The Effect of Targeted Hyperoxemia on Brain Immunohistochemistry after Long-Term, Resuscitated Porcine Acute Subdural Hematoma and Hemorrhagic Shock.

Epidemiological data suggest that moderate hyperoxemia may be associated with an improved outcome after traumatic brain injury. In a prospective, randomized investigation of long-term, resuscitated acute subdural hematoma plus hemorrhagic shock (ASDH + HS) in 14 adult, human-sized pigs, targeted hyperoxemia (200 < PaO2 < 250 mmHg vs. normoxemia 80 < PaO2 < 120 mmHg) coincided with improved neurological function. Since brain perfusion, oxygenation and metabolism did not differ, this post hoc study analyzed the available material for the effects of targeted hyperoxemia on cerebral tissue markers of oxidative/nitrosative stress (nitrotyrosine expression), blood-brain barrier integrity (extravascular albumin accumulation) and fluid homeostasis (oxytocin, its receptor and the H2S-producing enzymes cystathionine-ß-synthase and cystathionine-γ-lyase). After 2 h of ASDH + HS (0.1 mL/kgBW autologous blood injected into the subdural space and passive removal of 30% of the blood volume), animals were resuscitated for up to 53 h by re-transfusion of shed blood, noradrenaline infusion to maintain cerebral perfusion pressure at baseline levels and hyper-/normoxemia during the first 24 h. Immediate postmortem, bi-hemispheric (i.e., blood-injected and contra-lateral) prefrontal cortex specimens from the base of the sulci underwent immunohistochemistry (% positive tissue staining) analysis of oxidative/nitrosative stress, blood-brain barrier integrity and fluid homeostasis. None of these tissue markers explained any differences in hyperoxemia-related neurological function. Likewise, hyperoxemia exerted no deleterious effects.

Collagen fibre orientation in human bridging veins.

Bridging veins (BVs) drain the blood from the cerebral cortex into dural sinuses. BVs have one end attached to the brain and the other to the superior sagittal sinus (SSS), which is attached to the skull. Relative movement between these two structures can cause BV to rupture producing acute subdural haematoma, a head injury with a mortality rate between 30 and 90%. A clear understanding of the BVs microstructure is required to increase the biofidelity of BV models when simulating head impacts. Twelve fresh BV samples draining in the superior sagittal sinus (SSS) from a single human cadaver were cut open along their length and placed on an inverted multiphoton microscope. To ensure that the BVs were aligned with the axial direction an in-house built, uniaxial tension set-up was used. Two scans were performed per sample. Before the first scan, a minor displacement was applied to align the tissue; then, a second scan was taken applying 50% strain. Each BV was scanned for a length of 5 mm starting from the drainage site into the SSS. Imaging was performed on a Zeiss LSM780 microscope with an 25[Formula: see text] water immersion objective (NA 0.8), coupled to a tunable MaiTai DS (Spectraphysics) pulsed laser with the wavelength set at 850 nm. Second harmonic and fluorescence signals were captured in forward and backward direction on binary GaAsP (BiG) detectors and stored as four colour Z-stacks. Prior to the calculation of the local orientations, acquired Z-stacks were denoised and enhanced to highlight fibrillar structures from the background. Then, for each Z-plane of the stack, the ImageJ plugin OrientationJ was used to extract the local 2D orientations of the fibres based on structure tensors. Two kinds of collagen architectures were seen. The most common (8[Formula: see text]12 samples) was single layered and had a uniform distribution of collagen. The less common (4[Formula: see text]12 samples) had 2 layers and 7 to 34 times thicker collagen bundles on the outer layer. Fibre angle analysis showed that collagen was oriented mainly along the axial direction of the vessel. The von Mises fittings showed that in order to describe the fibre distribution 3 components were needed with mean angles [Formula: see text] at [Formula: see text] 0.35, 0.21, [Formula: see text] 0.02 rad or [Formula: see text] 20.2[Formula: see text], 12.1[Formula: see text], [Formula: see text] 1.2[Formula: see text] relative to the vessel's axial direction which was also the horizontal scan direction.

Predictors of subacute hematoma expansion requiring surgical evacuation after initial conservative treatment in patients with acute subdural hematoma.

BACKGROUND: The aim of this study was to clarify the factors associated with requiring subacute surgery in patients with acute subdural hematoma (ASDH) treated conservatively at admission. METHODS: Among the patients with ASDH admitted to our hospital from 2007 to 2018, we retrospectively reviewed data for 200 patients initially treated conservatively. We compared patients' characteristics, medical history, radiological findings, and clinical outcomes and differences between patients undergoing subacute surgery or no surgery. RESULTS: Of the 200 patients treated conservatively, 17 (8.5%) patients underwent subacute surgery due to deterioration of their clinical and/or computed tomography (CT) findings, while 183 (91.5%) patients did not undergo subacute surgery. There were significant differences in the presence of focal neurological deficits, modified Rankin Scale scores, degree of midline shift, hematoma thickness, hematoma volume, cella media index, Sylvian fissure ratio, and hematoma density between the two groups. CONCLUSIONS: Large hematoma, brain atrophy, and hematoma density may be useful predictors for the need for subacute surgery in patients with ASDH treated conservatively at admission. Intensive investigation of clinical findings or CT images is warranted in patients with adverse prognostic factors, even if their initial symptoms are mild.

Neurostereologic Lesion Volumes and Spreading Depolarizations in Severe Traumatic Brain Injury Patients: A Pilot Study.

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.

Leakage sign for acute subdural hematoma in clinical treatment.

BACKGROUND: Acute subdural hematoma (ASDH) is a serious traumatic disease, and predictive methods for hematoma growth are necessary to decide whether emergent operation is necessary. This study aimed to evaluate the incidence of "leakage" using computed tomography angiography (CTA) in patients with ASDH and to identify its prognostic value. METHODS: Sixty-seven patients with ASDH were examined using CTA (mean age 64.1 ± 20.6 years; 24 men) by analyzing two serial scans (CTA phase and delayed phase). We defined a positive leakage sign as a > 10% increase in Hounsfield units (HU) in the region of interest. Hematoma expansion was determined using plain CT after 24 h in patients who did not undergo emergent surgery. RESULTS: Of the 67 patients, conservative therapy was administered to 35 patients; of these patients, 9 showed hematoma expansion, and 8 of these 9 patients (88.9%) showed positive leakage signs. The sensitivity and specificity of leakage signs to hematoma expansion in the no-surgery group were 88.8% and 76.1%, respectively. All positive leakage signs were found within 4.5 h of injury; patients showing negative leakage signs showed a decreased tendency towards hematoma 24 h after injury. Patients presenting with positive leakage signs had poor outcomes. CONCLUSIONS: The results indicated that the leakage sign is a sensitive predictor of hematoma expansion and poor outcomes in ASDH. If the hematoma is small but leakage sign-positive, strict observation is necessary and aggressive surgery may improve outcomes.

Thrombin contributes to the injury development and neurological deficit after acute subdural hemorrhage in rats only in collaboration with additional blood-derived factors.

BACKGROUND: Acute subdural hemorrhage (ASDH) is a severe consequence of traumatic brain injury. The occurrence of subdural blood increases the lethality of these patients independent of the amount of blood or elevated intracranial pressure. Thrombin is one of the potential harmful blood components. Possible harmful effects of thrombin are mediated via the Protease-activated-receptor-1 (PAR1) and thus, translating the acute Thrombin release after ASDH into cell loss. The objectives of the present study were twofold, namely to examine (1) the impact of direct thrombin inhibition in the acute phase after hemorrhage on the long-term histological and functional deficits and (2) the early inhibition of PAR1 activation by thrombin with the selective antagonist SCH79797 on lesion volume at 14 days after ASDH. The effects of thrombin on the lesion size were investigated in two separate experiments via (1) direct thrombin inhibition in the subdural infused blood (Argatroban 600 µg) as well as by (2) intraventricular injection of the PAR-1 antagonist SCH79797 (1 µg or 5 µg). Lesion volume and behavior deficits using a neurological deficit score and a motor function test (beam balance test) were analyzed as outcome parameters at 14 days after injury. RESULTS: 59 Male Sprague-Dawley rats received a subdural infusion of 300 µl autologous blood or sham operation. Lesion volume at 14 days after ASDH tended to be smaller in the Argatroban-treated group when compared to the vehicle group (8.1 ± 1.1 vs. 10.1 ± 2.3 mm2, n.s.). Motor deficits in the beam balance test were not significantly less severe in the Argatroban-treated group. Animals treated with SCH79797 also showed a trend towards dose-dependent decreased lesion volume in comparison to the vehicle-treated group (1 µg: 4.3 ± 0.7 mm3; 5 µg: 3.8 ± 1.1 mm3; vehicle: 6.5 ± 2.0 mm3, n.s). CONCLUSIONS: Thrombin inhibition in the subdural blood and local cerebral blockade of PAR-1 cause a tendency towards reduced lesion volume or functional recovery. All results show a trend in favor of the acute treatment on the outcome parameters. Our results suggests that thrombin could be an important blood-derived factor during acute subdural hemorrhage that translates its deleterious effects in concert with other blood-induced factors.

Importance of effusion of blood under the dura mater in forensic medicine: A STROBE - compliant retrospective study.

Subdural hemorrhage is commonly associated with mechanical brain injury and has a correspondingly high mortality rate. Subdural hematomas may immediately provoke symptoms or may be initially asymptomatic, with further symptoms evolving rapidly and fatally.The data regarding forensic autopsy of victims were obtained from The State Forensic Medicine Service of Lithuania between the years 2013 and 2016. A retrospective study was performed including 110 patients, whose cause of death was subdural hemorrhage. 95% confidence intervals were calculated.It was calculated, that in cases of sudden death, after subdural hemorrhage was diagnosed, a higher concentration of ethyl alcohol in blood (mean 2.22 ±â€Š1.3%) demanded a smaller amount of blood under the dura matter (mean 81.6 ±â€Š60.5 g) in order for the patient to die. It was also noted that hospitalized patients with subdural hemorrhage had a smaller concentration of blood ethyl alcohol (mean 1.33 ±â€Š1%) and a larger amount of blood under the dura (mean 135.6 ±â€Š82.9 g).Due to the toxic effect of ethyl alcohol, even a small amount (81.6 ±â€Š60.5 g) of blood under the dura matter can determine a sudden death.

The Pathogenesis of Subacute Subdural Hematoma: A Report of 3 Cases and Literature Review.

OBJECTIVE: To discuss the pathologic mechanism of subacute subdural hematoma (sASDH). METHODS: Three typical cases of sASDH were reported, and related literature in Chinese published in the past 15 years was reviewed. RESULTS: Intervals from onset of acute subdural hematoma to surgery or symptom deterioration resulting in sASDH were 12.5-15.5 days (mean 14.1 days). Delayed liquefaction of hematoma clots occurred in all 3 reported cases. One patient achieved good curative effect after administration of dexamethasone, and another patient relapsed owing to poor drainage after evacuation of hematoma. CONCLUSIONS: The conversion of acute subdural hematoma to sASDH is an inflammatory reaction process with very regular in time, and it is speculated that the pathologic mechanism may be a delayed hypersensitivity reaction. Antigen released during the liquefaction process of blood clot, with subdural neomembrane cells as antigen-presenting cells, is presented to the T lymphocytes released from the capillaries in the neomembrane and forms sensitized T lymphocytes. When the subsequent antigen is released from the blood clots with a delayed liquefaction and is exposed to sensitized T lymphocytes, the delayed hypersensitivity process occurs.

Traumatic brain injury: Comparison between autopsy and ante-mortem CT.

PURPOSE: The aim of this study was to compare pathological findings after traumatic brain injury between autopsy and ante-mortem computed tomography (CT). A second aim was to identify changes in these findings between the primary posttraumatic CT and the last follow-up CT before death. METHODS: Through the collaboration between clinical radiology and forensic medicine, 45 patients with traumatic brain injury were investigated. These patients had undergone ante-mortem CT as well as autopsy. During autopsy, the brain was cut in fronto-parallel slices directly after removal without additional fixation or subsequent histology. Typical findings of traumatic brain injury were compared between autopsy and radiology. Additionally, these findings were compared between the primary CT and the last follow-up CT before death. RESULTS: The comparison between autopsy and radiology revealed a high specificity (≥80%) in most of the findings. Sensitivity and positive predictive value were high (≥80%) in almost half of the findings. Sixteen patients had undergone craniotomy with subsequent follow-up CT. Thirteen conservatively treated patients had undergone a follow-up CT. Comparison between the primary CT and the last ante-mortem CT revealed marked changes in the presence and absence of findings, especially in patients with severe traumatic brain injury requiring decompression craniotomy. CONCLUSION: The main pathological findings of traumatic brain injury were comparable between clinical ante-mortem CT examinations and autopsy. Comparison between the primary CT after trauma and the last ante-mortem CT revealed marked changes in the findings, especially in patients with severe traumatic brain injury. Hence, clinically routine ante-mortem CT should be included in the process of autopsy interpretation.

Aggressive medical management of acute traumatic subdural hematomas before emergency craniotomy in patients presenting with bilateral unreactive pupils. A cohort study.

BACKGROUND: The outcome of patients with severe traumatic brain injury (TBI) and acute traumatic subdural hematoma (aSDH) admitted to the emergency room with bilaterally dilated, unreactive pupils (bilateral mydriasis) is notoriously poor. METHODS: Of 2074 TBI patients consecutively admitted to our facility between 1997 and 2012, 115 had a first CT scan with aSDH, unreactive bilateral mydriasis, and a Glasgow Coma Score of 3 or 4. Sixty-two patients were unoperated and died within hours or a few days. The remaining 53 patients (2.5% of the 2074 consecutive patients) were scheduled for emergent evacuation of the aSDH. We compared three different dosages of mannitol to landmark different comprehensive levels of treatment: (1) a "basic" level of treatment characterized by a single conventional dose (18 to 36 g), (2) "reinforced" treatment landmarked by a single high dose (54 to 72 g), and (3) "aggressive" treatment landmarked by a single high dose (90 to 106 g). Doses above 36 g were administered intravenously over a period of 5 min. RESULTS: Of the 53 selected patients, 7 were aggressively managed (13.2%) and 24 (45.3%) received reinforced treatment. Rates of hyperventilation and barbiturate bolus administration were appropriately associated with increasing doses of mannitol. After adjustment for age, aggressive management was significantly associated with a lower risk of death and persistent vegetative state [adjusted OR 0.016 (95% 0.001-0.405)]. Patients surviving after aggressive management suffered more severe disability at 1 year. CONCLUSION: The study shows an association between reduced mortality and persistent vegetative state, albeit at the cost of increased long-term severe disability in survivors, and aggressive medical preoperative management of mydriatic patients with aSDH following TBI.

Symptomatic Acute-on-Chronic Subdural Hematoma: A Clinicopathological Study.

The pathophysiology of acute-on-chronic subdural hematoma (ACSDH) is complex and incompletely understood. Evidence to date indicates that the overall process is initiated by rotational force with movement of the brain inside the skull, which exerts tensile strain and rupture of bridging veins, leading in turn to acute hemorrhage in the subdural potential space. This is followed by the proliferation of mesenchymal elements with angiogenesis and inflammation, which in turn becomes a substrate for repeated hemorrhage and expansion of the lesion. Given the prevalence of traumatic subdural processes in the forensic setting and the importance of proper assessment of timing, etiology, risk factors, and clinicopathological correlation, we studied 47 patients presenting to the University of Maryland Shock Trauma Center, all of whom underwent craniotomy with resection of the outer membrane due to symptomatic ACSDH. The surgically resected tissue was examined for histopathologic features in all cases. Our findings highlight that ACSDH is a condition precipitated by trauma that affects middle-aged and older adults, is relatively indolent, is unilateral or asymmetric, and has a low in-hospital mortality rate. Pathological analysis demonstrates a substantial outer membrane in all cases with varying degrees of inflammation and organization that cannot be precisely dated as a function of clinical presentation. The extrapolation of adult ACSDH to mixed acute and chronic subdural hemorrhage in the pediatric setting is problematic due to substantial differences in clinical presentation, severity of underlying brain injury, gross and microscopic findings, and outcome.

On the assessment of bridging vein rupture associated acute subdural hematoma through finite element analysis.

Acute subdural hematoma (ASDH) is a type of intracranial haemorrhage following head impact, with high mortality rates. Bridging vein (BV) rupture is a major cause of ASDH, which is why a biofidelic representation of BVs in finite element (FE) head models is essential for the successful prediction of ASDH. We investigated the mechanical behavior of BVs in the KTH FE head model. First, a sensitivity study quantified the effect of loading conditions and mechanical properties on BV strain. It was found that the peak rotational velocity and acceleration and pulse duration have a pronounced effect on the BV strains. Both Young's modulus and diameter are also negatively correlated with the BV strains. A normalized multiple linear regression model using Young's modulus, outer diameter and peak rotational velocity to predict the BV strain yields an adjusted [Formula: see text]-value of 0.81. Secondly, cadaver head impact experiments were simulated with varying sets of mechanical properties, upon which the amount of successful BV rupture predictions was evaluated. The success rate fluctuated between 67 and 75%. To further increase the predictive capability of FE head models w.r.t. BV rupture, future work should be directed towards improvement of the BV representation, both geometrically and mechanically.

Blood Aggravates Histological and Functional Damage after Acute Subdural Hematoma in Rats.

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.

[A Case of Ruptured Internal Carotid-Posterior Communicating Artery Aneurysm Associated with Acute Subdural Hematoma, Extending from the Interhemispheric Space to the Posterior Fossa].

A 69-year-old woman was admitted to our hospital because of a sudden severe headache without a history of head trauma. CT and MRI revealed an acute subdural hematoma (ASDH) extending from the right interhemispheric space to the posterior fossa bilaterally, with a small amount of subarachnoid hemorrhage that was predominantly localized to the left side of the basal cistern. CT angiogram demonstrated a long protruding ruptured aneurysm at the junction of the right internal carotid and posterior communicating arteries (IC/PC AN) with a posteroinferior projection, associated with a small bleb located near the tentorial edge close to the ipsilateral posterior clinoid process, for which she received clipping surgery. Though rare, IC/PC AN could cause pure or nearly pure ASDH in the above-mentioned distribution. Therefore, in patients with such ASDH, especially without a history of head injury or precise information regarding the situation at the time of onset, urgent imaging evaluation and early intervention are essential to prevent devastating re-rupture events.

Contrecoup Traumatic Intracerebral Hemorrhage: A Geometric Study of the Impact Site and Association with Hemorrhagic Progression.

Traumatic intracerebral hemorrhage (TICH) represents 13-48% of the lesions after a traumatic brain injury (TBI). The frequency of TICH-hemorrhagic progression (TICH-HP) is estimated to be approximately 38-63%. The relationship between the impact site and TICH location has been described in many autopsy-based series. This association, however, has not been consistently demonstrated since the introduction of computed tomography (CT) for studying TBI. This study aimed to determine the association between the impact site and TICH location in patients with moderate and severe TBI. We also analyzed the associations between the TICH location, the impact site, the production mechanism (coup or contrecoup), and hemorrhagic progression. We retrospectively analyzed the records of 408 patients after a moderate or severe TBI between January 2010 and November 2014. We identified 177 patients with a total of 369 TICHs. We found a statistically significant association between frontal TICHs and impact sites located on the anterior area of the head (OR 5.8, p < 0.001). The temporal TICH location was significantly associated with impact sites located on the posterior head area (OR 4.9, p < 0.001). Anterior and lateral TICHs were associated with impact sites located at less than 90 degrees (coup) (OR 1.64, p = 0.03) and more than 90 degrees (contrecoup), respectively. Factors independently associated with TICH-HP obtained through logistic regression included an initial volume of <1 cc, cisternal compression, falls, acute subdural hematoma, multiple TICHs, and contrecoup TICHs. We demonstrated a significant association between the TICH location and impact site. The contrecoup represents a risk factor independently associated with hemorrhagic progression.

A case of acute subdural hematoma due to ruptured aneurysm detected by postmortem angiography.

Acute subdural hematoma (ASDH) is mostly caused by head trauma, but intrinsic causes also exist such as aneurysm rupture. We describe here a case involving a man in his 70s who was found lying on the bedroom floor by his family. CT performed at the hospital showed ASDH and a forensic autopsy was requested. Postmortem cerebral angiography showed dilatation of the bifurcation of the middle cerebral artery, which coincided with the dilated part of the Sylvian fissure. Extravasation of contrast medium into the subdural hematoma from this site was suggestive of a ruptured aneurysm. Autopsy revealed a fleshy hematoma (total weight 110 g) in the right subdural space and findings of brain herniation. As indicated on angiography, a ruptured saccular aneurysm was confirmed at the bifurcation of the middle cerebral artery. Obvious injuries to the head or face could not be detected on either external or internal examination, and intrinsic ASDH due to a ruptured middle cerebral artery aneurysm was determined as the cause of death. One of the key points of forensic diagnosis is the strict differentiation between intrinsic and extrinsic onset for conditions leading to death. Although most subdural hematomas (SDH) are caused by extrinsic factors, forensic pathologists should consider the possibility of intrinsic SDH. In addition, postmortem angiography can be useful for identifying vascular lesions in such cases.

Non-traumatic subdural hematoma secondary to septic brain embolism: A rare cause of unexpected death in a drug addict suffering from undiagnosed bacterial endocarditis.

Acute subdural hematomas are mostly due to blunt traumatization of the head. In rare instances, subdural bleeding occurs without evidence of a previous trauma following spontaneous hemorrhage, e.g. from a ruptured aneurysm or an intracerebral hematoma perforating the brain surface and the arachnoid. The paper presents the morphological, microbiological and toxicological findings in a 38-year-old drug addict who was found by his partner in a dazed state. When brought to a hospital, he underwent trepanation to empty a right-sided subdural hematoma, but he died already 4h after admission. Autopsy revealed previously undiagnosed infective endocarditis of the aortic valve as well as multiple infarctions of brain, spleen and kidneys obviously caused by septic emboli. The subdural hematoma originated from a subcortical brain hemorrhage which had perforated into the subdural space. Microbiological investigation of the polypous vegetations adhering to the aortic valve revealed colonization by Streptococcus mitis and Klebsiella oxytoca. According to the toxicological analysis, no psychotropic substances had contributed to the lethal outcome. The case reported underlines that all deaths of drug addicts should be subjected to complete forensic autopsy, as apart from intoxications also natural and traumatic causes of death have to be taken into consideration.

Optical clearing of the dura mater using glycerol: a reversible process to aid the post-mortem investigation of infant head injury.

PURPOSE: In cases of suspected abusive head trauma, a thorough and systematic study of the cranium and its contents is essential, preferably using the best available methods for observing the brain and its coverings. Building upon recent developments in skull bone removal techniques in infant autopsies, we have assessed the use of two optical clearing agents (OCAs), glycerol and mannitol, on pediatric dura mater in an attempt to increase the transparency of this tissue and thereby enhance the post-mortem assessment of infant head injuries, particularly subdural hematomas. METHODS: Extracorporeal testing revealed glycerol to be the more effective OCA. Therefore, in situ investigations were commenced using glycerol during 33 pediatric post-mortem examinations. RESULTS: An increase in the transparency of the dura was observed in 32 of the 33 cases, within 1 min of application of the OCA. In a 2 year old with cerebral palsy, only partial optical clearance of the dura was seen, most likely due to a significantly atrophic brain, prominent gelatinous leptomeninges, and abnormally thickened dura. This technique allowed for detection of minimal amounts of subdural bleeding over the convexities, before dissection of the dura, avoiding post-mortem blood spillage from artifactually disrupted bridging veins. Optical clearing of the dura aided in the evaluation of patterns of subdural hemorrhage in three cases of non-accidental head injury, three cases of peri-natal head injury and one case of overlaying, apparently resulting in minor crush injury to the head. CONCLUSIONS: We have demonstrated that glycerol is an effective and easy-to-use OCA to effect the readily reversible optical clearing of human infant calvarial dura at autopsy.