Secondary Injury To Perihematoma In Intracerebral Haemorrhage

ObjectiveThe incidence of intracerebral haemorrhage injury (ICH) is high and it is responsible for the disability and mortality of the patients. In western countries, intracereral haemorrhage injury(ICH) accounts for 8%-15% in the cerebral apoplexy of the whole country, while it reaches 21%-48% in our country. However, secondary injury to the intracerebral haemorrhage, especially the edema surrounding hematoma and the ultrastructure change are unknown to us. After the intracerebral haemorrhage , there exists a tissue damage and the district surrounded the hematoma aggravates edematization progresses. The ultrastructure change of this district is reversible within a certain period . If the patients could be received proper therapeutic measures at this time, the damage tissue can restore its function, this district is named the penumbra field of hematoma periph and semidarkness band. For the past few years, the ultrastructure change of cerebral hemorrhage hematoma periph tissue has drawn more and more researcher's attention, which becomes the highlight of cerebral hemorrhage now . This study draws the material from the surrounding of hematoma which look directly in operation. To observe the brain tissue's pathology and ultrastructure change at the different time which surrounding hematoma. Observe the secondary lesion's pathology processes and ultrastructure change of cerebral hemorrhage periph to identify pathophysiology processes and possible mechanism of the surrounding tissue's secondary injury caused by brain parenchymatous hemorrhage further. We want to observe the change and possible mechanism of cerebral hemorrhage peripheral edema band from pathology and ultrastructure, plan to take propotional therapeutic measures for ultrastructure change. These changes will have considerable reference value to the clinic.Methods1 The neural handicapped patients who were selected from the third hospital of He Bei medical university,International peace hospital and the second hospital of He Bei medical university were in hospital at 2005.02-2007.02, and confirm by head CT, according to Duo Tian formula videlicet: length(cm) X width(cm) X height (cm) Xπ/6, the patients of hypertension selected standard: the diagnosis main points of hypertensivc cerebral hemorrhagc consistent with the fourth cerebrovascular disease academic conference of the whole country in 1995, all confirmed by head CT or MRI; patients( intracranial hematoma and subdural hematoma ) caused by external injury consistent with the selected standard of the operation of craniocerebral injury from Wang Zhongcheng neurosurgery; total 100 instances, these patients were all needed operations. 64 instances among these were taken the operation of bonelet window, and the other 36 instances were taken the operation of removing bone lobe. These were divided into 5 groups: <6h, 6-24h, 24-72h , above 72h, according to the time after hemorrhage .2 According to head CT scanning we displayed hematoma location .At the same time of operations, unfolding bone lobe of skull and cerebral dura mater to find the hematoma and use keen Gillette blade to take a bit of brain tissue which was 1cm from the intracranial hematoma and near the cortex. they were put into neutrality Formaldehyde to conserve 24 hours for fixing ,paraffin imbedding, serial sections which thickness was 5um, Hematoxin Eosin( HE) coloretur, and observed pathology succession in general.3 The brain tissue around hematoma where was near the cortical field was took, and put in the 4%Glutaral. The time between taking brain tissue and putting it in the 4% Glutaral should be within 1 minute to prevent cytolysis. We conserved the sample in 4℃constant temperature refrigerator for 4 hours, clotting the brain tissue. We observed them at transmission electron microscope and light microscope.4 All the data were analyed by Software Packaged by Social Science ver 14.0 in the statistics. They were applied the linear tendency of grouped data which were in order to do test and correlation analysis. The difference was considered statistically significant(P<0.05). Results1 Histopathology change : Focal zone could be separated into hematoma zone,peripheral zone of hematoma and proximal normal tissue zone. HE coloretur showed: the brain tissue around the hematoma had no white infarct zone. Through light microscope, there was a peripheral zone between the hematoma and the normal brain tissue. Among this zone , we observed the tissue was loosen and cells had the edema in different degrees, astrocyte swelling, neural cells degeneration and necrosis, blood capillary hyperplasy and phlegmasia cells infiltration at the ambitus of hemorrhagic focus. In 3-6h, it had not visible edema around the hematoma . In 6-24 h, we could see sporadic neutrophil and oncotic gliocyte at the hematoma edge, and there were considerable engorge cells around the hematoma. The edema was significant outside the cells and around the blood vessel. The most neural cells showed (tigroid body disappearance, karyopycnosis, endochylema) devour tart degeneration. The most obvious edema turned up at the third day, and it started to appear foam cells around the hematoma which successed from carrier cells, gliocyte proliferation, neutrophilic leukocytosis. After this, the edema around the hematoma aggregated gradually, while foam cells became more and more. When it reaches to the 7d,there is considerable foam cells around the hematoma. The edema extincted obviously than before, and cellular swelling lightened. The part of cells died, and the edema outside the cells and around the blood vessel still existed .2 Ultrastructure change: The observation of electron microscope showed: At the nonage(3-6h) of the hematoma periph tissue, astrocyte body and ambitus foot process were swelling, and the intracytoplasm had a great quantity of edema by fluid. The swollen foot process oppressed the blood capillary and made the lumens narrow even blunt. The membrane structure of neural cells was complete, bioblast was swelling, cristae was decreasing, rough endoplasmic reticulum was broadening, part of endochylema change was liking vacuole, nuclear membrane was complete, and chromatin was decreasing. Medullary layers was vague, part abruptly, the neural plexus inside the neuraxis was normal on the whole. After 24h, astrocyte was swelling obviously, endochylema change was liking vacuole, and part of cells were degeneration and necrosis. Not only neural cells degenerated lightly and nucelus was pyknosis, but also the caryotin below caryotheca aggregated lightly. The electron density heightened. Part of the myelin sheath of layers were abrupt and disintegrated. The content of neuraxis was dissolving, the cell capillary endothelium was swelling, and blood brain barrier was breakdown. After 72h, the astrocyte was swelling highly, and the intracytoplasm could be found massive edema fluid. The nuclear chromatin eliminated and the part of the cell membrane disintegrated. The organs of cell in the intracytoplasm scattered outside the cells; we observed neural cell degenerated, endochylema vacuoleform, nuclear membrane umbilicated, intranuclear chromatin agglutinated, bioblast swollen, cristae disrupt, cell membrane uncomplete; myelin sheath layers disrupt and disintegrated, and capillary endothelium cell swelling, and lumens narrowing.ConclusionAfter the cerebral hemorrhage, the blood entered brain essence through ruptured blood vessels, caused a series of pathological change through mechanical injury, ischemia, inflam, edema, cytotoxicity , and so on in the neural cells . The results of electron microscope in this study showed: the brain tiusse around haematoma in different periods was injured in different degrees. The relation between the brain tiusse around haematoma and time were linear tendency. In 24h, most of cells were cytotoxic edema, part of cells were disrupt and necrosise. The myelin sheath injured differently. In 72h, cells swelled heavy, while organelle dissolved and pycnosis. The endotheliocyte intruded lumina and made them narrowed. In 7d, except heavy edema, the necrosis was more. The foot process of astrocyte extruded and blocked the capillary wall. The resistance of microcirculation increased and the blood-brain barrier destroyed. The tiny hemorrhagic focus appeared around blood vessel.