A nomogram for estimating intracranial pressure using acute subdural hematoma thickness and midline shift.

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.

Visualization of cortical cerebral blood flow dynamics during craniotomy in acute subdural hematoma using laser speckle imaging in a rat model.

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.

Initial Factors Affecting 6-month Outcome of Patients Undergoing Surgery for Acute Post-traumatic Subdural and Epidural Hematoma.

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.

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.

Fluid-structure interaction simulation of the brain-skull interface for acute subdural haematoma prediction.

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.

Development of Delayed Posttraumatic Acute Subdural Hematoma.

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.

Influence of rapidly successive head impacts on brain strain in the vicinity of bridging veins.

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.

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

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

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.

Seizures and Epileptiform Discharges in Patients With Acute Subdural Hematoma.

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.

Spontaneous resolution of traumatic acute subdural haematomas: A systematic review / Resolución espontánea de hematoma subdural agudo traumático: una revisión sistemática

Introduction: Traumatic subdural haematomas often require emergency surgical evacuation. Spontaneous resolution of traumatic acute subdural haematomas (TASDH) is under-reported. Two patients are described with spontaneous resolution of TASDH correlating with previous reports. A discussion is presented on the clinical, pathological and radiological features of TASDH. Methods: A review of the literature was performed using PubMed (Medline), Embase, and Cochrane Library for similar cases. Results: A total 21 articles were included, involving 27 cases well detailed of TASDH with spontaneous resolution or neurological and radiological improvement in less than 24h. Conclusions: There are two main mechanisms for the spontaneous resolution of acute subdural haematomas: dilution in subarachnoid space and redistribution of the haematoma in the subdural space. The primary radiological characteristic of these lesions is a hypodense rim on the outer surface of the clot. Spontaneous resolution of TASDH is unusual. Clinical and radiological surveillance is essential for appropriate management of these patients (AU)

Introducción: Los hematomas subdurales agudos traumáticos (HSDAT) requieren tratamiento quirúrgico de urgencia. Muy raras veces se describen casos de resolución espontánea de HSDAT. Describimos 2 casos de resolución espontánea de HSDAT y revisamos la bibliografía pertinente. Se discuten los aspectos clínicos, patológicos y radiológicos de resolución espontánea de HSDAT. Métodos: Revisamos la literatura en Pubmed (Medline), Embase y Cochrane Library en busca de casos similares. Resultados: Se incluyeron 21 artículos con 27 casos bien detallados de HSDAT con resolución espontánea o mejora clínica y radiológica en 24h. Conclusiones: Existen 2 mecanismos principales para la resolución espontánea de hematomas subdurales agudos: la dilución en el espacio subaracnoideo y la redistribución del hematoma en el espacio subdural. La principal característica radiológica de estas lesiones es una cerco hipodenso en la superficie exterior del coágulo. La resolución espontánea de HSDAT es rara. La vigilancia clínica y radiológica es esencial para el manejo adecuado de estos pacientes (AU)

Spontaneous rapid resolution of acute subdural hematoma in children.

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.

A case of type B lactic acidosis as a complication of chronic myelomonocytic leukaemia: a case report and review of the literature.

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.

Acute subdural hematoma after aortic surgery: a retrospective comparative study.

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.

Spontaneous acute subdural hematoma and intracerebral hemorrhage in a patient with thrombotic microangiopathy during pregnancy.

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.