Gross-total hematoma removal of hypertensive basal ganglia hemorrhages: A long-term follow-up

BACKGROUND AND PURPOSE 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.

[1]  L. Schilling,et al.  Clazosentan, an endothelin receptor antagonist, prevents early hypoperfusion during the acute phase of massive experimental subarachnoid hemorrhage: a laser Doppler flowmetry study in rats. , 2008, Journal of neurosurgery.

[2]  M. D. Del Bigio,et al.  Antisense Oligodeoxynucleotide Inhibition of Tumor Necrosis Factor-&agr; Expression Is Neuroprotective After Intracerebral Hemorrhage , 2001, Stroke.

[3]  J. Broderick,et al.  Relative Edema Volume Is a Predictor of Outcome in Patients With Hyperacute Spontaneous Intracerebral Hemorrhage , 2002, Stroke.

[4]  S M Davis,et al.  Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage , 2006, Neurology.

[5]  G. Ling,et al.  Quantitative analysis of injured, necrotic, and apoptotic cells in a new experimental model of intracerebral hemorrhage , 2001, Critical care medicine.

[6]  A. Mendelow,et al.  Surgery in Intracerebral Hemorrhage: The Uncertainty Continues , 2000, Stroke.

[7]  O. Sakowitz,et al.  Serial diffusion and perfusion MRI analysis of the perihemorrhagic zone in a rat ICH model. , 2008, Acta neurochirurgica. Supplement.

[8]  Seung-Up Kim,et al.  Anti-inflammatory mechanism of intravascular neural stem cell transplantation in haemorrhagic stroke. , 2008, Brain : a journal of neurology.

[9]  R. Keep,et al.  Iron-induced oxidative brain injury after experimental intracerebral hemorrhage. , 2006, Acta neurochirurgica. Supplement.

[10]  T. Schallert,et al.  Long-term effects of experimental intracerebral hemorrhage: the role of iron. , 2006, Journal of neurosurgery.

[11]  A. Fleischer,et al.  Plasma 6-keto prostaglandin F1α and thromboxane B2 in sick preterm neonates , 1985 .

[12]  D. Graham,et al.  Experimental intracerebral hemorrhage: early removal of a spontaneous mass lesion improves late outcome. , 1990, Neurosurgery.

[13]  M. Yenari,et al.  Post-ischemic inflammation: molecular mechanisms and therapeutic implications , 2004, Neurological research.

[14]  G. Chang.  Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage , 2006, Neurology.

[15]  E. Topol,et al.  Decreased perihematomal edema in thrombolysis-related intracerebral hemorrhage compared with spontaneous intracerebral hemorrhage. , 2000, Stroke.

[16]  J. Roh,et al.  Erythropoietin reduces perihematomal inflammation and cell death with eNOS and STAT3 activations in experimental intracerebral hemorrhage , 2006, Journal of neurochemistry.

[17]  J. Kalita,et al.  Prognostic predictors of thalamic hemorrhage , 2005, Journal of Clinical Neuroscience.

[18]  J. Broderick,et al.  Asymptomatic sinovenous thrombosis in a healthy neonate , 2006, Neurology.

[19]  A J Thompson,et al.  Measuring change in disability after inpatient rehabilitation: comparison of the responsiveness of the Barthel Index and the Functional Independence Measure , 1999, Journal of neurology, neurosurgery, and psychiatry.

[20]  T Brott,et al.  The ABCs of measuring intracerebral hemorrhage volumes. , 1996, Stroke.

[21]  O. Sakowitz,et al.  MRI of the Perihemorrhagic Zone in a Rat ICH Model: Effect of Hematoma Evacuation , 2008, Neurocritical care.

[22]  Joseph P Broderick,et al.  Natural History of Perihematomal Edema in Patients With Hyperacute Spontaneous Intracerebral Hemorrhage , 2002, Stroke.

[23]  T. Dalkılıç,et al.  The effects on prognosis of surgical treatment of hypertensive putaminal hematomas through transsylvian transinsular approach. , 2003, Surgical Neurology.

[24]  A. Mendelow,et al.  Comparison of protein carbonyl and antioxidant levels in brain tissue from intracerebral haemorrhage and control cases. , 2001, Clinica chimica acta; international journal of clinical chemistry.

[25]  P. Gaetani,et al.  Effect of Nimodipine on arachidonic acid metabolites after subarachnoid hemorrhage , 1987, Acta neurologica Scandinavica.

[26]  A. Algra,et al.  Long-term prognosis after recovery from primary intracerebral hemorrhage , 2002, Neurology.

[27]  Garnette R. Sutherland,et al.  Primary intracerebral hemorrhage , 2006, Journal of Clinical Neuroscience.

[28]  J. Murthy,et al.  Decompressive craniectomy with clot evacuation in large hemispheric hypertensive intracerebral hemorrhage , 2005, Neurocritical care.

[29]  R. Cheung.  Update on medical and surgical management of intracerebral hemorrhage. , 2007, Reviews on recent clinical trials.

[30]  A. Kleindienst,et al.  Spontaneous intracerebral hemorrhage , 1997 .

[31]  M. Sessa.  Intracerebral hemorrhage and hypertension , 2008, Neurological Sciences.

[32]  Lucas Elijovich,et al.  Intracerebral Hemorrhage , 2008, Seminars in neurology.

[33]  H. Feys,et al.  The European Stroke Scale , 1994, Stroke.

[34]  G. Pantazis,et al.  Early surgical treatment vs conservative management for spontaneous supratentorial intracerebral hematomas: A prospective randomized study. , 2006, Surgical neurology.