Venous or arterial blood components trigger more brain swelling, tissue death after acute subdural hematoma compared to elderly atrophic brain with subdural effusion (SDE) model rats.

Acute subdural hematoma (ASDH) is a frequent complication of severe head injury, whose secondary ischemic lesions are often responsible for the severity of the disease. We focused on the differences of secondary ischemic lesions caused by the components, 0.4ml venous- or arterial-blood, or saline, infused in the subdural space, evaluating the differences in vivo model, using rats. The saline infused rats are made for elderly atrophic brain with subdural effusion (SDE) model. Our data showed that subdural blood, both venous- and arterial-blood, aggravate brain edema and lesion development more than SDE. This study is the first study, in which different fluids in rats' subdural space, ASDH or SDE are compared with the extension of early and delayed brain damage by measuring brain edema and histological lesion volume. Blood constituents started to affect the degree of ischemia underneath the subdural hemorrhage, leading to more pronounced breakdown of the blood-brain barrier and brain damage. This indicates that further strategies to treat blood-dependent effects more efficiently are in view for patients with ASDH.

Detection of cerebrospinal fluid leakage in intracranial hypotension with radionuclide cisternography and blood activity monitoring.

UNLABELLED: Radionuclide cisternography is an indispensable examination to detect cerebrospinal fluid (CSF) leakage in patients suspected of having spontaneous intracranial hypotension (SIH). However, it sometimes fails to demonstrate the site of CSF leakage, and in such cases, early bladder visualization is utilized for the diagnosis of SIH as an indirect finding. The aim of this work is to improve the diagnostic ability of radionuclide cisternography and to reevaluate the reliability of early bladder visualization as an indirect finding of CSF leakage. METHODS: We obtained serial images during the first hour after injection as well as the following time points in 4 patients with SIH and 5 with normal pressure hydrocephalus (NPH) as a control. We also performed blood sampling over time to measure blood radioactivity concentrations. RESULTS: All 4 patients with SIH demonstrated leakage, 2 of 4 within one hour after injection. Bladder visualization was observed falsely in 4 of 5 patients with NPH, considered to be the result of a lumbar puncture complication. In this false bladder visualization, blood radioactivity showed a more rapid raise and fall than in CSF leakage of SIH. CONCLUSIONS: The combination of radionuclide cisternography, including early time points and blood sampling, may enable accurate diagnosis of SIH.

Local hypercoagulative activity precedes hyperfibrinolytic activity in the subdural space during development of chronic subdural haematoma from subdural effusion.

The involvement of coagulation and fibrinolysis in the development of chronic subdural haematoma (CSH) from subdural effusion was investigated. Subdural fluid and venous blood samples were obtained from 34 patients with CSH and 9 patients with subdural effusion, and analyzed using enzyme-linked immunosorbent assays for thrombin-antithrombin III complex (TAT), prothrombin fragment F1 + 2 (F1 + 2), tissue factor, tissue factor pathway inhibitor (TFPI) and D-dimer. CSH was classified into the layering type, believed to be active, and other types according to x-ray computed tomography. All markers in the blood of both patient groups were similar to the values of normal subjects. Levels of TAT and F1 + 2 were much higher in the subdural fluid than in the blood of patients with CSH (P < 0.001, P < 0.001) and with subdural effusion (P < 0.05, P < 0.05). The level of D-dimer in the subdural fluid was significantly higher than in the blood (P < 0.001) in patients with CSH, but not in patients with subdural effusion. All markers in the subdural fluid of layering type CSH, except TFPI, were significantly higher than in the other types (P < 0.05). Local hypercoagulative activity in the subdural space is present in subdural effusion and precedes hyperfibrinolytic activity in CSH. Thrombin generation as indicated by TAT and F1 + 2 might be involved in the development of CSH. Propagation of CSH may be modulated by the coagulation system including the extrinsic pathway and fibrinolysis.

Serum protein exudation in chronic subdural haematomas: a mechanism for haematoma enlargement?

A study was conducted to investigate the role of serum protein exudation in the aetiology of chronic subdural haematoma (SDH). Scintigraphy after intravenous injection of 99mTc-labelled human serum albumin (HSA) was performed in three patients with chronic SDH and a patient with subdural effusion. In another 60 haematomas, the amounts of total protein and albumin as indices of serum exudation were measured, and then compared among low-density, iso-density and high-density haematomas. Accumulation of 99mTc-HSA in the haematoma cavity was seen 6 h after isotope injection and became more evident at 24 h. However, the protein concentrations and albumin ratios in the haematomas exhibited a reciprocal relationship, suggesting that not all the protein in the haematomas was derived from serum exudation. The higher the total protein concentration in the haematoma became, the higher the haematoma density which was observed on CT. The albumin concentration in low-density haematomas was lower than that in iso-density and high-density haematomas, whereas no significant difference was seen between the latter two haematoma types. These results provide morphological evidence for serum protein exudation into the haematoma cavity, and therefore it is possible that serum protein exudation plays a role in the progression of chronic SDH and is related to changes in haematoma density on CT.