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  • br Discussion Traumatic asphyxia has characteristic pathophy

    2018-11-12


    Discussion Traumatic asphyxia has characteristic pathophysiologic mechanisms, including elevation of thoracoabdominal pressure with closure of the glottis and the airway (Figure 5). Venous backflow and an increasing capillary pressure may cause inadequate tissue perfusion and capillary rupture. The most common clinical manifestations are craniocervical cyanosis, edema, and petechiae; in addition, neurologic symptoms are commonly associated with traumatic asphyxia and determine the patient outcome. Brain edema and central nervous system ischemia have been described in various cases. In 1992, Jongewaard et al reported 14 cases of sustained thoracic compression associated with varying degrees of neurologic symptoms, including loss of consciousness, brachial plexopathy, visual disturbance, and paralysis. In 2008, Senoglu et al reported Perthes syndrome associated with an intramedullary spinal cord hemorrhage in a 4-year-old girl who sustained thoracic compression. In the present case, the patient experienced a temporary head contusion when he was roughly extricated from the machine by his colleague but was conscious and alert. The patient showed a delayed change in consciousness and MRI revealed nf-κb inhibitor lesions. Traumatic asphyxia combined with diffuse axonal injury has not been reported previously. Cervical venous drainage in the head and neck is divided by internal and external jugular veins. The external jugular vein has two pairs of valves, including the lower pair at its entrance into the subclavian vein and the upper pair approximately 4 cm above the clavicle. The internal jugular vein contains a pair of valves, which are bilaterally placed 2.5 cm above the termination of the vessel. They are protected against venous backflow to the face and brain when the vascular pressure is less than 45 mmHg. Venous hypertension and capillary rupture may result in tissue or organ hemorrhages, including bulbar conjunctiva hemorrhage and facial and cerebral petechiae. The definite mechanism of diffuse axonal injury is the acceleration and deceleration of inertial forces, and the microscopic features include axonal stretch injury and Wallerian-type axonal degeneration. The image-specific findings of diffuse axonal injury show multifocal puncture hemorrhages at the corticomedullary junction, corpus callosum, deep gray matter, and upper brain stem. Brain CT findings may often be normal but MRI may show obvious injury. A T2-weighted MRI demonstrated multifocal hyperintense foci at characteristic locations, diffusion-weighted MRI demonstrated hyperintense foci of restricted diffusion, and susceptibility-weighted MRI depicted more than T2* gradient-echo sequence. Clinicians should be aware of the fact that diffuse axonal injury can accompany traumatic asphyxia.
    Conclusion
    Introduction Glioblastoma multiforme (GBM) is the most common primary brain tumor and the most malignant of the astrocytomas, representing ∼12–15% of all intracranial tumors and 50–75% of astrocytomas. GBM is an aggressive malignant astrocytoma classified as a World Health Organization Grade IV astrocytoma and has poor differentiation. The mean survival time of affected patients is usually < 2 years. GBMs have various spread patterns, including white-matter metastases, which is the most common route, cerebrospinal fluid (CSF) dissemination, ependymal and subependymal spread, skull–dura invasion, and extra-central nervous system (CNS) metastases. Cases of extracranial lesions are < 2%, with the lung and pleura, regional lymph nodes, spine, bone marrow, and liver being common sites. In this study, in addition to reviewing relevant literature, we present an extremely rare and devastating case of regional skin invasion by GBM.
    Case Report In December 2012, a 50-year-old woman presented with right hemiparesis with a muscle power of 3–4 and Broca\'s aphasia. Imaging studies revealed the presence of a brain tumor on the left frontal–parietal area with peritumoral edema, for which she underwent immediate surgery. The tumor was pathologically confirmed to be GBM and after surgery, her clinical symptoms improved. Two weeks after the operation, she was administered concurrent radiotherapy with 6000 cGy for 30 courses and chemotherapy with temozolomide at 75 mg/m2/d for 42 days. Additionally, she received a 5-day course of adjuvant chemotherapy with temozolomide at 200 mg/m2/d every 28 days.