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Poor outcome following traumatic acute subdural hematoma (ASDH) is associated with the severity of the primary injury and secondary injury including cerebral edema and ischemia. However, the underlying secondary injury mechanism contributing to elevated intracranial pressure (ICP) and high mortality rate remains unclear. Cerebral edema occurs in response to the exposure of the intracellular fixed charge density (FCD) after cell death, causing ICP to increase. The increased ICP from swollen tissue compresses blood vessels in adjacent tissue, restricting blood flow and leading to ischemic damage. We hypothesize that the mass occupying effect of ASDH exacerbates the ischemic injury, leading to ICP elevation, which is an indicator of high mortality rate in the clinic. Using FEBio (febio.org) and triphasic swelling biomechanics, this study modeled clinically relevant ASDHs and simulated post-traumatic brain swelling and ischemia to predict ICP. Results showed that common convexity ASDH significantly increased ICP by exacerbating ischemic injury, and surgical removal of the convexity ASDH may control ICP by preventing ischemia progression. However, in cases where the primary injury is very severe, surgical intervention alone may not effectively decrease ICP, as the contribution of the hematoma to the elevated ICP is insignificant. In addition, interhemispheric ASDH, located between the cerebral hemispheres, does not significantly exacerbate ischemia, supporting the conservative surgical management generally recommended for interhemispheric ASDH. The joint effect of the mass occupying effect of the blood clot and resulting ischemia contributes to elevated ICP which may increase mortality. Our novel approach may improve the fidelity of predicting patient outcome after motor vehicle crashes and traumatic brain injuries due to other causes., (© 2024. The Author(s) under exclusive licence to Biomedical Engineering Society.)

Although criteria for surgical treatment of acute subdural hematoma (SDH) have been proposed, interaction exists between SDH, midline shift (MLS), and intracranial pressure (ICP). Based on our half sphere finite-element model (FEM) of the supratentorial brain parenchyma, tools for ICP estimation using SDH thickness (SDHx) and MLS were developed. We performed 60 single load step, structural static analyses, simulating a left-sided SDH compressing the cerebral hemispheres. The Young's modulus was taken as 10,000 Pa. The ICP loads ranged from 10 to 80 mmHg with Poisson's ratios between 0.25 and 0.49. The SDHx and the MLS results were stored in a lookup table. An ICP estimation equation was derived from these data and then was converted into a nomogram. Numerical convergence was achieved in 49 model analyses. Their SDHx ranged from 0.79 to 28.3 mm, and the MLS ranged from 1.5 to 16.9 mm. The estimation formula was log(ICP) = 0.614-0.520 log(SDHx) + 1.584 log(MLS). Good correlations were observed between invasive ICP measurements and those estimated from preoperative SDHx and MLS data on images using our model. These tools can be used to estimate ICP noninvasively, providing additional information for selecting the treatment strategy in patients with SDH.

Mass evacuation with decompressive craniotomy is considered a standard intervention for acute subdural hematoma (ASDH). However, hemispheric swelling complicates the intraoperative and postoperative management of ASDH patients, and previous studies have revealed that this approach can damage ischemic/reperfusion (I/R) injury. Few studies have focused on the cerebrovascular response following traumatic brain injury (TBI). To characterize the relative cerebral blood flow (rCBF) before and after removal of the hematoma, rats were injured by a subdural infusion of 400 μL of venous blood or paraffin oil. MRI scans were performed. Then, we monitored cortical rCBF during hematoma removal in real time using laser speckle imaging (LSCI) in ASDH rats. The CBF of arteriovenous and capillary regions were quantified and normalized to their own baseline values via a custom algorithm. In the sham group, the cortical CBF was higher post-craniotomy than pre-craniotomy. However, in the hematoma injection group, the CBF of arteries and capillaries was higher while the venous CBF was lower post-craniotomy than pre-craniotomy. The difference in the changes in vein CBF that occurred between the two groups was statistically significant. The three components of the vascular system showed heterogeneous responses to craniotomy, which may be the basis for secondary brain injury., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Introduction: The most frequent consequences of a traumatic brain injury are acute subdural (SDH) and epidural hematoma (EDH), which usually require a surgical treatment. Most of the factors affecting the prognosis have been analyzed on a wide group of traumatic brain injuries. Nonetheless, there are few studies analyzing factors influencing the prognosis regarding patients with EDH and SDH. The aim of the study is to identify factors which have prognostic value in relation to 6-month outcome of patients undergoing surgery for acute hematoma., Patients and Methods: The study included a group of 128 patients with isolated craniocerebral injuries. The patients were divided into two groups, namely a group of 28 patients operated on due to epidural hematoma and a group of 100 patients operated on due to acute subdural hematoma. All patients were operated and treated in the Department of Neurosurgery at the Medical University in Lublin from 1.10.2014 to 31.08.2017. The following factors from the groups were analyzed: demographic data, physiological factors, laboratory factors, computed tomography scan characteristics, and time between the trauma and the surgery. All the factors were correlated with six-month outcome in Glasgow outcome scale., Results: The univariate analysis has confirmed the influence of many factors affecting the outcomes., Conclusion: It is interesting that the factors such as GSC score, saturation, respiratory rate, and systolic blood pressure were associated with outcome with highly statistically significant differences in both group. These are factors that, with an appropriate treatment, could be normalized at the place of the accident., (This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Background: Spreading depolarizations (SDs) occur in 50-60% of patients after surgical treatment of severe traumatic brain injury (TBI) and are independently associated with unfavorable outcomes. Here we performed a pilot study to examine the relationship between SDs and various types of intracranial lesions, progression of parenchymal damage, and outcomes., Methods: In a multicenter study, fifty patients (76% male; median age 40) were monitored for SD by continuous electrocorticography (ECoG; median duration 79 h) following surgical treatment of severe TBI. Volumes of hemorrhage and parenchymal damage were estimated using unbiased stereologic assessment of preoperative, postoperative, and post-ECoG serial computed tomography (CT) studies. Neurologic outcomes were assessed at 6 months by the Glasgow Outcome Scale-Extended., Results: Preoperative volumes of subdural and subarachnoid hemorrhage, but not parenchymal damage, were significantly associated with the occurrence of SDs (P's < 0.05). Parenchymal damage increased significantly (median 34 ml [Interquartile range (IQR) - 2, 74]) over 7 (5, 8) days from preoperative to post-ECoG CT studies. Patients with and without SDs did not differ in extent of parenchymal damage increase [47 ml (3, 101) vs. 30 ml (- 2, 50), P = 0.27], but those exhibiting the isoelectric subtype of SDs had greater initial parenchymal damage and greater increases than other patients (P's < 0.05). Patients with temporal clusters of SDs (≥ 3 in 2 h; n = 10 patients), which included those with isoelectric SDs, had worse outcomes than those without clusters (P = 0.03), and parenchymal damage expansion also correlated with worse outcomes (P = 0.01). In multivariate regression with imputation, both clusters and lesion expansion were significant outcome predictors., Conclusions: These results suggest that subarachnoid and subdural blood are important primary injury factors in provoking SDs and that clustered SDs and parenchymal lesion expansion contribute independently to worse patient outcomes. These results warrant future prospective studies using detailed quantification of TBI lesion types to better understand the relationship between anatomic and physiologic measures of secondary injury.

Traumatic brain injury is a leading cause of disability and mortality. Finite element-based head models are promising tools for enhanced head injury prediction, mitigation and prevention. The reliability of such models depends heavily on adequate representation of the brain-skull interaction. Nevertheless, the brain-skull interface has been largely simplified in previous three-dimensional head models without accounting for the fluid behaviour of the cerebrospinal fluid (CSF) and its mechanical interaction with the brain and skull. In this study, the brain-skull interface in a previously developed head model is modified as a fluid-structure interaction (FSI) approach, in which the CSF is treated on a moving mesh using an arbitrary Lagrangian-Eulerian multi-material formulation and the brain on a deformable mesh using a Lagrangian formulation. The modified model is validated against brain-skull relative displacement and intracranial pressure responses and subsequently imposed to an experimentally determined loading known to cause acute subdural haematoma (ASDH). Compared to the original model, the modified model achieves an improved validation performance in terms of brain-skull relative motion and is able to predict the occurrence of ASDH more accurately, indicating the superiority of the FSI approach for brain-skull interface modelling. The introduction of the FSI approach to represent the fluid behaviour of the CSF and its interaction with the brain and skull is crucial for more accurate head injury predictions.

Background: Prior studies have shown that most patients with mild traumatic brain injury or negative computed tomography (CT) scans of the head rarely decline or require neurosurgical interventions. One common reason for a delayed decline is an intracranial hemorrhage that presents within 24-48 hours. This is typically seen in elderly patients and/or patients on antiplatelet or anticoagulation agents. We describe a case of a delayed subdural hemorrhage presenting in a young adult not on any antiplatelet or anticoagulation therapy., Case Description: A 19-year-old male presented to the emergency department after being involved in a motor vehicle accident. He had a Glasgow Coma Scale of 15, and an initial CT was negative for any intracranial hemorrhage or pathology, so he was then admitted to the intensive care unit for further care. The patient received 1 dose of aspirin 325 mg the following day for treatment of blunt cerebrovascular injury. Six hours later he reported a severe headache and had an episode of emesis with a subsequent rapid neurologic decline. Repeat CT showed an acute right subdural hematoma, and he underwent an emergent right decompressive hemicraniectomy., Conclusions: In rare cases, patients with negative initial head CT scans neurologically deteriorate as a result of a delayed acute subdural hematoma. We present an unusual case of a young patient on no medications with no CT findings of an intracranial injury who neurologically declined due to a delayed acute subdural hematoma., (Copyright © 2018 Elsevier Inc. All rights reserved.)

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., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Acute subdural hematoma due to a bridging vein rupture is a devastating but rare injury. There has to date been no satisfactory biomechanical explanation for this infrequent but costly injury. We surmise that it may be associated with multiple head impacts. Though numerical models have been used to estimate vein strains in single impact events, none to date have examined the influence on localized brain strain of rapidly consecutive impacts. Using the Simulated Injury Monitor, we investigated the hypothesis that such double impacts can increase strain beyond that created by any single impact. Input to our parametric study comprised hypothetical biphasic rotational head accelerations producing a maximum angular velocity of 40rad./s. In each of 19 simulations, two identical angular inputs are applied at right angles to each other but with time separations varying from 0 to 40ms. For these double impacts, it has been generally found that strain in the region of the bridging veins is different, than what would be associated with any corresponding single impact. In some cases, the effect is to actually reduce the tissue strain. In others, the strain in the region of the bridging veins is increased markedly. The mechanistic explanation for the strain increase is that the tissue strain from the first impact has not diminished fully when strain from the second impact is initiated. Rapidly consecutive impacts could be a potential mechanism leading to vein rupture that warrants further investigation., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Acute subdural hematoma (ASDH) is associated with high morbidity and mortality. Whether the volume effect of the hematoma and increase of intracranial pressure (ICP) or the local effect of blood are responsible for this severe pathophysiology is unclear. Therefore, we compared subdural infusion of autologous blood and paraffin oil in a rat model of ASDH. In a histological study, we investigated the effects on acute ICP, cerebral perfusion pressure (CPP), cerebral blood flow (CBF), tissue oxygen changes, and brain damage at 2, 24, and 96 h post-infusion. Inflammatory reaction was analyzed by immuno-staining for microglia (ionized calcium binding adaptor molecule 1 [Iba1]) and activated astrocytes (glial fibrillary acidic protein [GFAP]). Besides acute ICP and CBF changes, we investigated the development of behavior (neuroscore and beamwalk test) for up to 4 days after injury in a behavioral study. Despite comparably increased ICP, there was a more pronounced lesion growth in the blood infusion group during the first 96 h. Further, there was an increased peri-lesional immunoreactive area of Iba1 and GFAP 96 h post-infusion, primarily in the blood infusion group, whereas hippocampal damage was comparable in both infusion groups. In the behavioral evaluation, paraffin-infused animals showed a better recovery, compared with the blood infusion group. In conclusion, comparable acute time-course of ICP, CPP, and CBF clearly indicates that the differences in lesion size, inflammatory reaction, and behavioral deficits after blood- and paraffin oil-induced ASDH are partially due to blood constituents. Therefore, current data suggest that subdural hematomas should be completely removed as quickly as possible; decompression alone may not be sufficient to prevent secondary brain damage.

Purpose: Subdural hematomas (SDH) are associated with seizures and epileptiform discharges, but little is known about the prevalence and impact of seizures, status epilepticus (SE), and epileptiform discharges on outcomes in patients with isolated acute SDH (aSDH)., Methods: Continuous EEG reports from 76 adult patients admitted to Rush University Medical Center with aSDH between January 2009 and March 2012 were reviewed. Clinical and radiographic findings, comorbidities, treatment, and outcome parameters, such as mortality, discharge destination, need for tracheostomy/percutaneous endoscopic gastrostomy placement, and length of stay (LOS), were assessed. Univariate and multivariate analyses were performed to assess the impact of clinical seizures, SE, and epileptiform EEG on outcomes., Results: Of 76 patients with aSDH who underwent EEG monitoring, 74 (97.4%) received antiseizure prophylaxis. Thirty-two (41.1%) patients had seizures, most of which were clinical seizures. Twenty-four (32%) patients had epileptiform EEG findings. Clinical or nonconvulsive SE was diagnosed in 12 (16%) patients. Clinical seizures were not associated with outcome parameters. Epileptiform EEG findings were independently associated with longer hospital LOS (13 vs. 8 days, P = 0.04) and intensive care unit LOS (10 vs. 4 days, P = 0.002). The SE also predicted longer intensive care unit LOS (10 vs. 4 days, P = 0.002). Neither epileptiform EEG nor SE was significantly related to mortality, discharge destination, or need for tracheostomy/percutaneous endoscopic gastrostomy placement., Conclusions: Seizures and epileptiform EEG findings are very common in patients with aSDH despite antiseizure prophylaxis. While clinical seizures did not affect outcomes, the presence of epileptiform EEG findings and SE was independently associated with longer intensive care unit LOS and hospital LOS.

Background: Spontaneous rapid resolution of acute subdural hematoma developing secondary to trauma has been reported in the literature, yet it is very rare in pediatric population. The aim of the present review is to analyze mechanisms, characteristics, and outcomes of pediatric acute subdural hematoma cases with spontaneous rapid resolution in conjunction with an exemplary case of ours., Case Description: A 3-year-old boy was admitted to our emergency department following mild head trauma secondary to a fall from 2 m. He was alert and has a GCS of 15. He had no motor or sensorial deficit on neurological examination. On the emergent brain computed tomography image, an acute subdural hematoma over left frontoparietal lobe was observed. There was a midline shift of 8.3 mm and the width of the hematoma at the thickest portion was 11.2 mm. Surgery was postponed with a close neurological follow-up of the patient in pediatric intensive care unit, due to his well neurological status without any increased ICP findings. On the fourth hour follow-up head CT image, amount of midline shift and hematoma thickness were observed to have regressed dramatically. At the second week, the hematoma resorbed totally with only conservative approach, and he was discharged to home in well status., Discussion and Conclusion: Analysis of 12 pediatric patients revealed a mean and median ages of 6.87 and 3.9 years, respectively (range = 8 months-18 years). Causes for ASH development were fall, traffic accident, struggle, and child abuse. Main clinical presentations were with depressed sensorium, coma, stupor, drowsiness, headache, motor weakness, lethargy, and seizure. Close follow-up with conservative treatment should be mode of approach in pediatric patients with ASH, if neurological and radiological findings are favorable. However, if patients' neurological status deteriorates after admission to hospital, surgery should be conveyed with no further delay.

Introduction: Type B lactic acidosis represents a rare and often lethal complication of haematological malignancy. Here, we present a patient who developed a type B lactic acidosis presumably due to a concurrent chronic myelomonocytic leukaemia. Upon swift initiation of cytoreductive chemotherapy (doxorubicin), the lactic acidosis was rapidly brought under control. This case adds to the literature reporting other haematological malignancies that can cause a type B lactic acidosis and its successful treatment., Case Presentation: We report the case of a 77-year-old Caucasian man brought to our Accident and Emergency department following an unwitnessed collapse; he was found surrounded by coffee-ground vomit. Although haemodynamically stable on admission, he rapidly deteriorated as his lactic acid rose. An initial arterial blood gas revealed a pH of 7.27 and lactate of 18mmol/L (peaking at 21mmol/L)., Conclusions: A high degree of clinical suspicion for haematological malignancy should be held when presented with a patient with lactic acidosis in clinical practice, even without evidence of poor oxygenation or another cause. Treatment with emergency chemotherapy, in lieu of a definitive diagnosis, was rapidly successful at lowering lactate levels within 8 hours. This may suggest a causal and perhaps direct relationship between lactic acid production and the presence of leukemic cells. Veno-venous haemofiltration had no apparent effect on reducing the lactic acidosis and therefore its benefit is questioned in this setting, especially at the cost of delaying chemotherapy. In the face of a life-threatening lactic acidosis, pragmatic clinical judgement alone may justify the rapid initiation of chemotherapy.

Background: Acute subdural hematoma is uncommon following open-heart surgery, but may result in increased mortality and morbidity., Methods: A retrospective analysis was performed involving all patients who underwent thoracic aortic surgery from January 2009 to February 2013. There were 53 patients who had thoracic aortic repair with open distal anastomosis and required selective cerebral perfusion with or without retrograde cerebral perfusion. We evaluated the incidence of postoperative acute subdural hematoma. The patients were divided into two groups: a subdural hematoma group who had symptomatic subdural hematoma postoperatively, and a non-subdural hematoma group who had no subdural hematoma. The variables were compared between the 2 groups., Results: Eight (15.1%) patients had a transient symptomatic subdural hematoma; none required surgical evacuation of the hematoma. There were significant differences between the two groups in terms mean and maximum retrograde cerebral perfusion flow, and the volume of intraoperative platelet transfusion. Multivariate analysis revealed that a significant risk factor for acute subdural hematoma following thoracic aortic surgery was the amount of intraoperative platelet transfusion (odds ratio = 0.9, 95% confidence interval: 0.81-0.98, p = 0.015)., Conclusions: This retrospective study demonstrated that the subdural hematoma group received fewer units of platelets, thus it appears to be important to give platelets appropriately. Strict flow regulation or avoidance of retrograde cerebral perfusion is suggested., (© The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.)

Acute subdural hematoma (ASDH) is a severe insult with a high mortality rate, and emergent surgical evacuation is recommended in the vast majority of such cases. Generally, resolution of the hemorrhage requires weeks and months in patients treated conservatively. However, numerous cases of rapid spontaneous resolution of ASDH, occurring within 72h after the trauma, have been reported to date in the literature. Several possible hypotheses have been suggested, primarily involving redistribution and dilution, or washing out the ASDH. In this study, we present the relevant images of such a case, review the mechanisms of the rapid spontaneous resolution in the literature, and also propose a new hypothesis to explain the occurrence of the rapid spontaneous resolution of ASDH. We indicate that the fluctuation of intra-parenchymal cerebral pressure that drives the rapid spontaneous resolution of ASDH., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

The high incidence of subdural hematoma (SDH) from birthing was first identified with MRI by Looney in 2007 and was then more accurately determined by Rooks in 2008. Rooks screened 101 "normal" deliveries and demonstrated that 46% of the babies in her series and by inference, approximately 46% of the 4 million born normally in the US have SDH that formed in the perinatal (birthing) period during labor. Both metabolic strain and physical forces exerted on the head damage the capillaries within the dura (the intradural capillary bed), which is the source of the blood in the SDH that results from labor and delivery or at times from labor alone. While child abuse pediatricians relying on Rooks, maintain that no permanent complications result, her study was limited to 101 subjects and the sole criteria for resolution was the resolution of the SDH as seen on follow-up MRI. In fact, Rooks did have one patient (1%) who had complications that lead to symptoms and findings often associated with abuse. The purpose of this article is to explore if there is a complication rate for perinatal (PSDH) that supports that 1% of complications that are definable by different criteria. Next, if there are complications, how many of the roughly 2,000,000 cases of perinatal acute subdural hematoma every year in the United States will suffer them? Then, what are the clinical manifestations of the complications if they occur? Lastly, do the complications cause or mimic some or all of the findings that are offered by board certified child abuse pediatricians as evidence of child abuse? The article argues that a small percentage, but significant number of neonates, suffer birth related complications and findings secondary to the development of chronic subdural hematoma CSDH) that are often misdiagnosed as abusive head trauma., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Recombinant human erythropoietin (EPO) has been successfully tested as neuroprotectant in brain injury models. The first large clinical trial with stroke patients, however, revealed negative results. Reasons are manifold and may include side-effects such as thrombotic complications or interactions with other medication, EPO concentration, penetration of the blood-brain-barrier and/or route of application. The latter is restricted to systemic application. Here we hypothesize that EPO is neuroprotective in a rat model of acute subdural hemorrhage (ASDH) and that direct cortical application is a feasible route of application in this injury type. The subdural hematoma was surgically evacuated and EPO was applied directly onto the surface of the brain. We injected NaCl, 200, 2000 or 20,000IU EPO per rat i.v. at 15min post-ASDH (400μl autologous venous blood) or NaCl, 0.02, 0.2 or 2IU per rat onto the cortical surface after removal of the subdurally infused blood t at 70min post-ASDH. Arterial blood pressure (MAP), blood chemistry, intracranial pressure (ICP), cerebral blood flow (CBF) and brain tissue oxygen (ptiO2) were assessed during the first hour and lesion volume at 2days after ASDH. EPO 20,000IU/rat (i.v.) elevated ICP significantly. EPO at 200 and 2000IU reduced lesion volume from 38.2±0.6mm(3) (NaCl-treated group) to 28.5±0.9 and 22.2±1.3mm(3) (all p<0.05 vs. NaCl). Cortical application of 0.02IU EPO after ASDH evacuation reduced injury from 36.0±5.2 to 11.2±2.1mm(3) (p=0.007), whereas 0.2IU had no effect (38.0±9.0mm(3)). The highest dose of both application routes (i.v. 20,000IU; cortical 2IU) enlarged the ASDH-induced damage significantly to 46.5±1.7 and 67.9±10.4mm(3) (all p<0.05 vs. NaCl). In order to test whether Tween-20, a solvent of EPO formulation 'NeoRecomon®' was responsible for adverse effects two groups were treated with NaCl or Tween-20 after the evacuation of ASDH, but no difference in lesion volume was detected. In conclusion, EPO is neuroprotective in a model of ASDH in rats and was most efficacious at a very low dose in combination with subdural blood removal. High systemic and topically applied concentrations caused adverse effects on lesion size which were partially due to increased ICP. Thus, patients with traumatic ASDH could be treated with cortically applied EPO but with caution concerning concentration., (Copyright © 2013 IBRO. Published by Elsevier Ltd. All rights reserved.)

Preeclampsia, HELLP syndrome (hemolysis, elevated liver enzymes, and low-platelet count), and acute fatty liver of pregnancy are the main causes of thrombotic microangiopathy and evere liver dysfunction during pregnancy and represent different manifestations of the same pathological continuum. The case of a 35-week pregnant woman who was admitted to an intensive care unit immediately after a Cesarean section due to fetal death and the presence of nausea, vomiting, and jaundice is reported. Postpartum preeclampsia and acute fatty liver of pregnancy were diagnosed. The patient developed an acute subdural hematoma and an intracerebral hemorrhage, which were subjected to neurosurgical treatment. The patient died from refractory hemolytic anemia and spontaneous bleeding of multiple organs. Preeclampsia HELLP syndrome, and acute fatty liver of pregnancy might overlap and be associated with potentially fatal complications, including intracranial hemorrhage, as in the present case. Early detection and diagnosis are crucial to ensure management and treatment success.

Introduction: To review the outcome of patients with post-traumatic acute subdural haematoma (ASDH) before and after the establishment of a hospital trauma team at a designated trauma centre., Method: A retrospective analysis was conducted on 82 consecutive patients who underwent surgery for post-traumatic ASDH. The 'PRE' and 'POST' groups included patients admitted before and after the establishment of a hospital trauma team, respectively. Injury severity was assessed by the admission Glasgow coma score, imaging findings, and the revised trauma score. Clinical outcome measures were the hospital length of stay and the Glasgow outcome score (GOS) upon hospital discharge., Results: The overall mortality rate was 53.7%. No significant difference was found between the PRE and POST groups. The mean length of hospital stay was also comparable between the two groups. The functional status of those who survived acute hospital care was significantly better in the POST group. Good outcome (GOS of 4 or 5) was achieved in 66.7% of the survivors in the POST group, compared with 25.0% in the PRE group (p=0.024)., Conclusion: Post-traumatic ASDH carried a poor prognosis. The mortality rate and hospital length of stay of patients were not found to be reduced after the establishment of a hospital trauma team. The latter, however, was associated with significantly better functional outcome amongst survivors. Although causality cannot be established due to the multitude of factors which may have affected patient outcome, our findings nonetheless provide further support for the introduction of a multidisciplinary hospital trauma team for the optimal care of trauma patients., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Acute subdural hemorrhage (ASDH) is a frequent and devastating consequence of traumatic brain injury. Tissue damage develops rapidly and makes treatment even more difficult. Management of increased intracranial pressure (ICP) due to extravasated blood volume and brain swelling is often insufficient to control all adverse effects of ASDH. In addition to sheer volume, spontaneously triggered cortical spreading depression (CSD) that leads to cell death following ischemia or trauma may contribute to injury development after ASDH. Therefore, we explored the occurrence of CSD by tissue impedance (IMP) measurement in a rat model subjected to ASDH. IMP and intraventricular and mean arterial pressure were monitored before (baseline), during (blood infusion), and after ASDH for 3 h.Tissue impedance increased by around 203% of baseline during subdural infusion of 300 μl of autologous, venous blood and dropped back to baseline within 22 min. Fifty-six minutes after the start of ASDH a cluster of four short-lasting (3-3.5 min; 140-160% of baseline) IMP increases started that reflected spontaneous CSDs. This pattern presumes that CSD occurs early after ASDH and therefore may contribute to the rapid lesion development in this disease.

An acute subdural hematoma (ASDH) induces pathomechanisms which worsen outcome after traumatic brain injury, even after a small hemorrhage. Synergistic effects of a small ASDH on brain damage are poorly understood, and were studied here using neuromonitoring for 10 h in an injury model of controlled cortical impact (CCI) and ASDH. Pigs (n = 32) were assigned to 4 groups: sham, CCI (2.5 m/s), ASDH (2 ml) and CCI + ASDH. Intracranial pressure was significantly increased above sham levels by all injuries with no difference between groups. CCI and ASDH reduced ptiO(2) by a maximum of 36 ± 9 and 26 ± 11%, respectively. The combination caused a 31 ± 11% drop. ASDH alone and in combination with CCI caused a significant elevation in extracellular glutamate, which remained increased longer for CCI + ASDH. The same two groups had significantly higher peak lactate levels compared to sham. Somatosensory evoked potential (SSEP) amplitude was persistently reduced by combined injury. These effects translated into significantly elevated brain water content and histological damage in all injury groups. Thus, combined injury had stronger effects on glutamate and SSEP when compared to CCI and ASDH, but no clear-cut synergistic effects of 2 ml ASDH on trauma were observed. We speculate that this was partially due to the CCI injury severity., (Copyright © 2011 S. Karger AG, Basel.)

An 88-year-old woman presented with acute subdural hematoma (ASDH) which showed rapid resolution on computed tomography (CT) and magnetic resonance (MR) imaging. She was transferred to our hospital after falling out of bed. On admission, she was comatose with Japan Coma Scale score of 200 and Glasgow Coma Scale score of E1V1M2. Brain CT showed a thick left frontotemporal ASDH. Conservative treatment consisted of 200 ml of glycerol administered intravenously twice a day, and maintenance in the approximately 20 degree head-up position to reduce intracranial pressure. Three days later, her consciousness recovered to Japan Coma Scale score of 30 and Glasgow Coma Scale score of E2V4M5. CT showed obvious reduction of the hematoma without brain or scalp swelling. Spinal MR imaging detected no redistribution of hematoma to the spine. The present case illustrates that rapid spontaneous reduction of ASDH may occur by redistribution of hematoma, mainly to the supratentorial subdural space because of brain atrophy.

Acute subdural hematoma (ASDH) patients presenting in a severe condition tend to have poor outcomes due to the significant brain edema required to maintain the ICP at less than 20-25 mmHg. This study compared the surgical outcomes of 16 critically ill patients with ASDH who underwent hematoma irrigation with trephination therapy (HITT) based on their initial ICP values. The initial mean GCS score upon admission was four. A unilateral dilated pupil was seen in one and bilateral dilated pupils were seen in seven patients. The co-existence of a brain contusion was seen in seven patients, brain swelling was noted in six patients, and both basal cistern effacement and a midline shift greater than 5 mm were observed in all patients. The mean initial ICP value was 45 mmHg (range: 3 to 85 mmHg). Ten patients (62.5%) underwent a rapid external decompression to evacuate the hematoma. By using the Glasgow Outcome Scale upon discharge a score of good recovery (GR) was assigned to two (12.5 %), moderate disability (MD) to four (25.0 %), vegetative state (VS) to two (12.5 %), and death (D) to eight (50.0 %) patients. All six patients who showed an initial ICP greater than 60 mmHg died despite intensive care. Eight patients who showed an initial ICP less than 40 mmHg had a favorable outcome, but two patients deteriorated due to a traumatic cerebrovascular disorder. It seems that the initial ICP monitoring with HITT for ASDH patients in critical condition may be an important factor for predicting both surgical outcome and clinical course.

Acute subdural hematoma (ASDH) is a critical condition following the onset of traumatic brain injury, and it is essential to immediately reduce elevated intracranial pressure (ICP). Single burr hole surgery/twist drill craniostomy is commonly performed in patients with ASDH as an emergency surgical intervention, usually preceding decompressive craniotomy. A novel method using a cerebrospinal fluid (CSF) drainage catheter kit for rapid drainage of ASDH is described. Percutaneous twist drill craniostomy using a CAMINO(®) micro ventricular bolt pressure-temperature monitoring kit was performed in the emergency room in 12 patients with severe ASDH. The kit contained a closed-system CSF drainage and pressure-temperature monitoring catheter, which allowed aspiration of the hematoma and monitoring of the ICP. The tip of the catheter was inserted into the hematoma from the forehead. The mean initial ICP was 61 mmHg, with a range of 31 to 120 mmHg. The liquid hematoma was aspirated, and the ICP was temporarily controlled to the normal range. Pupil dilation recovered immediately after aspiration of the hematoma in 3 patients. No complications occurred either during or after the operation. This new method for craniostomy is easy, safe, and effective to monitor and rapidly control ICP in the emergency room. This technique also offers the possibility of evaluating the patient's prognosis and determining indications for further decompressive craniectomy by the continuation of ICP control under ICP monitoring and evaluation of the reversibility of pupillary findings in ASDH patients.

The majority of acute post-traumatic subdural hematomas (ASDH) require urgent surgical evacuation. Spontaneous resolution of ASDH has been reported in some cases. We report here on a case of a patient with a large amount of ASDH that was rapidly reduced. A 61-yr-old man was found unconscious following a high speed motor vehicle accident. On initial examination, his Glasgow Coma Score scale was 4/15. His pupils were fully dilated and non-reactive to bright light. Brain computed tomography (CT) showed a massive right-sided ASDH. The decision was made to treat him conservatively because of his poor clinical condition. Another brain CT approximately 14 hr after the initial scan demonstrated a remarkable reduction of the previous ASDH and there was the new appearance of high density in the subdural space adjacent to the falx and the tentorium. Thirty days after his admission, brain CT revealed chronic SDH and the patient underwent surgery. The patient is currently able to obey simple commands. In conclusion, spontaneous rapid resolution/reduction of ASDH may occur in some patients. The mechanisms are most likely the result of dilution by cerebrospinal fluid and the redistribution of hematoma especially in patients with brain atrophy.

A rare case is described of acute disseminated intravascular coagulation (DIC) following isolated mild head injury with acute subdural haematoma, coagulopathy onset preceding craniotomy. Surgical treatment of the cause followed by swift diagnosis and treatment soon after surgery enabled a good outcome. Post-operative recollection of subdural and extadural blood was treated by further surgery. DIC following isolated mild head injury without axonal damage is rare, but fatal if missed. Thrombocytopaenia in head injured patients should be investigated expediently. Post-operative interim imaging (if not standard practice) should also be considered to exclude haemorrhagic recollection requiring further surgery.

Blunt and rotational head impacts due to vehicular collisions, falls and contact sports cause relative motion between the brain and skull. This increases the normal and shear stresses in the (skull/brain) interface region consisting of cerebrospinal fluid (CSF) and subarachnoid space (SAS) trabeculae. The relative motion between the brain and skull can explain many types of traumatic brain injuries (TBI) including acute subdural hematomas (ASDH) and subarachnoid hemorrhage (SAH) which is caused by the rupture of bridging veins that transverse from the deep brain tissue to the superficial meningeal coverings. The complicated geometry of the SAS trabeculae makes it impossible to model all the details of the region. Investigators have compromised this layer with solid elements, which may lead to inaccurate results. In this paper, the failure of the cerebral blood vessels due to the head impacts have been investigated. This is accomplished through a global/local modelling approach. Two global models, namely a global solid model (GSM) of the skull/brain and a global fluid model (GFM) of the SAS/CSF, were constructed and were validated. The global models were subjected to two sets of impact loads (head injury criterion, HIC = 740 and 1044). The relative displacements between the brain and skull were determined from GSM. The CSF equivalent fluid pressure due to the impact loads were determined by the GFM. To locally study the mechanism of the injury, the relative displacement between the brain and skull along with the equivalent fluid pressure were implemented into a new local solid model (LSM). The strains of the cerebral blood vessels were determined from LSM. These values were compared with their relevant experimental ultimate strain values. The results showed an agreement with the experimental values indicating that the second impact (HIC = 1044) was strong enough to lead to severe injury. The global/local approach provides a reliable tool to study the cerebral blood vessel ruptures leading to ASDH and/or SAH.

A 55-year-old man presented with a rare lipomatous meningioma associated with acute subdural hematoma manifesting as sudden onset of severe headache, but no neurological deficit. No evidence of trauma or underlying predisposition to hemorrhage was seen. Fluid-attenuated inversion-recovery magnetic resonance imaging showed a thin hyperintense area in the right temporal convexity, and an extra-axial mass appearing as mixed hypointensity and hyperintensity. Two weeks later, right temporal craniotomy was performed and the tumor was totally resected with the attached dura. The hematoma was localized at the inferior margin of the mass and connected directly with the tumor. Histological examination of the resected specimen revealed typical meningothelial meningioma admixed with mature adipose tissue. Longstanding intratumoral congestion probably caused hyaline deposition in the tissue, leading to vessel rupture.

Traumatic brain injury (TBI) is often complicated by acute subdural hemorrhage (ASDH) with a high mortality rate. The pathophysiological mechanisms behind such an injury type and the contribution of blood to the extent of an injury remain poorly understood. Therefore, the goals of this study were to establish a porcine ASDH model in order to investigate pathomechanisms of ASDH and to compare effects induced by blood or sheer volume. Thus, we infused 2, 5, and 9 mL of blood (up to 15% of intracranial volume), and we compared a 5-mL blood and paraffin oil volume to separate out effects of extravasated blood on brain tissue. An extended neuromonitoring was applied that lasted up to 12 h after injury and included intracranial pressure (ICP), cerebral perfusion pressure (CPP), tissue oxygen concentration (ptiO(2)), biochemical markers (glutamate, lactate), somatosensory evoked potentials (SEP), brain water content, and histological assessment (Lesion Index [LI]). Volume-dependent changes were detected mainly during the first hours after injury. ICP increased to significant levels (p < 0.05) of 36.89 +/- 1.59, 15.52 +/- 0.48, and 11.25 +/- 0.35 mm Hg after 9, 5, and 2 mL of subdural blood, respectively (sham, 4.85 +/- 0.06 mm Hg). The ptiO(2) dropped drastically after 9 mL of subdural blood without recovery in both hemispheres to below 20% of baseline, but was affected little after 2 and 5 mL in the acute monitoring period (maximal drop to 71% of baseline). Later, 5 mL of blood led to a significant increase of ptiO(2) compared to 2 mL ipsilaterally (p < 0.05). Glutamate and lactate showed a comparable pattern with a long-lasting increase after 9 mL of blood and short-lasting changes after 2 and 5 mL. The two smaller volumes caused an increased brain swelling (2 mL, 80.60 +/- 0.34%; 5 mL, 81.20 +/- 0.66%; p < 0.05 vs. sham), a significant LI (sham, 6.4 +/- 1.4; 2 mL, 30.0 +/- 0.95; 5 mL, 32.1 +/- 1.2; p < 0.05 vs. sham), and a reduced SEP amplitude (5 mL, p < 0.05 vs. baseline) at the end of the experiment. A 9-mL led to herniation during the experiment causing dramatical brain swelling and acute histological damage. Comparison of blood volume with paraffin oil showed no significance, indicating that volume alone determines the acute pathophysiological processes leading to a rapidly developing histological damage. Additional effects due to blood contact with brain tissue (e.g., inflammation) may be detected only at later time points (>12 h).

Objective: The treatment of acute subdural hematoma (ASDH) consists mainly of surgical evacuation of the hematoma. It is conceivable that early preoperative neuroprotection with hypertonic/hyperoncotic treatment (HHT) can improve survival rates. The present study investigated the benefit of treatment with hypertonic/hyperoncotic solution on functional and histologic outcome as supportive therapy accompanying surgical intervention., Design: Laboratory experiment., Setting: University laboratory., Subjects: Male Sprague-Dawley rats weighing 296-350 g (n = 56)., Interventions: ASDH was induced through subdural infusion of 400 microL of autologous venous blood. Thirty minutes after subdural blood infusion, the rats received either HyperHAES (7.2% saline/6% hydroxyethyl starch) or vehicle (NaCl 0.9%) intravenously, followed by surgical evacuation of the hematoma 1 hr after ASDH induction in those rats scheduled for surgical treatment. The experiment was divided into two parts: an acute study, which explored acute effects of HHT on blood variables, ASDH-induced changes of intracranial pressure (ICP), and cerebral perfusion pressure (CPP), and a chronic study, which investigated the chronic effects of HHT, surgical blood clot evacuation, and the combination of both on the functional and histologic outcome following ASDH (12 days)., Measurements and Main Results: In the acute study, HHT expectedly raised the serum sodium concentration and lowered hematocrit. ASDH increased ICP and decreased CPP in all groups. HHT improved CPP by reducing ICP. In the chronic study, all treated groups showed a better recovery with respect to neurologic function and neuronal cell death compared with the vehicle-treated ASDH group. HHT with surgical evacuation or HHT alone improved functional and histologic outcome slightly more than surgical evacuation alone., Conclusions: In this rat model, HHT led to a decrease of ICP after ASDH. This significantly improved functional and histologic outcome, which was comparable to the effects after blood evacuation alone. The combination of evacuation of subdural blood and early HHT improved histologic outcome further but not significantly, which was due to the strong effects of single treatments and a ceiling effect of the combined treatment in this model.

A 39-year-old man presented with headache, weight loss, bilateral subdural hematomas, pansinusitis, and visual loss. The neuro-ophthalmologic examination disclosed deep choroidal lesions and bilateral optic disc edema. Orchiectomy for testicular torsion showed acute vasculitis consistent with polyarteritis nodosa (PAN). Polymerase chain reaction (PCR) testing revealed hepatitis C. This is the first reported case of PAN due to hepatitis C with early findings of choroidal and optic nerve infarction.

Aim: Acute subdural haematoma (ASDH) is seldom an isolated lesion and it is difficult to understand the mechanisms which determine the poor prognosis associated to this occurrence. Aim of this study was estimating the outcome of patients with ASDH without any companion lesions by analysing the haematoma volume, its thickness and midline shift., Methods: Twenty-eight severely head injured patients (Glasgow Coma Scale, GCS =/<8) with isolated unilateral ASDH admitted in intensive care unit (ICU) were retrospectively studied. The haematoma thickness, the midline shift, the ASDH volume were obtained from the first emergency computerized tomography (CT) scan and analysed by a computer assisted programme (Osiris). Patients' outcome was scored according to the Glasgow Outcome Scale (GOS) 6 months after the event. According to their GOS the patients were further divided in 2 groups (favourable outcome: GOS 4-5, poor outcome: GOS 1-2-3)., Results: Midline shift ranged from 0 to 19.2 mm; we found a larger midline shift in those patients who died and in patients with severe disability or vegetative state 6 months after the trauma., Conclusion: The presence and size of midline shift was a more important determinant of outcome than ASDH volume or its thickness.

Background: Traumatic brain injury (TBI) is a major health problem, both in terms of the economic cost to society and the survivor's quality of life. The development of devices to protect against TBI requires criteria that relate observed injury to measurements of head kinematics. The objective of this study is to find the best statistical correlates to impact-induced TBI in nonhuman primates using a qualified, self-consistent set of historical kinematic and TBI data from impact tests on nonhuman primates., Methods: A database was constructed and qualified from historical head impact tests on nonhuman primates. Multivariate logistic regression analysis with backwards stepwise elimination was performed. Variables considered are the peak rotational acceleration (Omegamax), the peak linear acceleration (Amax), and the number of impacts (N)., Results: Bivariate combinations of angular acceleration and the number of impacts are the best correlates to all modes of TBI considered, i.e., concussion, subarachnoid hemorrhage, brain contusion, and subdural hematoma. For a nonhuman primate with 100-g brain mass, the criteria that the probability of TBI is less than 10% by injury mode are:Concussion: OmegamaxN(0.84) < 70 krad/s/s SAH: OmegamaxN(0.70) < 160 krad/s/s Contusion: Omegamax N(0.35) < 160 krad/s/s SDH: Omegamax N(0.60) < 280 krad/s/s, Conclusions: Based on this dataset, the best statistically based risk factor for all modes of TBI in nonhuman primates is the bivariate combination of rotational acceleration and number of impacts.

Traumatic brain injury is associated with acute subdural hematoma (ASDH) that worsens outcome. Although early removal of blood can reduce mortality, patients still die or remain disabled after surgery and additional treatments are needed. The blood mass and extravasated blood induce pathomechanisms such as high intracranial pressure (ICP), ischemia, apoptosis and inflammation which lead to acute as well as delayed cell death. Only little is known about the basis of delayed cell death in this type of injury. Thus, the purpose of the study was to investigate to which extent caspase-dependent intracellular processes are involved in the lesion development after ASDH in rats. A volume of 300microL blood was infused into the subdural space under monitoring of ICP and tissue oxygen concentration. To asses delayed cell death mechanisms, DNA fragmentation was measured 1, 2, 4 and 7 days after ASDH by TUNEL staining, and the effect of the pan-caspase inhibitor zVADfmk on lesion volume was assessed 7 days post-ASDH. A peak of TUNEL-positive cells was found in the injured cortex at day 2 after blood infusion (53.4+/-11.6 cells/mm(2)). zVADfmk (160ng), applied by intracerebroventricular injection before ASDH, reduced lesion volume significantly by more than 50% (vehicle: 23.79+/-7.62mm(3); zVADfmk: 9.06+/-4.08). The data show for the first time that apoptotic processes are evident following ASDH and that caspase-dependent mechanisms play a crucial role in the lesion development caused by the blood effect on brain tissue.

Object: Based on data from primate experiments it is known that rotational acceleration in the sagittal plane and in a forward direction is most likely to produce acute subdural hematomas due to bridging vein rupture. For protection against these lesions, knowledge of rotational acceleration tolerance levels in humans is required. In the present study the authors analyze human tolerance levels for bridging vein rupture by performing head impact tests in cadavers., Methods: Ten unembalmed cadavers were subjected to 18 occipital impacts producing head rotation in the sagittal plane with varying rotational acceleration magnitudes and pulse durations. Rotational acceleration was calculated from the linear acceleration histories recorded by three uniaxial accelerometers mounted on the side of the head. Bridging vein ruptures were detected by injecting contrast dye into the superior sagittal sinus under fluoroscopy and by autopsy procedures. Bridging vein ruptures were produced in six head impact tests: one test with a pulse duration of 5.2 msec and a peak rotational acceleration of 13,411 rad/second2; three tests with a pulse duration between 7 and 8 msec and a peak rotational acceleration of 12,558, 10,607, and 8567 rad/second2; and two tests with a pulse duration longer than 10 msec and a peak rotational acceleration as low as 5267 rad/second2., Conclusions: This is the only cadaveric study of bridging vein rupture focused on short pulse durations, which are usually associated with falls. The data suggest a tolerance level of approximately 10,000 rad/second2 for pulse durations shorter than 10 msec, which seems to decrease for longer pulse durations.

The aim of this study was to clarify the mechanism of hemodynamic changes leading to intraoperative hypotension during evacuation of acute subdural hematoma. To our knowledge, little data is available about the mechanism of hemodynamic changes during surgical interventions to decrease intracranial pressure after severe head injury. The influence of preoperative hypotension on intraoperative hypotension was examined. Hemodynamic studies (pulmonary artery catheterization) were carried out in 15 patients before and after acute subdural hematoma evacuation. All patients were assessed for hemodynamic parameters, evacuated hematoma volume, and intracranial pressure measurements. Comparison between just before and after evacuation of the hematoma showed that the mean arterial pressure, pulmonary arterial pressure, systemic vascular resistance, pulmonary vascular resistance, central venous pressure, and pulmonary capillary wedge pressure all decreased after hematoma evacuation. However, the cardiac index was unchanged after hematoma evacuation. Mean arterial blood pressure is dependent on the cardiac index and vascular resistance, so the decrease in arterial blood pressure during hematoma evacuation was the result of a decline in vascular resistance. The influence of preoperative blood pressure on intraoperative hemodynamic changes was analyzed by dividing the patients into two groups, the preoperative hypotension group and preoperative nonhypotension group. The decrease in mean arterial blood pressure was more marked in the preoperative hypotension group than in the preoperative nonhypotension group. Intraoperative hypotension during evacuation of acute subdural hematoma is caused by a decrease in vascular resistance. Preoperative hypotension is a also risk factor for intraoperative hypotension.

Objective: To develop a highly reproducible rat model and behavioral tests for acute subdural hematoma (ASDH) and to investigate the role of intravascular coagulation and thrombin in the pathogenesis of brain injury in this model., Methods: A new method was implemented to inject 200 microl of autologous blood subdurally in rats. Immunohistochemistry was used to investigate intravascular fibrin deposition and thrombin levels in the cortex underlying the ASDH. Effectiveness of systemic heparin, argatroban, or ginkgolide B treatment was determined by histological lesion volume, number of occluded microvessels, and neurological deficits. Neurological deficits were monitored for 7 days after ASDH by use of forelimb placing, forelimb use asymmetry, and corner turn tests., Results: Consistent brain damage and sensorimotor deficits were observed in all animals with ASDH. Histological analysis demonstrated occluded microvessels and enlarged perivascular spaces in the underlying cortex starting 1 hour after hematoma induction. Fibrin and thrombin immunoreactivity were increased in the lesioned cortical parenchyma at 4 and 24 hours. However, no intravascular fibrin deposition was detected. Heparin induced hemorrhagic transformation in the cortical lesion and did not attenuate microvessel occlusion. Argatroban and ginkgolide B did not induce hemorrhage but failed to improve microvessel occlusion, lesion volume, and neurological deficits., Conclusion: Intravascular coagulation and thrombin are not the major mediators of brain damage after ASDH. The model and behavioral tests presented in this study can be used to investigate other putative mechanisms of injury and to test future therapeutic interventions in ASDH.

Objective: The objective was to evaluate cerebral hemodynamics in young children with acute subdural hematoma (SDH) and the impact of surgical treatment using transcranial Doppler (TCD)., Design: The design was a prospective study of infants with SDH requiring surgical evacuation., Setting: The setting was the neuro intensive care unit of a university hospital., Interventions: Indications for surgical evacuation were based upon clinical and radiological arguments. Surgery included emergency needle aspiration followed by external or/and internal shunting as required. A TCD evaluation was performed before needle aspiration, and after each surgical drainage procedure. It included a pressure provocation test to assess cerebral compliance. Preoperative and postoperative middle cerebral artery (MCA) velocities, Gosling pulsatility (PI) and Pourcelot resistivity (RI) indexes and compliance were compared with Student's t-test, or Fisher's exact test as indicated., Measurements and Main Results: Out of 26 infants, 23 (88%) had injuries that had possibly been inflicted, and 3 had accidental injuries. Initial TCD evaluation demonstrated intracranial hypertension with decreased diastolic velocity, increased PI and RI, and decreased compliance. Surgical evacuation resulted in statistically significant improvement in cerebral hemodynamics (diastolic velocity: 17.2+/-10 cm/s vs. 31.1+/-10 cm/s, p<0.0015, PI: 2.5+/-1.3 vs. 1.4+/-0.8, p<0.002, RI: 0.8+/-0.2 vs. 0.6+/-0.1, p<0.005) in all but 3 infants, who eventually died. Surgical drainage (primary shunting or external drainage) was needed in 23 infants and resulted in further improvement in cerebral hemodynamics. Finally, 73% of the infants made a good recovery., Conclusions: Children with acute bilateral HSD have a high incidence of increased intracranial pressure as assessed by TCD. Surgical evacuation improves cerebral hemodynamics. TCD could be used for assessing the need for, and the efficiency of surgical drainage.

We report a case of 57 year-old man with documented posttraumatic acute subdural hematoma and a linear temporal bone fracture. He suffered from a blunt head injury and presented with sudden loss of consciousness. Within 2 hours he became alert and oriented. Follow-up CT scan of brain 2 hours after the initial one showed resolution and redistribution of the subdural hematoma. To our knowledge, this is the first case in the literature about spontaneous resolution of an acute subdural hematoma in a patient with a linear fracture and the fastest resolution period. In this article, the authors discuss the underlying pathophysiology of this uncommon phenomenon.

The aim of this study was to develop a new rat model of diffuse brain injury (DBI) associated with acute subdural hemorrhage (SDH). In order to make this model more clinically relevant, we determined whether the varying hematoma volume, severity of DBI, or the presence of hypoxemia could influence the physiological consequence. SDH was made by an autologous blood injection, while DBI was induced using the impact acceleration model (mild, 450 g/1 m, severe, 450 g/2 m). Physiological parameters measured included intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral blood flow (CBF), and brain tissue water content. In the first series, 23 rats were randomized into the five following groups: Group 1, sham; Group 2, 400 (microL SDH; Group 3, SDH400 + mild DBI; Group 4, SDH400 + severe DBI; and Group 5, SDH300 + severe DBI. Results suggested that SDH300 + severe DBI (Group 5) may be the most suitable model, in which the MABP and CBF temporarily decreased during the SDH induction, but thereafter recovered to the baseline. Conversely, ICP was persistently elevated throughout the experiment. The water content was also significantly higher in both hemispheres compared to that of sham. In the second series, the animal was exposed to a hypoxemic insult (10 or 30 min) in addition to SDH300 + severe DBI (Group 6). The prolonged hypoxemia caused both a severe CBF reduction without recovery and a bilateral brain swelling, whereas the brief hypoxemia showed a gradual CBF recovery from the transient reduction and an increased water content only in the SDH side. These results suggest that these models may be potentially useful to study the combination of DBI and SDH with or without hypoxemia.

Acute subdural hematomas are usually neurosurgical emergencies, although a conservative therapy is indicated in selected cases. In some of these patients a progressive resolution is appreciated. However, rapid spontaneous resolution of an acute suddural hematoma is seldom reported. A patient with antecedent of chronic alcoholism and spontaneous resolution of acute subdural hematoma in less than 18 hours after the head injury is described. The possible mechanisms of this rapid resolution are discussed. A tear in the arachnoid with spilling of CSF into the subdural space and the effect of intracranial antihypertensive measures together with cerebral atrophy, are factors that possibly contribute to dilution and redistribution of blood with hematoma disappearing in CT scan.

Acute postraumatic subdural hematoma is known to have bad prognosis. Traditionally, its treatment consisted in urgent surgical evacuation. Rapid spontaneous resolution of the hematoma has been infrequently observed. We report a case of a patient with an acute traumatic subdural hematoma which disappeared without surgery. CT-scan showed a left-sided subdural hematoma with marked mass effect. A low density layer, which implied involvement of CSF in the subdural space, was observed between the hematoma and the inner wall of the skull. We think that the spontaneous resolution of the hematoma was due to the dilution and washing-out by the CSF through an arachnoid tear. Another suggested mechanism in the literature is blood redistribution in the subdural space. Selected patients with an acute subdural hematoma can be managed with conservative treatment.