Acute Subdural Hemorrhage Research Articles

Sport-Related Structural Brain Injury: 3 Cases of Subdural Hemorrhage in American High School Football

The risk of sport-related concussion (SRC) has emerged as a major public health concern. In rare instances, sport-related head injuries can be even more severe, such as subdural hemorrhage, epidural hemorrhage, or malignant cerebral edema. Unlike SRCs, sport-related structural brain injury (SRSBI) is rare, may require neurosurgical intervention, and can lead to permanent neurologic deficit or death. Data characterizing SRSBI are limited, and many have recognized the need to better understand these catastrophic brain injuries. The goal of the current series is to describe, in detail, the presentation, management, and outcomes of examples of these rare injuries. During the fall of 2015, three high school football players presented with acute subdural hemorrhages following in-game collisions and were treated at our institution within a span of 2 months. For the 2 athletes who required surgical intervention, a previous SRC was sustained within 4 weeks before the catastrophic event. One year after injury, 2 players have returned to school, though with persistent deficits. One patient remains nonverbal and wheelchair bound. None of the athletes has returned to sports. Acute subdural hemorrhage resultant from an in-game football collision is rare. The temporal proximity of the reported SRSBIs to recent SRCs emphasizes the importance of return-to-play protocols and raises questions regarding the possibility of second impact syndrome. Although epidemiologic conclusions cannot be drawn from this small sample, these cases provide a unique opportunity to demonstrate the presentation, management, and long-term outcomes of SRSBI in American high school football.

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.

Immobile cerebral veins in the context of positional brain shift: an undescribed risk factor for acute subdural hemorrhage

Changes in head position are thought to cause a degree of brain shift in the intracranial cavity. However, little is known on the concurrent shift of the cerebral veins. The present study aimed to investigate the positional shift of the cerebral veins that accompanies brain shift. Sagittal T2-weighted magnetic resonance imaging was performed on 21 consecutive patients lying in the supine and prone positions, using the same sequence. For each patient, imaging data were obtained for the two positions as a pair of images with morphologically best-matched cerebral contours. The subarachnoid spaces in the parasagittal frontal convexity showed variable reductions related to a postural change from a supine to a prone position, with a mean percent reduction (%Δ) of 17.8 ± 11.7%. Additionally, cerebral cisterns ventral to the brainstem and upper cervical cord were reduced in most patients when lying in a prone position, with a mean %Δ of 16.6 ± 8.7%. In contrast, none of these 130 pairs of identical venous segments located in the parasagittal cerebral convexity showed positional shift. Cadaveric dissections found that the major cortical veins were superficially upheld by the arachnoid membranes. The parasagittal major cortical and bridging veins do not seem to show positional shifts. Positional change in the posterior-anterior direction causes a shearing between the frontal cortices and the distributing veins and can be a risk factor for acute subdural hemorrhage, in case of severe head trauma.

Diagnostic Challenge of Diffusion Tensor Imaging in a Patient With Hemiplegia After Traumatic Brain Injury.

A 51-year-old man showed hemiplegia on his right side after a traumatic brain injury (TBI). On initial brain computed tomography (CT) scan, an acute subdural hemorrhage in the right cerebral convexity and severe degrees of midline shifting and subfalcine herniation to the left side were evident. On follow-up brain magnetic resonance imaging (MRI), there were multiple microhemorrhages in the left parietal and occipital subcortical regions. To explain the occurrence of right hemiplegia after brain damage which dominantly on the right side of brain, we used diffusion tensor imaging (DTI) to reconstruct the corticospinal tract (CST), which showed nearly complete injury on the left CST. We also performed motor-evoked potentials, and stimulation of left motor cortex evoked no response on both sides of upper extremity. We report a case of patient with hemiplegia after TBI and elucidation of the case by DTI rather than CT and MRI.

The Association between Psychiatric Comorbidities and Outcomes for Inpatients with Traumatic Brain Injury.

It is well established that traumatic brain injury (TBI) is associated with the development of psychiatric disorders. However, the impact of psychiatric disorders on TBI outcome is less well understood. We examined the outcomes of patients who experienced a traumatic subdural hemorrhage and whether a comorbid psychiatric disorder was associated with a change in outcome. A retrospective observational study was performed in the California Office of Statewide Health Planning and Development (OSHPD) and the Nationwide Inpatient Sample (NIS). Patients hospitalized for acute subdural hemorrhage were identified using International Classification of Diseases, Ninth Revision (ICD-9) diagnosis codes. Patients with coexisting psychiatric diagnoses were identified. Outcomes studied included mortality and adverse discharge disposition. In OSPHD, diagnoses of depression (OR = 0.64, p < 0.001), bipolar disorder (OR = 0.45, p < 0.05), and anxiety (OR = 0.37, p < 0.001) were associated with reduced mortality during hospitalization for TBI, with a trend toward psychosis (OR = 0.56, p = 0.08). Schizophrenia had no effect. Diagnoses of psychosis (OR = 2.12, p < 0.001) and schizophrenia (OR = 2.60, p < 0.001) were associated with increased adverse discharge. Depression and bipolar disorder had no effect, and anxiety was associated with reduced adverse discharge (OR = 0.73, p = 0.01). Results were confirmed using the NIS. Analysis revealed novel associations between coexisting psychiatric diagnoses and TBI outcomes, with some subgroups having decreased mortality and increased adverse discharge. Potential mechanisms include pharmacological effects of frequently prescribed psychiatric medications, the pathophysiology of individual psychiatric disorders, or under-coding of psychiatric illness in the most severely injured patients. Because pharmacological mechanisms, if validated, might lead to improved outcome in TBI patients, further studies may provide significant public health benefit.

Subdural hemorrhages in acute lymphoblastic leukemia: case report and literature review

Acute lymphoblastic leukemia is a rare hematological malignancy. Pure subdural hemorrhages in a patient with acute lymphoblastic leukemia patient are extremely rare. This case presented acute spontaneous subdural hemorrhage without head trauma at first, and acute lymphoblastic leukemia was diagnosed later. The second time, the patient was admitted with multiple pure subdural hemorrhages in different locations and periods with a history of slight head trauma. Pure subdural hemorrhages can occur in a patient with acute lymphoblastic leukemia. More care would be needed for pure subdural hemorrhages without obvious head trauma, and patients with hematological malignancies should be protected from even mild head trauma.

Early progressive mobilisation following acute subarachnoid or subdural haemorrhage: An observational pilot study

Background/Aims: There is little research regarding early mobilisation following non-traumatic acute subarachnoid (SAH) or subdural haemorrhage (SDH). The aim of this prospective observational study was to document the feasibility and safety of our usual practice regarding the early progressive mobilisation of patients following acute SAH or SDH. Method: Mobilisation was defined as sitting on the edge of the bed or greater. All participants were screened regarding their suitability for mobilisation to commence/continue. Results: Fifty participants were included: 42 mobilised at least once as part of their physiotherapy intervention. The 50 participants received a total of 373 physiotherapy sessions, with mobilisation occurring during 50% of sessions. Neurological reasons most frequently prevented mobilisation. All 42 participants who mobilised at least once achieved the mobility milestone of sitting on the edge of the bed and 86% progressed to walking, usually by 4–5 days post-admission. Poor neurological status on admission was associated with delayed achievement of mobility milestones. Adverse events associated with mobilisation were infrequent (1.6%), transient and self-limiting. Conclusion: Following appropriate screening, early progressive mobilisation of patients following non-traumatic acute SAH or SDH was feasible and safe. Further research is required to confirm its safety and benefits, and establish the most effective dose.

Spontaneous Acute Subdural Hemorrhage with Rupture of Intracranial Aneurysm: A Series of Two Cases and Review of Literature

We present a rare series of two cases of spontaneous intracranial aneurysmal hemorrhage associated with acute subdural hematoma. One patient was having ruptured anterior communicating artery aneurysm and acute subdural hematoma with no evidence of subarachnoid hemorrhage and the other patient presented with subarachnoid hemorrhage with bleeding in subdural, intraparenchymal, and intraventricular location with rupture of posterior communicating artery aneurysm. In this report, we are describing the pathophysiology and radiological features of subdural hematoma with aneurysm bleed.

Dating of Acute and Subacute Subdural Haemorrhage: A Histo-Pathological Study.

Microscopic study of the organization of the Subdural Haemorrhage (SDH) verified against the time period can help us in the determination of its age which has serious medico-legal implications. Very few studies concerning the dating of SDH are present in the literature. This study was conducted for dating the early subdural haemorrhage by routine histopathological stains. A prospective analytical study was conducted during July 2009 to December 2010. A total of 100 cases (50 males and 50 females) fulfilling the inclusion and exclusion criteria were included in this study. Routine histopathological staining of the subdural haematoma was done. Correlation between the frequency of a given histomorphological phenomenon and the length of the Post-Traumatic Interval (PTI) was evidential. All the histomorphological features, when correlated with PTI groups, were found to be statistically significant, except for Polymorphonuclear Leukocytes (PMN). We concluded that routine histopathology was reliable in the dating of early subdural haemorrhages.

Diagnosis and Genetic Analysis of Glutaric Acidaemia Type I: Very rarely seen inborn error of metabolism.

Diagnosis and Genetic Analysis of Glutaric Acidaemia Type I: Very rarely seen inborn error of metabolism.

54 Days Without Anticoagulation in a Patient with Metallic Mitral Valve

In patients with a mechanical heart valve, adequate anticoagulation is extremely important, as coagulation poses a risk of embolism and thrombosis of the valve. However, in patients with a metallic heart valve suffering an intracranial bleed, there is a high mortality rate. This can become a management dilemma, as limited evidence is available to guide clinical decision-making in this situation. Each case must be assessed individually, ideally with a multidisciplinary team approach. Here, we report the case of a woman in her 80s presenting with acute massive subdural hemorrhage because of a fall. We examine the complex repercussions of specific decisions in a very critical clinical scenario. Furthermore, we suggest that a revision of anticoagulation guidelines may be necessary.

Endotracheal tube cuff leak: Minor product defect or lack of cuff pressure monitoring?

Sir, We report a leak in the pilot inflation line of an endotracheal tube (ETT) resulting in partial loss of tidal volume and increased risk of pulmonary aspiration. It also brings out the significance of intra-operative cuff pressure monitoring. A 60-year-old man, body mass index 30 kg/m2, a case of acute subdural hematoma and subarachnoid hemorrhage with increased intracranial pressure and deteriorating sensorium (Glasgow Coma Scale 6) was admitted to the intensive care unit. The history of preoperative fasting and other co-morbidities was unreliable. After a quick routine pre check for cuff patency of the ETT by inflation and cuff inspection followed by rapid deflation, the patient was intubated with a size 8.0 mm ID ETT (Ruschelit® Safety Clear Plus, Teleflex Medical Sdn Bhd, Kamunting, Malaysia) and the cuff was inflated with air and manually palpated to assess adequacy of its pressure. He was mechanically ventilated and other measures to control intracranial pressure were initiated. The patient was shifted to the operation theatre for an emergency craniotomy. Nitrous oxide and oxygen 60:40 sub-minimum alveolar concentration isoflurane and propofol infusion 50–100 μg/kg/min were used for maintenance. During the period of approximately 45 min from the time of intubation to the beginning of surgery, a loss of tidal volume was noticed. A check laryngoscopy ruled out tube migration. The cuff appeared lax and was re-inflated but the events repeated in the same manner again. The ETT was changed with another one and examined for obvious leaks. This ETT was then immersed in a bowl of water and the cuff inflated with an aneroid manometer (Mallinckrodt Medical Athlone, Ireland). Multiple air bubbles were noticed to appear at higher cuff pressures (>100 cm H2O), but as the pressure was reduced gradually, their size, number and speed lowered, and the bubbling stopped at the cuff pressure below 40 cm H2O. The leak was detected from the point where the transparent pilot inflation line entered the blue stem of the pilot cuff [shown by the arrow in [Figure 1]. The product defect was communicated to the manufacturers. Figure 1 Arrow showing air bubbles in water at higher cuff pressure; inset showing pilot inflation line entering the pilot cuff with the arrow showing the probable leak site A leak from any part of the ETT assembly can be alarming, more so in cases of difficult airway or in surgeries involving limited access to airway (non-supine position and head and neck surgery) where a change of tube may not be possible intra-operatively.[1] It may cause increased risk of pulmonary aspiration and inadequate ventilation (inadequate depth of anesthesia, intra-operative awareness, and hemodynamic instability). The leaks in the cuffs and the various ways to tackle them are well known but a defect in the pilot inflation line has been sparsely reported in the literature.[2] Various methods using continuous inflation with air, saline or lignocaine jelly or use of three-way stopcock to maintain cuff pressure are documented, though most of them are no more than a rescue measure.[1] This report alarms the caregiver to be vigilant at all times as even minor leaks from unusual sites may have clinically significant and long-standing consequences. Besides, it also reinforces the need for objective monitoring of the ETT cuff pressure, especially in the presence of nitrous oxide (which readily diffuses into the cuff and increases its pressure). Manual assessment of cuff pressure may be grossly incorrect and may underestimate pressures.[3] The pressure can be high as to manifest minor leaks (even when high volume low-pressure cuffs are used), as seen in the case reported. The effects of the leak due to the minor product defect could have been avoided if the cuff pressure was measured and maintained within the safe range of 20–30 cm of H2O.[4]

Ruptured distal anterior cerebral artery aneurysm presenting as subdural hemorrhage

We report on a 64-year-old man with no history of trauma who went into a deep coma after aneurysmal rupture. The brain computed tomography (CT) scan showed interhemisphere and convexity subdural hemorrhage (SDH) without detectable subarachnoid hemorrhage. The CT angiography confirmed a rare condition of pericallosal aneurysmal rupture. We emphasize that when a patient with an unclear history of head trauma presented with acute convexity and interhemispheric SDH, the possibility of distal pericallosal artery aneurysmal rupture should be considered. We also recommend CT angiography must be performed as soon as possible to determine the cause of bleeding.

Perioperative Glycemic Status of Adult Traumatic Brain Injury Patients Undergoing Craniotomy

Patients of traumatic brain injury (TBI) may have hyperglycemia and when they undergo craniotomy, hyperglycemia may be exacerbated and worsen outcome. However, epidemiology of perioperative hyperglycemia in these patients is unknown. The epidemiological study has been undertaken to address the correlation between intraoperative blood glucose variability in nondiabetic adult TBI patients undergoing craniotomy with the severity and type of brain trauma and patients' demographic variables. A total of 200 adult nondiabetic patients undergoing emergency craniotomy for TBI were recruited in this prospective single-group observational study. Baseline capillary blood glucose (CBG) measurement was performed immediately before induction of anesthesia and then at half hourly interval until the end of surgery and 1 hour after the end of surgery. Incidence of at least 1 episode of intraoperative hyperglycemia (CBG≥180 mg/dL) is 20% in patients with TBI during emergency craniotomy. Independent predictors of intraoperative hyperglycemia are severe head injury (Glasgow-Coma score [GCS] <9) and acute subdural hemorrhage. Baseline CBG also correlates with subsequent intraoperative and postoperative CBG. Hyperglycemia is common during emergency craniotomy in TBI patients. We recommend routine monitoring of blood glucose in the intraoperative and postoperative period at least in severe head injury patients.

Risk factors for development of significant chronic subdural hematoma following conservative treatment of acute subdural hemorrhage

Objective. One of the complications of untreated acute subdural hemorrhage (aSDH) is the late development of chronic subdural hematomas (cSDH). cSDH may cause major neurologic deficits, requiring their surgical evacuation. The aim of our work was to find risk factors for the development of significant cSDH requiring surgery following conservative treatment of trauma-related aSDH. Methods. In a retrospective manner, we analyzed the data of 95 adult patients admitted with a non-surgical, traumatic aSDH. The patients were divided into two groups. The first group contained 52 patients who did not, on follow-up, develop cSDH requiring surgery. The second group contained 43 patients who ended up with a significant cSDH, based on clinical and radiological criteria, requiring surgical evacuation. Data acquisition and comparison between the two groups was performed by analyzing the patients’ charts for diverse medical conditions and other trauma-related parameters. Results. The operation rate was significantly higher in patients with medical history of ischemic heart disease (IHD) or hypertension (66.7% vs. 38%, p = 0.019 and 56.9% vs. 20%, p < 0.01, respectively), with a 4-fold increase in the risk for developing surgical cSDH in patients with IHD and a 6-fold increase in the risk in patients with hypertension (odds ratio 4.2 [95% CI for odds, 1.3–13.1] and 5.9 [95% C.I for odds, 1.6–21.5], respectively). Among 21 patients, 20 (95%) patients, who were either on more than 1 anti-aggregant agents (AAA), used Clopidrogrel, or took anti-coagulant drug were in the operative group (OG). A larger initial thickness of the aSDH was statistically significant in the OG as compared to the non-OG (8.9 mm ± 4.6 vs. 5.5 mm ± 2.1, p < 0.001). Conclusion. Head-trauma patients with a medical history of IHD or hypertension, patients on more than one AAA or anti-coagulant agents and patients with worse initial CT scan parameters are at risk of developing significant cSDH requiring surgery after conservative treatment of aSDH and consequently should have closer follow-up.

Supratentorial Subdural Hemorrhage of a Previous Head Injury and Cerebellar Hemorrhage After Cervical Spinal Surgery

Case report. To report a case of an acute supratentorial subdural hemorrhage (SDH) of a previous head injury site and cerebellar hemorrhage, after an incidental dural tear during spine surgery. Intracranial hemorrhage, such as subdural, cerebellar, subarachnoid, and epidural hemorrhage after a dural tear during spinal surgery, is a rare and poorly recognized complication. Moreover, only 3 cases in patients with concurrent SDH and cerebellar hemorrhage have been described in the literature, and none of these reports demonstrated the bleeding point on the adhesion site of the dural at the regions of the previous head injury. A case report and literature review are presented. A 46-year-old male underwent occipital cervical surgery for os odontoideum. Intraoperatively, a dural tear was noted and repaired, but he later developed postoperative disturbance of consciousness. A head computed tomographic scan revealed a supratentorial SDH and cerebellar hemorrhage. Evacuation of the supratentorial SDH was performed via craniotomy, and the bleeding point was revealed to be on the adhesion site of the dural where the patient had experienced a previous head injury. The patient made a full recovery. This report illustrates that cerebrospinal fluid leakage after a dural tear during spinal surgery may cause intracranial hemorrhage. A previous head trauma could be a risk factor for such hemorrhagic complications. Headache, nausea, and postoperative stupor after spinal surgery, especially after an accidental durotomy, should be considered possible indications of intracranial hemorrhage, and affected patients should be investigated with computed tomography or magnetic resonance imaging. N/A.

Atypical meningioma and acute subdural hemorrhage.

Atypical meningioma and acute subdural hemorrhage.

G452 Horse related injuries in children-Our experience in PICU

IntroductionHorse riding and horse handling are risk prone activities and can cause fatal injuries. Horse related injuries are not uncommon in children and could account for significant morbidity.ObjectivesTo review the...

Intracerebral aneurysmal bleed presenting as acute subdural haemorrhage

Acute subdural haemorrhage (aSDH) secondary to an aneurysmal bleed is a surgical emergency that requires urgent decision making. Major dilemmas are whether preoperative diagnostic studies should precede surgery and whether obliteration of the aneurysm should be performed during haematoma evacuation or as a separate delayed intervention after resuscitation. We successfully operated on a 44-year-old patient with aneurysmal aSDH, and discuss the challenges involved with such patients. Case report A 44-year-old man was brought unconscious to hospital by paramedics. Immediate family members or friends were not available to give a reliable history. On admission his Glasgow Coma Score (GCS) was 6/15 (E1 M4 V1). His right pupil was dilated and unreactive to light and he had features of Cushing’s reflex with bradycardia and hypertension. He was immediately intubated and underwent an urgent computed tomography (CT) scan (Fig. 1), which revealed a large, right frontotemporo-parietal acute subdural haematoma with effacement of basal cisterns and evidence of mass effect and midline shift. The scan also showed thick blood in the right sylvian fissure and a thrombus in the superior temporal gyrus on the right side. Because of features of uncal herniation, an emergency craniotomy was performed immediately. On draining the aSDH, the brain became lax and pulsatile. The sylvian fissure was thereafter opened proximal to distal. The arachnoid membrane across the sylvian fissure could clearly be seen in the proximal fissure, but distally, over the aneurysm, it was obliterated by the thick thrombus surrounding the fundus of a large bi-lobed aneurysm at the middle cerebral artery (MCA) bifurcation. The thrombi were carefully removed and the aneurysm neck was dissected out and clipped using a large curved Yasargil clip. Postoperatively he was ventilated for 24 hours and then gradually weaned off the ventilator. His postoperative recovery was slow but steady. On last followup six months after surgery he had made significant recovery with a modified Rankin score of 2. He was independent for activities of daily living but had not yet resumed his earlier vocation.

Kernohan-Woltman Notch Phenomenon Caused by Acute Traumatic Subdural Haematoma

A 27-year-old man suffered from right hemiparesis after a closed head injury. Computed tomography (CT) revealed a right hemisphere subdural haematoma with midline structure shifted to the left. The CT finding was believed to be mislabeled because the site of haematoma did not correlate with an ipsilateral hemiparesis. Magnetic resonance imaging revealed a right transtentorial uncal herniation and a small lesion within left cerebral peduncle, suggesting Kernohan-Woltman notch phenomenon (KWNP). KWNP has been rarely seen in patients with acute traumatic subdural haemorrhage. Anatomical small maximum tentorial notch width is the possible anatomical factor predisposing our patient to this phenomenon. (Hong Kong j.emerg.med. 2014;21:116-119)