = 0.001), poor clinical grade (P = 0.04), and female sex (P = 0.008). After controlling for these variables, all TCD mBFV thresholds between 120 and 180 cm/s added a modest degree of incremental predictive value for DCI at nearly all time points, with maximal sensitivity by SAH day 8. However, the sensitivity of any mBFV more than 120 cm/s for subsequent DCI was only 63%, with a positive predictive value of 22% among patients with Hunt and Hess grades I to III and 36% in patients with Hunt and Hess grades IV and V. Positive predictive value was only slightly higher if mBFV exceeded 180 cm/s. CONCLUSION Increased TCD flow velocities imply only a mild incremental risk of DCI after SAH, with maximal sensitivity by day 8. Nearly 40% of patients with DCI never attained an mBFV more than 120 cm/s during the course of monitoring. Given the poor overall sensitivity of TCD, improved methods for identifying patients at high risk for DCI after SAH are needed.


2016 ◽  
Vol 37 (5) ◽  
pp. 1829-1840 ◽  
Author(s):  
Fumiaki Oka ◽  
Ulrike Hoffmann ◽  
Jeong Hyun Lee ◽  
Hwa Kyoung Shin ◽  
David Y Chung ◽  
...  

Spontaneous spreading depolarizations are frequent after various forms of human brain injury such as ischemic or hemorrhagic stroke and trauma, and worsen the outcome. We have recently shown that supply-demand mismatch transients trigger spreading depolarizations in ischemic stroke. Here, we examined the mechanisms triggering recurrent spreading depolarization events for many days after subarachnoid hemorrhage. Despite large volumes of subarachnoid hemorrhage induced by cisternal injection of fresh arterial blood in rodents, electrophysiological recordings did not detect a single spreading depolarization for up to 72 h after subarachnoid hemorrhage. Cortical susceptibility to spreading depolarization, measured by direct electrical stimulation or topical KCl application, was suppressed after subarachnoid hemorrhage. Focal cerebral ischemia experimentally induced after subarachnoid hemorrhage revealed a biphasic change in the propensity to develop peri-infarct spreading depolarizations. Frequency of peri-infarct spreading depolarizations decreased at 12 h, increased at 72 h and normalized at 7 days after subarachnoid hemorrhage compared with sham controls. However, ischemic tissue and neurological outcomes were significantly worse after subarachnoid hemorrhage even when peri-infarct spreading depolarization frequency was reduced. Laser speckle flowmetry implicated cerebrovascular hemodynamic mechanisms worsening the outcome. Altogether, our data suggest that cerebral ischemia is required for spreading depolarizations to be triggered after subarachnoid hemorrhage, which then creates a vicious cycle leading to the delayed cerebral ischemia syndrome.


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