Gross-total hematoma removal of hypertensive basal ganglia hemorrhages: a long-term follow-up.
OBJECTIVE
Hypertensive basal ganglia hemorrhage (HBGH) accounts for 35%-44% of cases of hypertensive intracranial hemorrhage (ICH), which is one of the most devastating forms of cerebrovascular disease. In this study, intracerebral hematoma was evacuated with a burr hole craniectomy. The relationships of residue hematoma volume to brain edema, inflammation factors and the long-term prognosis of HBGH patients were studied.


METHODS
One hundred and seventy-six patients with HBGH were randomly divided into gross-total removal of hematoma (GTRH) and sub-total removal of hematoma (STRH) groups. The pre-operative and post-operative data of the patients in the two groups were compared. The pre-operative data included age, sex, hematoma volume, time from the ictus to the operation, Glasgow Coma Scale (GCS) scores, and the European Stroke Scale (ESS) scores. The post-operative information included edema grade, level of thromboxane B2 (TXB2), 6-keto-prostaglandin F1a (6-K-PGF1a), tumor necrosis factor-a (TNF-a) and endothelin (ET) in hematoma drainage or cerebral spinal fluid (CSF), ESS and Barthel Index (BI).


RESULTS
There was no statistical difference between the two groups (P>0.05) in the pre-operative data. The levels of TXB2, 6-K-PGF1a, TNF-a and ET in the GTRH group were significantly lower than those in the STRH group at different post-operative times. The ESS in the GTRH group increased rapidly after the operation and was higher than that in the STRH group. There was a significant difference between the two groups (P<0.05). The post-operative CT scan at different times showed that the brain edema grades were better in the GTRH group than in the STRH group. The BI was higher in the GTRH group than in the STRH group (P<0.05).


CONCLUSIONS
GTRH is an effective method to decrease ICH-induced injury to brain tissue. Such effect is related to decreased perihematomal edema formation and secondary injury by coagulation end products activated inflammatory cascade.
Zuo
Yi
Y
Department of Neurosurgery, Xijing Hospital of the Fourth Military Medical University, Xi'an, China.
Cheng
Gang
G
Gao
Da-Kuan
DK
Zhang
Xiang
X
Zhen
Hai-Ning
HN
Zhang
Wei
W
Xiao
San-Chao
SC
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis / Q000097:blood / Q000134:cerebrospinal fluid; D000368:Aged; D020145:Basal Ganglia Hemorrhage / Q000150:complications / Q000503:physiopathology* / Q000601:surgery*; D015415:Biomarkers / Q000032:analysis / Q000097:blood / Q000134:cerebrospinal fluid; D001929:Brain Edema / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D018450:Disease Progression; D004660:Encephalitis / Q000209:etiology / Q000503:physiopathology*; D016232:Endothelins / Q000032:analysis / Q000097:blood / Q000134:cerebrospinal fluid; D005260:Female; D005500:Follow-Up Studies; D015600:Glasgow Coma Scale; D006801:Humans; D006973:Hypertension / Q000150:complications*; D018836:Inflammation Mediators / Q000032:analysis / Q000097:blood / Q000134:cerebrospinal fluid; D008297:Male; D008875:Middle Aged; D019635:Neurosurgical Procedures / Q000379:methods; D011183:Postoperative Complications / Q000209:etiology / Q000503:physiopathology; D011237:Predictive Value of Tests; D011379:Prognosis; D013929:Thromboxane B2 / Q000032:analysis / Q000097:blood / Q000134:cerebrospinal fluid; D013997:Time Factors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000097:blood / Q000134:cerebrospinal fluid
D015415:Biomarkers; D016232:Endothelins; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha