2019Unpublished venueRequires access

Effect of Directional targeted soft channel intracranial hematoma drainage combined with autologous serum or urokinase in the treatment of hypertensive cerebral hemorrhage

Zhanbiao Li, Honglei Zhang, Zhu Chun-yan

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Abstract

Objective To explore the clinical effect of targeted soft channel intracranial hematoma drainage combined with urokinase and autologous serum on hypertensive cerebral hemorrhage. Methods Form October 2016 to October 2017, 120 patients with hypertensive cerebral hemorrhage were selected as the research objects in Handan First Hospital.In accordance with the principle of random number rule, they were divided into two groups, 60 cases in each group, the study group was given directional soft channel with autologous serum treatment, the control group was given directional soft channel joint urokinase for treatment of intracranial hematoma drainage, and then nerve function, clinical curative effect, inflammatory factors and endothelial function of two groups were compared. Results Before treatment, the National Institutes of HealthStroke Scale (NIHSS) score of the study group and the control group were (4.70±0.99) and (4.71±1.02), after treatment were (9.57±1.54) and (6.63±1.35), respectively.The difference between the two groups before treatment was not statistically significant (t=0.054, P=0.957). After treatment, the NIHSS scores of patients in both groups were significantly higher than those before treatment (Study group t=20.605, P=0.000, Control group t=8.790, P=0.000), The NIHSS score of the study group was significantly higher than that of the control group and the difference was statistically significant (t=11.120, P=0.000). Before treatment, Interleukin-6 (Il-6) in the study group and the control group were(45.61±4.13) ng/L and (44.98±2.19) ng/L, after treatment were (13.72±2.19) ng/L and (26.17±2.51) ng/L, respectively, and the two groups before treatment showed no significant difference (t=0.065, P=0.948). After treatment, IL-6 in both the study group and the control group decreased significantly (Study group t=52.841, P=0.000, Control group t=43.740, P=0.000), and IL-6 in the study group was significantly lower than that in the control group (t=28.951, P=0.000). Before treatment, the Tumor necrosis factor-α(TNF-α) of the study group and the control group were(63.01±4.22) μg/L and(62.96±4.21) μg/L, after treatment were(40.92±3.12) μg/L and(55.67±4.02) μg/L, respectively.The difference between the two groups before treatment was not statistically significant (t=0.065, P=0.948). TNF-α in both the study group and the control group significantly decreased after treatment (Study group t=32.604, P=0.000, Control group t=9.933, P=0.000). TNF-α in the study group was significantly lower than the control group (t=22.453, P=0.000). Before treatment, the nitric oxide of the study group and the control group were (33.46±4.27) μmol/L and(32.97±4.25) μmol/L, after treatment were(54.15±3.11) μmol/L and (43.17±3.22) μmol/L.No statistically significant difference was observed between the two groups before treatment (t=0.630, P=0.530). After treatment, nitric oxide was significantly increased in both the study group and the control group (Study group t=30.339, P=0.000, Control group t=14.818, P=0.000). Nitric oxide in the study group was significantly higher than that in the control group (t=18.999, P=0.000). Before treatment, the Endothelin-1 of the study group and the control group before and after treatment were (84.43±4.22) μg/L and (84.51±4.26) μg/L, after treatment were(57.47±5.07) μg/L and (70.14±5.12) μg/L.There was no statistically significant difference between the two groups before the treatment (t=0.335, P=0.738). After the treatment, endothelin-1 in both the study group and the control group was significantly reduced (Study group t=22.889, P=0.000, Control groupt=10.662, P=0.000), and endothelin-1 in the study group was significantly lower than that in the control group (t=9.226, P=0.000). The total effective rate of the study group after treatment was 88.33% (53/60), significantly higher than that of the control group (73.33%) (44/60). The difference between the two groups was statistically significant (χ2=4.357, P=0.037). Conclusion Targeted soft channel intracranial hematoma drainage combined with autologous serum was effective in the treatment of hypertensive cerebral hemorrhage, which is worthy of clinical application. Key words: Hypertensive; Cerebral hemorrhage; Directional soft channel intracranial hematoma drainage; Urokinase; Autologous serum

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Objective To explore the clinical effect of targeted soft channel intracranial hematoma drainage combined with urokinase and autologous serum on hypertensive cerebral hemorrhage. Methods Form October 2016 to October 2017, 120 patients with hypertensive cerebral hemorrhage were selected as the research objects in Handan First Hospital.In accordance with the principle of random number rule, they were divided into two groups, 60 cases in each group, the study group was given directional soft channel with autologous serum treatment, the control group was given directional soft channel joint urokinase for treatment of intracranial hematoma drainage, and then nerve function, clinical curative effect, inflammatory factors and endothelial function of two groups were compared. Results Before treatment, the National Institutes of HealthStroke Scale (NIHSS) score of the study group and the control group were (4.70±0.99) and (4.71±1.02), after treatment were (9.57±1.54) and (6.63±1.35), respectively.The difference between the two groups before treatment was not statistically significant (t=0.054, P=0.957). After treatment, the NIHSS scores of patients in both groups were significantly higher than those before treatment (Study group t=20.605, P=0.000, Control group t=8.790, P=0.000), The NIHSS score of the study group was significantly higher than that of the control group and the difference was statistically significant (t=11.120, P=0.000). Before treatment, Interleukin-6 (Il-6) in the study group and the control group were(45.61±4.13) ng/L and (44.98±2.19) ng/L, after treatment were (13.72±2.19) ng/L and (26.17±2.51) ng/L, respectively, and the two groups before treatment showed no significant difference (t=0.065, P=0.948). After treatment, IL-6 in both the study group and the control group decreased significantly (Study group t=52.841, P=0.000, Control group t=43.740, P=0.000), and IL-6 in the study group was significantly lower than that in the control group (t=28.951, P=0.000). Before treatment, the Tumor necrosis factor-α(TNF-α) of the study group and the control group were(63.01±4.22) μg/L and(62.96±4.21) μg/L, after treatment were(40.92±3.12) μg/L and(55.67±4.02) μg/L, respectively.The difference between the two groups before treatment was not statistically significant (t=0.065, P=0.948). TNF-α in both the study group and the control group significantly decreased after treatment (Study group t=32.604, P=0.000, Control group t=9.933, P=0.000). TNF-α in the study group was significantly lower than the control group (t=22.453, P=0.000). Before treatment, the nitric oxide of the study group and the control group were (33.46±4.27) μmol/L and(32.97±4.25) μmol/L, after treatment were(54.15±3.11) μmol/L and (43.17±3.22) μmol/L.No statistically significant difference was observed between the two groups before treatment (t=0.630, P=0.530). After treatment, nitric oxide was significantly increased in both the study group and the control group (Study group t=30.339, P=0.000, Control group t=14.818, P=0.000). Nitric oxide in the study group was significantly higher than that in the control group (t=18.999, P=0.000). Before treatment, the Endothelin-1 of the study group and the control group before and after treatment were (84.43±4.22) μg/L and (84.51±4.26) μg/L, after treatment were(57.47±5.07) μg/L and (70.14±5.12) μg/L.There was no statistically significant difference between the two groups before the treatment (t=0.335, P=0.738). After the treatment, endothelin-1 in both the study group and the control group was significantly reduced (Study group t=22.889, P=0.000, Control groupt=10.662, P=0.000), and endothelin-1 in the study group was significantly lower than that in the control group (t=9.226, P=0.000). The total effective rate of the study group after treatment was 88.33% (53/60), significantly higher than that of the control group (73.33%) (44/60). The difference between the two groups was statistically significant (χ2=4.357, P=0.037). Conclusion Targeted soft channel intracranial hematoma drainage combined with autologous serum was effective in the treatment of hypertensive cerebral hemorrhage, which is worthy of clinical application. Key words: Hypertensive; Cerebral hemorrhage; Directional soft channel intracranial hematoma drainage; Urokinase; Autologous serum

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Available abstract

Objective To explore the clinical effect of targeted soft channel intracranial hematoma drainage combined with urokinase and autologous serum on hypertensive cerebral hemorrhage. Methods Form October 2016 to October 2017, 120 patients with hypertensive cerebral hemorrhage were selected as the research objects in Handan First Hospital.In accordance with the principle of random number rule, they were divided into two groups, 60 cases in each group, the study group was given directional soft channel with autologous serum treatment, the control group was given directional soft channel joint urokinase for treatment of intracranial hematoma drainage, and then nerve function, clinical curative effect, inflammatory factors and endothelial function of two groups were compared. Results Before treatment, the National Institutes of HealthStroke Scale (NIHSS) score of the study group and the control group were (4.70±0.99) and (4.71±1.02), after treatment were (9.57±1.54) and (6.63±1.35), respectively.The difference between the two groups before treatment was not statistically significant (t=0.054, P=0.957). After treatment, the NIHSS scores of patients in both groups were significantly higher than those before treatment (Study group t=20.605, P=0.000, Control group t=8.790, P=0.000), The NIHSS score of the study group was significantly higher than that of the control group and the difference was statistically significant (t=11.120, P=0.000). Before treatment, Interleukin-6 (Il-6) in the study group and the control group were(45.61±4.13) ng/L and (44.98±2.19) ng/L, after treatment were (13.72±2.19) ng/L and (26.17±2.51) ng/L, respectively, and the two groups before treatment showed no significant difference (t=0.065, P=0.948). After treatment, IL-6 in both the study group and the control group decreased significantly (Study group t=52.841, P=0.000, Control group t=43.740, P=0.000), and IL-6 in the study group was significantly lower than that in the control group (t=28.951, P=0.000). Before treatment, the Tumor necrosis factor-α(TNF-α) of the study group and the control group were(63.01±4.22) μg/L and(62.96±4.21) μg/L, after treatment were(40.92±3.12) μg/L and(55.67±4.02) μg/L, respectively.The difference between the two groups before treatment was not statistically significant (t=0.065, P=0.948). TNF-α in both the study group and the control group significantly decreased after treatment (Study group t=32.604, P=0.000, Control group t=9.933, P=0.000). TNF-α in the study group was significantly lower than the control group (t=22.453, P=0.000). Before treatment, the nitric oxide of the study group and the control group were (33.46±4.27) μmol/L and(32.97±4.25) μmol/L, after treatment were(54.15±3.11) μmol/L and (43.17±3.22) μmol/L.No statistically significant difference was observed between the two groups before treatment (t=0.630, P=0.530). After treatment, nitric oxide was significantly increased in both the study group and the control group (Study group t=30.339, P=0.000, Control group t=14.818, P=0.000). Nitric oxide in the study group was significantly higher than that in the control group (t=18.999, P=0.000). Before treatment, the Endothelin-1 of the study group and the control group before and after treatment were (84.43±4.22) μg/L and (84.51±4.26) μg/L, after treatment were(57.47±5.07) μg/L and (70.14±5.12) μg/L.There was no statistically significant difference between the two groups before the treatment (t=0.335, P=0.738). After the treatment, endothelin-1 in both the study group and the control group was significantly reduced (Study group t=22.889, P=0.000, Control groupt=10.662, P=0.000), and endothelin-1 in the study group was significantly lower than that in the control group (t=9.226, P=0.000). The total effective rate of the study group after treatment was 88.33% (53/60), significantly higher than that of the control group (73.33%) (44/60). The difference between the two groups was statistically significant (χ2=4.357, P=0.037). Conclusion Targeted soft channel intracranial hematoma drainage combined with autologous serum was effective in the treatment of hypertensive cerebral hemorrhage, which is worthy of clinical application. Key words: Hypertensive; Cerebral hemorrhage; Directional soft channel intracranial hematoma drainage; Urokinase; Autologous serum

Key concepts: Medicine, Urokinase, Hematoma, Surgery, Intracranial hematoma, Anesthesia

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Effect of Directional targeted soft channel intracranial hematoma drainage combined with autologous serum or urokinase in the treatment of hypertensive cerebral hemorrhage — Research Paper | ScholarLens