scholarly journals A Case of Impalement Brain Injury That Could Achieve Good Neurological Outcome by Introducing Early Sedation and Immobilization Strategy

2018 ◽  
Vol 2018 ◽  
pp. 1-4 ◽  
Author(s):  
Wataru Takayama ◽  
Kaho Yamasaki ◽  
Akira Endo ◽  
Yasuhiro Otomo
Keyword(s):  
Brain Injury ◽  
Foreign Body ◽  
Vital Signs ◽  
Neurological Deficits ◽  
Secondary Brain Injury ◽  
Related Complication ◽  
Imaging Evaluation ◽  
Initial Management ◽  
Major Vessel ◽  
The Right

Impalement brain injury is rare, and the initial management of this condition is not well-established. We present a case of a well-managed brain injury caused by impalement with a metal bar. A 29-year-old man whose head had been impaled by a metal bar was transferred to our hospital. Upon arrival, he was agitated, with an unsteady gait and prominent odor of alcohol on his breath. He exhibited normal vital signs and neurological findings, except for his level of consciousness. To address the risk of secondary brain injury caused by movement of the foreign body, we immediately administered a sedative agent and muscle relaxant after the initial neurological evaluation. The imaging evaluation revealed the insertion of a metal bar into the right frontal lobe at a depth of >100 mm through the frontal bone; however, there was no apparent major vessel injury-related complication. Three hours after arrival at the hospital, a craniotomy was performed to remove the foreign body. The patient’s postoperative course was uneventful, and he was discharged after rehabilitation without any neurological deficits. The strategy of immediate immobilization to prevent the secondary brain injury is important in the initial management of a patient who has survived an impalement brain injury and presented to an emergency department.

scholarly journals Case Report: Transorbital approach for the management of an orbito-temporal penetrating brain injury (skull base region) secondary to wooden spikes

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 1283
Author(s):  
Tedy Apriawan ◽  
Abdul Hafid Bajamal ◽  
Ditto Darlan ◽  
Yusriandi Ramadhan
Keyword(s):  
Brain Injury ◽  
Foreign Body ◽  
Magnetic Resonance ◽  
Petrous Bone ◽  
Primary Treatment ◽  
Surgical Approaches ◽  
Penetrating Brain Injury ◽  
Body Location ◽  
The Right ◽  
Base Of The Skull

Background and importance: Transorbital penetrating brain injury (PBI) due to a non-projectile foreign body is rare. It can lead to life-threatening severe neurovascular damage. Surgery is the primary treatment choice; however, there are a number of approaches that can be considered based on the patient's condition in terms of foreign body location and state of the patient. Clinical presentation: An 18-year-old male carpenter was hit by a log and sustained transorbital PBI while cutting wood with a machine. Computed tomography (CT) scan showed a wooden spike that was approximately 11 cm from the left medial orbital to the superior part of the posterolateral of the petrous bone, crossing the right side at the base of the skull. CT angiography (CTA), magnetic resonance angiography (MRA), and magnetic resonance venography (MRV) revealed no internal carotid artery (ICA) and cavernous sinus lesions, respectively. We had a 3D-printed model for preoperative planning, and surgery was performed using a transorbital approach to extract the wood 14 days after the accident. The impacted wood was removed without any complications. Conclusion: There are many surgical approaches for transorbital PBI. We decided to perform the transorbital approach because it is perpendicular to the entry zone. Surgeons should consistently perform minimally invasive procedures based on the clinical and radiological findings.

scholarly journals A Case of Right Shoulder Penetrating Injury Inflicted by a Hollow Metal Fence

2020 ◽  
Author(s):  
Peng-chao Guo ◽  
Guang-feng Zhao ◽  
Mao Zhang
Keyword(s):  
Foreign Body ◽  
Vital Signs ◽  
Ulnar Artery ◽  
Emergency Operation ◽  
Penetrating Injury ◽  
Abnormal Breathing ◽  
Comminuted Fractures ◽  
Unbearable Pain ◽  
Gcs Score ◽  
The Right

Abstract Background: Right shoulder penetrating injury are rare and challenging diagnoses that should not be missed.Case presentation: The patient, a 30-year-old male, had a clear mind, stable vital signs, a gcs score of 15 points, unbearable pain in his right shoulder and chest wall, and no abnormal breathing. His right radial artery was unclear, and the right ulnar artery was thin and unclear, suggesting comminuted fractures of the right humeral shaft and scapula. After the multi-disciplinary discussion in the emergency department, we planned to perform an emergency operation to take out the foreign body from his right shoulder.Conclusions: Penetrating injury is very important to systematically and comprehensively assess the peripheral vascular nerve and muscle tissue at the site of injury. The foreign body should be carefully removed during the operation to avoid further damage to the patient, and it is necessary to perform fluoroscopy again after the removal of the foreign body. The placement of drainage, secondary debridement and sutures, and fixation can effectively reduce postoperative infection.

scholarly journals GOLGA2/GM130 is a Novel Target for Neuroprotection Therapy in Intracerebral Hemorrhage

2021 ◽  
Author(s):  
Shuwen Deng ◽  
Qing Hu ◽  
Qiang He ◽  
Xiqian Chen ◽  
Wei Lu
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Tight Junction ◽  
Neurological Deficits ◽  
Blue Staining ◽  
Autophagic Flux ◽  
Secondary Brain Injury ◽  
Associated Proteins ◽  
Novel Target

Abstract Blood–brain barrier (BBB) impairment after intracerebral hemorrhage (ICH) can lead to secondary brain injury and aggravate neurological deficits. Currently, there are no effective methods for its prevention or treatment partly because of to our lack of understanding of the mechanism of ICH injury to the BBB. Here, we explored the role of Golgi apparatus protein GM130 in the BBB and neurological function after ICH. The levels of the tight junction-associated proteins ZO-1 and occludin decreased, whereas those of LC3-II, an autophagosome marker, increased in hemin-treated Bend.3 cells (p < 0.05). Additionally, GM130 overexpression increased ZO-1 and occludin levels, while decreasing LC3-II levels (p < 0.05). GM130 silencing reversed these effects and mimicked the effect of hemin treatment (p < 0.05). Moreover, tight junctions were disrupted after hemin treatment or GM130 silencing and repaired by GM130 overexpression. GM130 silencing in Bend.3 cells increased autophagic flux, whereas GM130 overexpression downregulated this activity. Furthermore, GM130 silencing-induced tight junction disruption was partially restored by 3-methyladenine (an autophagy inhibitor) administration. Similarly, an in vivo ICH rat model showed elevated perihematomal ZO-1 and occludin expression and decreased LC3-II expression (p < 0.05); these results were reversed following GM130 silencing (p < 0.05). Perihematomal Evans Blue staining and brain water content were elevated in GM130-silenced ICH rats relative to control ICH rats. GM130 overexpression can protect BBB integrity from brain injury, inhibit excessive autophagy flux in ICH, and improve neurobehavioral prognosis. Therefore, therapy targeting GM130 regulation might represent a potential treatment for acute brain injury after ICH.

scholarly journals A case report of an unexpected traumatic brain injury following severe child abuse

2019 ◽  
Vol 6 (2) ◽  
pp. 109-111
Author(s):  
Seyed Reza Habibzadeh ◽  
Ehsan Bolvardi ◽  
Esmail Rayat Dost ◽  
Mahdi Foroughian
Keyword(s):  
Traumatic Brain Injury ◽  
Emergency Department ◽  
Child Abuse ◽  
Brain Injury ◽  
Blood Glucose Control ◽  
Pressure Control ◽  
Preperitoneal Space ◽  
Secondary Brain Injury ◽  
Arterial Blood ◽  
The Right

Introduction: Child abuse has been defined as allowing others to cause physical, emotional, and sexual harm, and also physical and emotional pain to a child. The present study was a report on a case of physical and sexual child abuse accompanied by traumatic brain injury (TBI) referred to an emergency department. Case Presentation: A 4-year-old child was rushed into an emergency department by her mother. At the time of hospital admission, the child was feeling confused and drowsy and had symptoms of hemorrhage in the right preperitoneal space as well as bleeding from the mouth. According to the pattern of the child’s admission to the emergency department, contradictory descriptions by parents, clinical examinations, and TBI pattern; the probability of a case of child abuse was raised. Thus; neurosurgery, legal medicine, gynecology, and surgery consultations were requested. With regard to the brain injury and epidural hematoma, immediate measures (i.e. head lifting, taking Dilantin, blood glucose control, blood pressure control, and maintaining adequate oxygen saturation in the arterial blood) were taken to put a stop to secondary brain injury, and the patient was then transferred to the intensive care unit (ICU) for further treatments. Conclusion: In the present case study, the child was seriously examined and followed up. In conclusion; 20 days later, the case was discharged from the pediatric ward with good medical conditions, and received counseling and psychiatric services for one year.

scholarly journals SS-31 Provides Neuroprotection by Reversing Mitochondrial Dysfunction after Traumatic Brain Injury

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Yihao Zhu ◽  
Handong Wang ◽  
Jiang Fang ◽  
Wei Dai ◽  
Jiang Zhou ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mitochondrial Dysfunction ◽  
Nuclear Translocation ◽  
Neurological Diseases ◽  
Neurological Deficits ◽  
Secondary Brain Injury ◽  
Neuroprotective Effects ◽  
Weight Drop ◽  
Ros Scavenger

SS-31, a novel mitochondria-targeted peptide, has been proven to provide neuroprotection in a variety of neurological diseases. Its role as a mitochondrial reactive oxygen species (ROS) scavenger and the underlying pathophysiological mechanisms in traumatic brain injury (TBI) are still not well understood. The aim of the designed study was to investigate the potential neuroprotective effects of SS-31 and fulfill our understanding of the process of the mitochondrial change in the modified Marmarou weight-drop model of TBI. Mice were randomly divided into sham, TBI, TBI + vehicle, and TBI + SS-31 groups in this study. Peptide SS-31 (5 mg/kg) or vehicle was intraperitoneally administrated 30 min after TBI with brain samples harvested 24 h later for further analysis. SS-31 treatment significantly reversed mitochondrial dysfunction and ameliorated secondary brain injury caused by TBI. SS-31 can directly decrease the ROS content, restore the activity of superoxide dismutase (SOD), and decrease the level of malondialdehyde (MDA) and the release of cytochrome c, thus attenuating neurological deficits, brain water content, DNA damage, and neural apoptosis. Moreover, SS-31 restored the expression of SIRT1 and upregulated the nuclear translocation of PGC-1α, which were proved by Western blot and immunohistochemistry. Taken together, these data demonstrate that SS-31 improves the mitochondrial function and provides neuroprotection in mice after TBI potentially through enhanced mitochondrial rebiogenesis. The present study gives us an implication for further clinical research.

Deferoxamine-induced attenuation of brain edema and neurological deficits in a rat model of intracerebral hemorrhage

2003 ◽  
Vol 15 (4) ◽  
pp. 1-7 ◽  
Author(s):  
Takehiro Nakamura ◽  
Richard F. Keep ◽  
Ya Hua ◽  
Timothy Schallert ◽  
Julian T. Hoff ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Iron Chelator ◽  
Iron Accumulation ◽  
Neurological Deficits ◽  
Sprague Dawley ◽  
Autologous Whole Blood ◽  
The Right

Object In the authors' previous studies they found that brain iron accumulation and oxidative stress contribute to secondary brain damage after intracerebral hemorrhage (ICH). In the present study they investigated whether deferoxamine, an iron chelator, can reduce ICH-induced brain injury. Methods Male Sprague–Dawley rats received an infusion of 100 μl of autologous whole blood into the right basal ganglia and were killed 1, 3, or 7 days thereafter. Iron distribution was examined histochemically (enhanced Perl reaction). The effects of deferoxamine on ICH-induced brain injury were examined by measuring brain edema and neurological deficits. Apurinic/apyrimidinic endonuclease/redox effector factor–1 (APE/Ref-1), a repair mechanism for DNA oxidative damage, was quantitated by Western blot analysis. Iron accumulation was observed in the perihematoma zone beginning 1 day after ICH. Deferoxamine attenuated brain edema, neurological deficits, and ICH-induced changes in APE/Ref-1. Conclusions Deferoxamine and other iron chelators may be potential therapeutic agents for treating ICH. They may act by reducing the oxidative stress caused by the release of iron from the hematoma.

scholarly journals Downregulation of phosphoglycerate mutase 5 improves microglial inflammasome activation after traumatic brain injury

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yuhua Chen ◽  
Kai Gong ◽  
Limin Guo ◽  
Bingchang Zhang ◽  
Sifang Chen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Mitochondrial Protein ◽  
Physiological Mechanism ◽  
Neurological Deficits ◽  
Phosphoglycerate Mutase ◽  
Inflammasome Activation ◽  
Secondary Brain Injury

AbstractTraumatic brain injury (TBI) is considered as the most common cause of disability and death, and therefore an effective intervention of cascade pathology of secondary brain injury promptly can be a potential therapeutic direction for TBI prognosis. Further study of the physiological mechanism of TBI is urgent and important. Phosphoglycerate mutase 5 (Pgam5), a mitochondrial protein, mediate mitochondrial homeostasis, cellular senescence, and necroptosis. This study evaluated the effects of Pgam5 on neurological deficits and neuroinflammation of controlled cortical impact-induced TBI mouse model in vivo and LPS + ATP-induced microglia model in vitro. Pgam5 was overexpressed post-TBI. Pgam5 depletion reduced pyroptosis-related molecules and improved microglia activation, neuron damage, tissue lesion, and neurological dysfunctions in TBI mice. RNA-seq analysis and molecular biology experiments demonstrated that Pgam5 might regulate inflammatory responses by affecting the post-translational modification and protein expression of related genes, including Nlrp3, caspase1, Gsdmd, and Il-1β. In microglia, Pgam5-sh abrogated LPS + ATP-induced Il-1β secretion through Asc oligomerization-mediated caspase-1 activation, which was independent of Rip3. The data demonstrate the critical role Pgam5 plays in nerve injury in the progression of TBI, which regulates Asc polymerization and subsequently caspase1 activation, and thus reveals a fundamental mechanism linking microglial inflammasome activation to Asc/caspase1-generated Il-1β-mediated neuroinflammation. Thus, our data indicate Pgam5 worsens physiological and neurological outcomes post-TBI, which may be a potential therapeutic target to improve neuroinflammation after TBI.

Evidence for a conditioning effect of inhalational anesthetics on angiographic vasospasm after aneurysmal subarachnoid hemorrhage

2020 ◽  
Vol 133 (1) ◽  
pp. 152-158 ◽  
Author(s):  
Umeshkumar Athiraman ◽  
Diane Aum ◽  
Ananth K. Vellimana ◽  
Joshua W. Osbun ◽  
Rajat Dhar ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Multivariate Logistic Regression Analysis ◽  
Secondary Brain Injury ◽  
Large Artery ◽  
Inhalational Anesthetics ◽  
Angiographic Vasospasm ◽  
Inhalational Anesthetic

OBJECTIVEDelayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH) is characterized by large-artery vasospasm, distal autoregulatory dysfunction, cortical spreading depression, and microvessel thrombi. Large-artery vasospasm has been identified as an independent predictor of poor outcome in numerous studies. Recently, several animal studies have identified a strong protective role for inhalational anesthetics against secondary brain injury after SAH including DCI—a phenomenon referred to as anesthetic conditioning. The aim of the present study was to assess the potential role of inhalational anesthetics against cerebral vasospasm and DCI in patients suffering from an SAH.METHODSAfter IRB approval, data were collected retrospectively for all SAH patients admitted to the authors’ hospital between January 1, 2010, and December 31, 2013, who received general anesthesia with either inhalational anesthetics only (sevoflurane or desflurane) or combined inhalational (sevoflurane or desflurane) and intravenous (propofol) anesthetics during aneurysm treatment. The primary outcomes were development of angiographic vasospasm and development of DCI during hospitalization. Univariate and logistic regression analyses were performed to identify independent predictors of these endpoints.RESULTSThe cohort included 157 SAH patients whose mean age was 56 ± 14 (± SD). An inhalational anesthetic–only technique was employed in 119 patients (76%), while a combination of inhalational and intravenous anesthetics was employed in 34 patients (22%). As expected, patients in the inhalational anesthetic–only group were exposed to significantly more inhalational agent than patients in the combination anesthetic group (p < 0.05). Multivariate logistic regression analysis identified inhalational anesthetic–only technique (OR 0.35, 95% CI 0.14–0.89), Hunt and Hess grade (OR 1.51, 95% CI 1.03–2.22), and diabetes (OR 0.19, 95% CI 0.06–0.55) as significant predictors of angiographic vasospasm. In contradistinction, the inhalational anesthetic–only technique had no significant impact on the incidence of DCI or functional outcome at discharge, though greater exposure to desflurane (as measured by end-tidal concentration) was associated with a lower incidence of DCI.CONCLUSIONSThese data represent the first evidence in humans that inhalational anesthetics may exert a conditioning protective effect against angiographic vasospasm in SAH patients. Future studies will be needed to determine whether optimized inhalational anesthetic paradigms produce definitive protection against angiographic vasospasm; whether they protect against other events leading to secondary brain injury after SAH, including microvascular thrombi, autoregulatory dysfunction, blood-brain barrier breakdown, neuroinflammation, and neuronal cell death; and, if so, whether this protection ultimately improves patient outcome.

scholarly journals TRAF3 mediates neuronal apoptosis in early brain injury following subarachnoid hemorrhage via targeting TAK1-dependent MAPKs and NF-κB pathways

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yan Zhou ◽  
Tao Tao ◽  
Guangjie Liu ◽  
Xuan Gao ◽  
Yongyue Gao ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Therapeutic Target ◽  
Cortical Neurons ◽  
Neuronal Apoptosis ◽  
Early Brain Injury ◽  
Neurological Deficits ◽  
Human Brain Tissue

AbstractNeuronal apoptosis has an important role in early brain injury (EBI) following subarachnoid hemorrhage (SAH). TRAF3 was reported as a promising therapeutic target for stroke management, which covered several neuronal apoptosis signaling cascades. Hence, the present study is aimed to determine whether downregulation of TRAF3 could be neuroprotective in SAH-induced EBI. An in vivo SAH model in mice was established by endovascular perforation. Meanwhile, primary cultured cortical neurons of mice treated with oxygen hemoglobin were applied to mimic SAH in vitro. Our results demonstrated that TRAF3 protein expression increased and expressed in neurons both in vivo and in vitro SAH models. TRAF3 siRNA reversed neuronal loss and improved neurological deficits in SAH mice, and reduced cell death in SAH primary neurons. Mechanistically, we found that TRAF3 directly binds to TAK1 and potentiates phosphorylation and activation of TAK1, which further enhances the activation of NF-κB and MAPKs pathways to induce neuronal apoptosis. Importantly, TRAF3 expression was elevated following SAH in human brain tissue and was mainly expressed in neurons. Taken together, our study demonstrates that TRAF3 is an upstream regulator of MAPKs and NF-κB pathways in SAH-induced EBI via its interaction with and activation of TAK1. Furthermore, the TRAF3 may serve as a novel therapeutic target in SAH-induced EBI.

scholarly journals Early Detection of Post-Endarterectomy Complication by Point-of-Care Ultrasound

Reports ◽  
2021 ◽  
Vol 4 (3) ◽  
pp. 21
Author(s):  
Bo-Ku Chen ◽  
Po-Wei Chiu ◽  
Chih-Hao Lin
Keyword(s):  
Femoral Artery ◽  
Point Of Care ◽  
Postoperative Bleeding ◽  
External Iliac Artery ◽  
Common Femoral Artery ◽  
Atheromatous Plaque ◽  
Point Of Care Ultrasound ◽  
Related Complication ◽  
Contrast Extravasation ◽  
The Right

Endarterectomy is an effective intervention to remove the atheromatous plaque in the inner lining of the artery, aiming to revascularize the occluded/stenosed vessel in patients with peripheral arterial occlusive disease (PAOD). The most common wound-related complication is postoperative bleeding, followed by infection, hematoma, and seroma. However, hematoma complications with air surrounded have rarely been reported in clinical cases. Case presentation: A 90-year-old female patient visited our emergency department because of a rapidly growing hematoma with pulsatile bleeding over her right groin area. She had received bilateral percutaneous transluminal angioplasty with endarterectomy for PAOD one month prior. A point-of-care ultrasound revealed a large hypoechoic mass, with a dirty shadow on the right groin area. Computed tomography angiography showed a hematoma over her right femoral region, with free air surrounding the right femoral artery. Angiography revealed an irregular shaped lesion on the right femoral artery without contrast extravasation. The patient was diagnosed with right-femoral post-endarterectomy infection with infected hematoma, with the inclusion of air. She underwent urgent excision and repair of the right femoral artery infectious lesion, debridement of the infectious hematoma and stenting of the right external iliac artery, common femoral artery and superficial femoral artery.

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