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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.

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.)

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.

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.

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.

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) 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.

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).

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.

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.

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.

The pupils in brainstem-dead patients are classically fixed and dilated. We present a case of a brainstem-dead patient whose pupils displayed persistent asynchronous pupillary constriction and dilatation independent of external physical stimuli. Central causes for the phenomenon were excluded leaving an unexplained peripheral cause as the most likely explanation. Early recognition of this phenomenon prevents delay in the diagnosis of brainstem death, lessening to some extent the distress for the family, and facilitating earlier organ donation and allowing the better use of resources.

Acute subdural haematoma is a well-entrenched nosological entity implying subdural collection of blood following acute head injury. Pathologically, it is usually associated with or, for that matter, secondary to cerebral contusion and laceration. Based on cumulated experience, clinical and pathological studies it is proposed that, for too long the neurosurgeons have put emphasis on the clot rather than the totality of the pathological anatomy and that they have focused their therapeutic strategy on removal of the accumulated blood, unmindful of the associated parenchymatous lesion. Not surprisingly, such attempts have been associated with a very high mortality. On the basis of nearly four decades of personal experience and critical review of the literature, evidence has been provided that to reduce the mortality associated with this condition, it is necessary to evolve a strategy, not only to evacuate the blood but comprehensively deal with the associated parenchymatous lesions and the cascade of secondary insult to the underlying brain.

A case of "spontaneous" acute subdural hematoma caused by cocaine abuse is described. As an isolated cerebrovascular event, related to cocaine abuse, this is the first report in the literature. It also represents a new differential diagnosis for nontraumatic acute subdural haematomas. The putative pathophysiology of the lesion is discussed.