Microstructural changes in the perihematomal area in case of the unfavourable course of spontaneous intracerebral hematomas

Abstract

Objective ‒ to determine the dependence of unfavourable treatment outcomes of spontaneous intracerebral hematomas (ICH) on the peculiarities of microstructural changes in the perihematomal area.Materials and methods. A prospective study was conducted that included 68 patients with haemorrhagic stroke and chronic arterial hypertension, as well as signs of ICH. Patients’ clinical condition and treatment outcomes were assessed. The brain data of five patients who died at different stages after the haemorrhagic stroke were analysed using the method of optical microscopy of autopsy material. Results. Patients’ age ranged from 38 to 59. At the time of hospitalization, the Glasgow Coma Scale score was 8 to 15. The inpatient period was less than 1 day for three patients with stem and medial ICH, and 10 and 34 days in case of subarachnoid haemorrhage (in the latter cater, there was an aneurism re-rapture 3 days before death). Blood in the ventricular system was observed in all patients. Gross examination data during the autopsy showed that the cortical layer above the affected area is thin; after 12‒24 hours, the perihematomal area is swollen, with small dotted, and sometimes coalesced haemorrhaging; after 3 and more days, it increased to 4–5 mm and turned reddish-brown. During histologic examination: brain tissue with signs of the swelling, perihematomal area is cell-like with nerve cells – ranging from minor changes to extreme dystrophia and coagulative necrosis (nuclei with signs of pyknosis, rhexis, lysis), homogenous eosinophilic cytoplasm, apparent pericellular swelling, cell shaft formed by lymphocytes, leukocytes, macrophages, hemosiderophages, and reactive increase in oligodendrocytes and astrocytes.Conclusions. Perihematomal area has been found to be not just a «perihematomal swelling» as described in the literature. The unfavourable course of the ICH of different localization (basal, stem) can be explained by a complex of pathomorphological changes in this area: reactive inflammatory activation of glia, dystrophic nerve cell changes, pericellular swelling. As seen from our observations, early development of these processes – as early as on the 1st day – and their progressing indicate the presence of common mechanisms of unfavourable outcome regardless of haemorrhagic stroke localisation.