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.

Delayed methotrexate excretion in infants and young children with primary central nervous system tumors and postoperative fluid collections.

PURPOSE: High-dose methotrexate (HD-MTX) has been used to treat children with central nervous system tumors. Accumulation of MTX within pleural, peritoneal, or cardiac effusions has led to delayed excretion and increased risk of systemic toxicity. This retrospective study analyzed the association of intracranial post-resection fluid collections with MTX plasma disposition in infants and young children with brain tumors. METHODS: Brain MRI findings were analyzed for postoperative intracranial fluid collections in 75 pediatric patients treated with HD-MTX and for whom serial MTX plasma concentrations (MTX) were collected. Delayed plasma excretion was defined as (MTX) ≥1 µM at 42 hours (h). Leucovorin was administered at 42 h and then every 6 h until (MTX) <0.1 µM. Population and individual MTX pharmacokinetic parameters were estimated by nonlinear mixed-effects modeling. RESULTS: Fifty-eight patients had intracranial fluid collections present. Population average (inter-individual variation) MTX clearance was 96.0 ml/min/m² (41.1 CV %) and increased with age. Of the patients with intracranial fluid collections, 24 had delayed excretion; only 2 of the 17 without fluid collections (P < 0.04) had delayed excretion. Eleven patients had grade 3 or 4 toxicities attributed to HD-MTX. No significant difference was observed in intracranial fluid collection, total leucovorin dosing, or hydration fluids between those with and without toxicity. CONCLUSIONS: Although an intracranial fluid collection is associated with delayed MTX excretion, HD-MTX can be safely administered with monitoring of infants and young children with intracranial fluid collections. Infants younger than 1 year may need additional monitoring to avoid toxicity.

Procollagen propeptides in chronic subdural hematoma reveal sustained dural collagen synthesis after head injury.

OBJECTIVE: To study the hypothesis that concentrations of procollagen propeptides of type I and III collagens (PICP and PIIINP, respectively) and the carboxyterminal telopeptide of type I collagen (ICTP) in subdural haematoma increase in a time-dependent manner as a sign of dural collagen synthesis after head injury. METHODS: Thirty-six patients with subdural haematoma were operated. Subdural haematoma fluid samples were assayed for the concentrations of PICP, PIIINP and ICTP by specific radioimmunoassays. RESULTS: High concentrations of PICP, PIIINP and ICTP were found in subdural haematoma. The mean concentration of PICP in the 36 subdural haematoma samples was 11.8 (SD 9.27) mg/l, the concentration of PIIINP 590 (SD 302) microg/l and that of ICTP 32.0 (SD 12.1) microg/l. The time elapsed from the alleged head injury to operation could be defined in 30 patients. The concentrations of PICP, PIIINP and ICTP in subdural haematoma increased rapidly during the first two weeks after head injury and then stayed high for at least three months. CONCLUSIONS: High concentrations of procollagen propeptides were found in subdural haematoma samples of different haematoma age. Concentrations of these propeptides seem to follow a time-dependent course. The elevation of the concentrations of procollagen propeptides in subdural haematoma may be regarded as a sign of sustained dural collagen synthesis after head injury.

High concentrations of procollagen propeptides in chronic subdural haematoma and effusion.

Procollagen propeptides increase in the CSF after subarachnoid haemorrhage, reflecting increased collagen synthesis in the arachnoid. We studied the induction of dural collagen synthesis after cerebral trauma by measuring the carboxyterminal propeptide of type I procollagen (PICP) and the aminoterminal propeptide of type III procollagen (PIIINP) in 17 subdural haematoma or effusion fluid samples obtained at operation on days 10-85 after head trauma. The concentration of PICP was 78-fold higher and that of PIIINP 156-fold higher, relative to that in the serum. These results indicate that meningeal trauma is followed by a long lasting increase in dural collagen synthesis, and suggest that enhanced synthesis of the various extracellular matrix components may have a role in the development of chronic subdural haematoma or effusion.

Inflammatory cytokines locally elevated in chronic subdural haematoma.

The involvement of inflammation in the development and propagation of chronic subdural haematoma (CSH) was investigated by measuring the levels of inflammatory cytokines (tumour necrosis factor [TNF] alpha, interleukin [IL]-1 beta, IL-6, and IL-8). Peripheral venous blood and subdural fluid were obtained at the time of burr hole surgery from 34 patients with CSH and from 9 with subdural effusion. The levels of the inflammatory cytokines were analysed by enzyme-linked immunosorbent assay. The blood levels of TNF alpha, IL-1 beta, IL-6, and IL-8 in both CSH and subdural effusion groups were almost within the range of normal subjects, and no differences were observed between the two groups. IL-6 and IL-8 in the subdural fluid were much higher than in the blood of both groups, and the levels in CSH patients were significantly higher (10 times) than in subdural effusion patients. Local elevation of inflammatory cytokines in the subdural space of both CSH and subdural effusion without systemic change suggests the presence of local inflammation in the two diseases. The same behavioural patterns of cytokines for these and higher levels of cytokines in the CSH also suggest that inflammatory cytokines may be involved in the continuous development from subdural effusion to CSH and propagation of CSH.

Rate constant of gadolinium (Gd)-DTPA transfer into chronic subdural hematomas.

Gadolinium (Gd) DTPA concentrations in subdural fluid and arterial blood were measured following intravenous Gd-DTPA injection by ion coupled plasma emission spectrometry in 31 chronic subdural hematomas and 12 with subdural effusions. Dynamic biological modeling analysis was used to calculate the unidirectional transfer rate constant (K) for Gd-DTPA influx into the subdural fluid. The Gd concentrations in subdural hematomas and subdural effusions were 36.3 +/- 3.7 nmol ml(-1) and 80.0 +/- 14.0 nmol ml(-1), respectively. The transfer rate constants (K) for subdural hematomas and subdural effusions were 12.4 +/- 1.5 (x10(-4)) min(-1) and 19.7 +/- 2.2(x10(-4)) min(-1), respectively. The Gd concentration and transfer rate constant for subdural effusions were significantly (p<0.05) higher than for subdural hematoma. The Gd transfer rate constant was significantly correlated with the interval from head injury to operation. The present study shows that the immature outer membrane has a high transfer rate constant, allowing extravasation of plasma components into the subdural space and increasing the volume of the subdural effusion; the rate constant decreases with aging of the subdural hematoma.

Subdural fat effusion complicating parenteral nutrition.

A preterm infant fed parenterally through a central venous catheter developed a subdural effusion containing fat emulsion. Subsequent postmortem examination failed to demonstrate any vascular abnormality that might have explained this rarely reported complication. Although retrograde flow of feeding solutions into cerebral veins seems a likely explanation, the exact mechanism remains uncertain.

Attenuation values of chronic subdural haematoma and subdural effusion in CT scans.

When peripheral blood is serially diluted with saline solution, the bloody colour is determined by the derivative of haemoglobin. Solutions over 10(5)/mm3 red cells or 0.5 g/dl haemoglobin are represented as being sanguineous. This is the lower limit for a subdural haematoma, because the name itself requires at least a bloody appearance of its contents. Diluted blood solutions less 0.5 X 10(4) red cells or 15 mg/dl haemoglobin are macroscopically translucent or watery clear. Solutions between bloody and translucent are xanthochromic. If the contents of a subdural collection is watery clear or xanthochromic, it must be called an effusion or hygroma. The haemoglobin in haematomas is the most important factor determining the attenuation values in the CT scan. Protein, iron or calcium ions have only minimal concentration in haematomas and are negligible for attenuation values of haematomas in the CT scan. The lightest sanguineous solution, that is a haematoma, corresponds to 15 Hounsfield's units measured by the CT scan.

Megalocephaly and hypodense extracerebral fluid collections.

Computed tomographic (CT) scans were identified and reviewed for 25 pediatric patients with enlarged heads and extracerebral fluid collections that showed cerebrospinal fluid-like attenuation. Mild to moderate enlargement of the subarachnoid space over the convexity, interhemispheric fissure, and the lateral ventricles was observed in most of the cases. The CT findings are not specific, and it is not always possible to determine the nature of the extracerebral fluid, whether it lies in the subarachnoid space, the subdural space, or both. The differential diagnosis included subdural effusions, hygromas, preclinical or external hydrocephalus, hypodense subdural hematomas, megalocephaly, and possibly a normal variant. CT remains the method of choice for the initial study of these patients and for subsequent follow-up in selected cases.

Benign subdural collections of infancy.

Four asymptomatic infants with macrocrania, abnormal transillumination, and characteristic computed tomography scans are described. All had bilateral subdural collections, normal brain size, modest ventricular enlargement, and prominent cerebral sulci and interhemispheric fissures. Although these latter findings are often interpreted as atrophy, these infants had normal development and rapidly growing heads. No treatment beyond diagnostic subdural punctures was performed. After up to 13 months of follow-up, the size of the subdural collections was either stable or decreasing in all four infants.

Real-time sonography of the brain through the anterior fontanelle.

Noninvasive, rapid evaluation of the neonate and young infants with reproducible results is feasible with real-time cranial sonography through the anterior fontanelle. Cerebral anatomy in coronal and sagittal planes is visualized, and the entire ventricular system and adjacent brain parenchyma are identified. This rapid (5-10 min) procedure can be done at/in the incubator making transport of sick neonates unnecessary, thus preserving their thermal stability. Images are recorded on videotape and "hard copy" is obtained afterward. Ventricular size, intracranial hemorrhage (both intraventricular and parenchymal), abnormalities of the the ventricular system, subdural effusion, and fluid-filled lesions are recognized by the usual sonographic criteria. In addition, "solid" parenchymal lesions such as diffuse hemangiomas and brain tumors are depicted as changes in sonographic parenchymal architecture.