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CEREBRAL EDEMA TREATMENT STEROIDSEdema sometimes caused by head trauma and gulati hours being. To treat cerebral edema, part of the skull must be removed to relieve the pressure on the brain. Cerebral edema is the swelling of the brain due to the accumulation of water outside or within brain cells. Everyone in Bali is born with one of four first names, based on birth order: Wayan, Made, Nyoman, or Ketut. Cerebral edema is most easily understood as a swelling of the brain because of excess water accumulation outside of, or within, the brain cells.
The primary cause of a patient's pathology will strongly influence aspects of his or her treatment for cerebral edema. Another form of treatment for cerebral edema is controlling the temperature of the brain and the rest of the body. Cerebral edema develops in response to and as a result of a variety of neurologic insults such as ischemic stroke, traumatic brain injury, and tumor. Pediatric Hyperglycemia and Diabetic Ketoacidosis (DKA) Third Edition, 2015 1 Illinois EMSC is a collaborative program between the Illinois Department.
Pediatric Hyperglycemia and Diabetic Ketoacidosis (DKA) Third Edition, 2015 1 Illinois EMSC is a collaborative program between the Illinois Department of Public Health and Loyola University Chicago. Today, almost a century after the discovery of insulin, the most common cause of death in a child with diabetes, from a global perspective, is lack of access to insulin or improper use of insulin.
Illinois Emergency Medical Services for Children (EMSC) ? Illinois EMSC is a collaborative program between the Illinois Department of Public Health and Loyola University Chicago, aimed at improving pediatric emergency care within our state. Science, Technology and Medicine open access publisher.Publish, read and share novel research. Radiation-Induced Brain Injury After Radiotherapy for Brain TumorZhihua Yang1, Shoumin Bai2, Beibei Gu3, Shuling Peng3, Wang Liao4 and Jun Liu4[1] Department of Neurology, the First Affiliated Hospital, Guangzhou Medical University, Guangdong, China[2] Department of Oncology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangdong, China[3] Department of Anesthesiology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangdong, China[4] Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangdong, China1.
Almost completely surrounded by the unyielding bony skull, the brain has little area to expand.
Although patients experience a combination of causes for cerebral edema as the pathology cascades along known symptoms, cerebral edema generally has been divided into three subtypes: cytotoxic, vasogenic and interstitial, also called hydrocephalic.
Brain cells that were injured by the original trauma or subsequent swelling require adequate oxygen to stay alive and to avoid releasing vasodilators that can further increase fluid in the area. Depending on the specific treatment facility's guidelines, hypothermic treatment might be started. Adequate blood volume and perfusion to the brain and brain cells is necessary to ensure proper oxygenation, but too much fluid can contribute to the edema.
It deforms brain tissue, resulting in localized mass effect and increase in intracranial pressure (ICP) that are associated with a high rate of morbidity and mortality. Illinois Department of Public HealthLoyola University Chicago ? Since 1994, Illinois EMSC has worked to enhance and integrate:Illinois EMSC Pediatric education Practice standards Injury prevention Data initiatives This educational activity is being presented without the provision of commercial support and without bias or conflict of interest from the planners and presenters. Lurie Children’s Hospital of Chicago Carolynn Zonia, DO, FACOEP, FACEP Chair, EMSC Facility Recognition Committee Loyola University Health System Paula Atteberry, RN, BSN Illinois Department of Public Health Joseph R. IntroductionRadiation therapy is used widely for the treatment of diffuse primary and metastatic brain tumors [1]. Expansion within the area that it naturally has can cause injury and cellular death even as the brain seeks to release excessive pressure by expanding through the foramen magnum — the opening where the spinal cord enters the brain — in a process known as herniation. Depending on which subtype it is, steroids and osmolytic fluids might or might not be used.
Brain cells lacking adequate oxygen or recognizing too much carbon dioxide often release these natural vasodilators in an effort to increase their local blood flow, increase oxygen and decrease carbon dioxide. In most cases, however, the goal is that of a normal body temperature, and prophylactic acetaminophen is often administered rectally. Osmolytic fluids might reduce intracellular cerebral edema, but too much of this type of infusion can result in systemic dehydration and decreased oxygen to the brain cells.
When administered in bolus form, hyperosmolar agents such as mannitol and hypertonic saline have been shown to reduce total brain water content and decrease ICP, and are currently the mainstays of pharmacological treatment. Around the world, forces have united to make it come true that no child should die from diabetes or its complications. Hageman, MD, FAAP NorthShore University Health System - Evanston Cheryl Lovejoy, RN, TNS Advocate Condell Medical Center Linnea O’Neill, RN, MPH Weiss Memorial Hospital Cathleen Shanahan, RN, BSN, MS Ann & Robert H. Fundus examination in radiation-induced optic neuropathy: ocular fundus showing flame-shaped and dot hemorrhage (bottom row, h, arrow) and cotton-wool spots (top row, bottom row, p). Especially for nasopharyngeal carcinoma (NPC), the most common type of cancer in southern China, radiation therapy is the first-choice treatment and sometimes the only effective management of the disease.
Sperduto, Neuropsychological effects of cranial radiation: current knowledge and future directions. Robbins, Inflammation and chronic oxidative stress in radiation-induced late normal tissue injury: therapeutic implications. Britten, Low (60 cGy) doses of (56)Fe HZE-particle radiation lead to a persistent reduction in the glutamatergic readily releasable pool in rat hippocampal synaptosomes. Cuando el corazon deja de funcionar la presion de las venas que van al pulmon se incrementa, el liquido entonces se introduce en los espacios de aire o alveolos de los pulmones.
Treatment almost always involves attention to the primary disease or condition that has resulted in the increased intracranial pressure (ICP). In situations involving cerebral edema, however, this reflexive action might result in even greater excess fluid and pressure.
A febrile state — a condition in which the body's temperature significantly increases and causes various side effects — are to be avoided at all costs. Postural treatment for cerebral edema can decrease ICP while putting certain patients at risk for additional complications.
However, surprisingly, little is known about the increasingly common clinical practice of inducing a state of sustained hypernatremia. Lurie Children’s Hospital of Chicago Maureen Bennett, RN, BSN Loyola University Health System Sandy Hancock, RN, MS Saint Alexius Medical Center Evelyn Lyons, RN, MPH Illinois Department of Public Health S. Lumps-like abnormal signal was shown in the right-basolateral region, heterogeneous high signal was shown on T2W, surrounded by low signal, a large fingerlike high signal of the white matter around lesions on T2W.
Necrosis of right-temporal and right-parietal lobe shows low signal intensity on T1WI and high signal on T2WI with enhanced boundary. As many as 200,000 patients receive partial large-field or whole-brain irradiation every year, and the population of long-term cancer survivors keeps on growing. First, however, treatment for cerebral edema often requires immediate measures to mechanically relieve the ICP, such as drilling a small hole as in ventriculostomy or removing part of the skull in decompressive craniectomy, along with the administration of osmolytic fluids to draw excess fluid from within the brain. Osmolytic fluids reduce intracellular water by drawing out excessive water using concentrated intravenous (IV) fluids. The rationale behind these treatments is the theoretical assumption that feverish brain cells require more oxygen and therefore a greater volume of blood flow. The treatment for cerebral edema is thus almost always conducted in a neurological intensive care unit where careful monitoring can help avoid complications. Margaret Paik MD, FAAP University of Chicago Comer Children’s Hospital Herbert Sutherland, DO, FACEP Central DuPage Hospital Mark Cichon, DO, FACOEP, FACEP Loyola University Health System Sheri Hey, RN, BSN Edward Hospital Patricia Metzler, RN, TNS, SANE-A Carle Foundation Hospital Parul Soni, MD, MPH, FAAP Ann & Robert H. Cerebral gyrus of the frontal and parietal lobe narrow and cerebral sulcus widen which is the sign of cerebral atrophy. Edema of the left-temporal lobe shows finger like low signal intensity on T1WI and high signal on T2WI with non-enhanced boundary.
Anisotropic map shows low signal in the bilateral temporal lobe and white matter fiber of the normal temporal lobe shows high signal and blurred.5. During treatment, however, some healthy brain tissues are also exposed to the radiation inevitably, and consequently many patients may experience neurological symptoms associated with damage to these healthy tissues after radiotherapy. Insufficient evidence exists to recommend pharmacologic induction of hypernatremia as a treatment for cerebral edema.
Si el edema pulmonar es grave o no responde a los medicamentos via oral requiere hospitalizacion y uso de diureticos intravenosos.Si el edema ha sido causado por otros trastornos no cardiacos como infeccion grave requerira otro tratamiento como antibioticosPronosticoEl pronostico dependera de la causa. The strategy of vigilant avoidance of hyponatremia is currently a safer, potentially more efficacious paradigm.
This is known as acute and chronic radiation-induced brain injury (RIBI), also known as radiation encephalopathy (RE).

Approximately 100,000 primary and metastatic brain tumor patients each year in the US survive long enough (>6 months) to experience RIBI [2]. For example, the incidence of RIBI for patients with NPC in Guangdong province is up to 3 per 100,000, to our knowledge, 40 times higher than the world average and is the most common one among head and neck tumor. RIBI includes a series of clinical manifestations, such as focal neurological deficits, secondary epilepsy, mental and behavioural disorders, elevated intracranial pressure, and the progressive deterioration of the hippocampal-associated learning and memory functions [3],which can be especially devastating to patients and caregivers.The American Cancer Society center (ACS) stresses that in order to maximize the quality of life for tumor patients after radiotherapy, the future research should focus on preventing and curing complications of cancer therapy. RIBI, a common and devastating complication of radiotherapy for brain tumor, is now emerging as a major health problem in the treatment of brain tumor.2. PathogenesisBased on the time between onset of clinical expression and radiation therapy administration, RIBI has been classified into acute, early delayed, and late delayed injury, which was first reported by Sheline [4].
Early delayed brain injury occurs 6–12 weeks post-irradiation [5], while some other researchers consider this time course is 1-6 months [6]. Although both of these early injuries can result in severe reactions, they rarely occur and normally resolve spontaneously or reversible after short-term treatment. Oxidative stressIt is reported that in the unilaterally irradiated animals, irradiated hemispheres showed similarly significant changes in oxygenation compared to unirradiated controls. These cells then produce reactive oxygen species (ROS) whose production and detoxification are normal physiological processes. Nevertheless, an imbalance between ROS production and ROS removal may lead to oxidative stress [13, 14].Several components of ROS can cause damage to cardinal cellular components, such as lipids, proteins, and DNA, initiating subsequent cell death via necrosis or apoptosis [15]. Thus, ROS can be contributed to neuronal toxicity and implicated in both acute injury and chronic neuropathological conditions [16].Many related molecules have been reported.
Nonspecific inflammationIrradiation can caused an acute endothelial cell apoptosis which lead to BBB breakdown, chronic hypoxia and peritumoral tissue edema.
Microglias could also be activated by quantity of irradiation through rapid proliferation, as well as increased production of ROS and other cytokines which are involved in mediating neuroin?ammation [22].Plenty of experiments have found up-regulation of pro-inflammatory transcription factors after irradiation which constituted the evidence of nonspecific inflammation cascades in the process of RIBI.
And the further research demonstrated that anti-inflammation factor (TNF-alpha) successfully inhibited radiation-induced effects in the local as well as abscopal region in the brain. And the effectiveness of PPAR-gamma agonists is also a strong demonstration of nonspecific inflammation.
Since all the brain gliocytes including oligodendrocyte, astrocytes and microglia would participate in the radioactive damage process in different ways and RIBI is predominated by white matter necrosis and demyelination, the pathological mechanism is well known as Gliocyte Hypothesis. However, there is conflicting conclusion that the targeted anti-in?ammatory agent has no effect on gliocytes, but can still ameliorate RIBI [26].
Consequently, pathological mechanism of RIBI cannot be explained so simply by the Gliocyte Hypothesis despite the large amount of evidence supporting this hypothesis.Due to the synergistic effect of oxidative stress and nonspecific inflammation after irradiation, endothelial cell nuclear, blood vessel density, and blood vessel length are vulnerable to have a reduction. Paradoxically, radiation-induced necrosis has also been reported in the absence of vascular changes [27]. In addition, the PPAR? agonist, pioglitazone, and the ACE inhibitor, ramipril, which are believed to prevent RIBI in the rat do not reverse the reduction in vascular density and length that occurs after fWBI [28, 29].Therefore, RIBI cannot be completely explained by any single cell or tissue despite a host of evidence supporting these hypotheses. Blood Brain Barrier(BBB) disruptionA number of data from laboratory animals has demonstrated acute BBB disruption which was initiated by apoptosis of endothelial cells and mediated by the ASMase pathway after irradiation [18].
As a result, change of BBB permeability has been thought to be the most sensitive and reliable index for detection of early RIBI.
Apoptosis and neurogenesis inhibitionThe pathogenesis of RIBI may also relate to the process of neuronal apoptosis and inhibition of neurogenesis.Even gray matter contains neuronal cell bodies which is quite oxygen-dependent, neurons have been considered radioresistant since they could no longer divide.
However, it is reported that apoptosis occurs in the young adult rat brain after ionizing irradiation and recent studies also demonstrated that there exists direct radiation-induced damage to hippocampal neurons with associated cognitive decline. Irradiating the hippocampus resulted in an increase in apoptosis in the subgranular zone of the DG which are capable of both self-renewal and generating neurons, astrocytes, and oligodendrocytes [32, 33]. And blocking neurogenesis which was associated with alterations of microenvironment including disruption of the microvascular angiogenesis and increase in the number and activation status of microglia within the neurogenic zone can contribute to the deleterious side effects of radiation treatment.
Chandler reported the time interval between the end of radiotherapy to the onset of RIBI was 1 month to 16 years [35]. Early delayed effects of post-irradiation and usually show reversible symptoms generalized weakness and somnolence, partly resulting from a transient demyelination. Take NPC for example, since inferior temporal lobes inevitably expose to the radiation, the prominent and earliest seen symptom of RIBI is distinctive cognitive impairment. The feature of cognitive impairment is different from those with Alzheimer’s disease, it is characterized by decreased verbal memory, spatial memory, attention, novel problem-solving ability, and even executive function. Patients usually accompanied with negative emotions including depression, anxiety as well as somatization.
Mental disorders such as stupor state, hallucinations and delusions could also be observed as the injury progresses [20].It should be noted that signi?cant cognitive impairment can be seen in the absence of radiographic or clinical evidence of demyelination or white matter necrosis after irradiation [40].
Therefore, conducting cognitive evaluations shortly post-irradiation at regular intervals is becoming more and more important. Once cognitive decline is detected, no matter whether there is imaging findings of brain lesions, prophylactic treatment should be given to the patients immediately.
The mini-mental status examination (MMSE), a test to assess global cognitive function, is relatively insensitive to radiation-induced cognitive impairment [39, 41]. As the cognitive domains that are most affected by brain irradiation is distinct from the common causes of dementia such as Alzheimer's disease and vascular dementia, current Radiation Therapy Oncology Group (RTOG) study has established a series of tests that focuses on the cognitive domains affected by brain irradiation, such as Dutch adult reading test for assessing intelligence, vline bisection test for perception, visual verbal learning test for memory and stroop color word test for executive function [42].
The Montreal cognitive assessment (MoCA) is used to assess different cognitive domains including attention and concentration, executive functions, memory, language, visuoconstructional skills, conceptual thinking, calculations, and orientation. If the pathogenesis develops persistently, the area of edema could expand to the parietal lobes and then cause rapidly deteriorating clinical course. Signs of increased intracranial pressure such as headache, nausea and vomiting would get worse progressively. Severe cerebral edema could result in compression of cerebral peduncle and cerebral hernia, which would lead to hemiplegia and even to death. Moreover, cerebral edema could at last get liquefactive necrosis with formation of cystic spaces. Brain stem and cranial typeIt has been reported that each pair of cranial nerve could get involved in injury after irradiation in NPC patients [43].
Due to the irradiation fields mainly cover the lower part of brain stem, the last four cranial nerves, glossopharyngeal nerve, vagus nerve, accessory nerve and hypoglossal nerve, were commonly affected and leading to corresponding clinical manifestations, such as atrophy of tongue muscle, dysphagia, dysphonia and dysdipsia. And the frequency of upper cranial nerve injury increased greatly if the patients have to conduct re-radiotherapy.Some other common involved cranial nerve is cochleovestibular nerve caused by not only direct effect of irradiation to the nerve but also the indirect effect of the inner ear damage after radiotherapy such as secretory otitis media or even intractable suppurative otitis media.
The prime symptoms of disorders of the cochleovestibular nerve are vertigo, tinnitus and pain. Irreversible hearing loss caused by nerve deafness, conduction deafness and mixed deafness will happen in the end [43].Radiation-induced optic neuropathy (RION) is a rare but usually devastating side effect of radiotherapy for NPC. The most frequent clinical symptoms of RION typically present with sudden, painless, irreversible vision loss in one or both eyes after radiotherapy, and occur most commonly from 3 months to more than 9 years after radiotherapy. Ophthalmologic examinations showed flake bleeding in the retina, optic nerve atrophy and cotton-wool spots.
Damage to descending sympathetic nerve fibers, which anatomically run along the brain stem, may result in hazardous syncope as well as Horner syndrome. Damage to cerebellum results in edema of cerebellar hemisphere and leads to symptoms such as vertigo, stumbling, ataxia and other discomfort. Value of neuroimaging in RIBI diagnosisNeuroimaging, including computed tomography (CT), magnetic resonance imaging (MRI) especially neurological functional imaging technology, provide valuable information in early diagnosis and differential diagnosis of RIBI. Computed Tomography (CT)CT foundings of focal radiation brain edema and necrosis are generally low density, while the affected white matter is usually symmetric and exhibit no enhancement or irregular peripheral enhancement with contrast material.
The brain lesions would range from small foci near the frontal or occipital horns to a confluent band extending from the ventricles to the corticomedullary junction. Magnetic resonance Imaging (MRI)MRI is definitely more valuable for the diagnosis of RIBI than CT.
The appearence of finger like edema and focal necrosis which shows low signal intensity on T1WI and high signal on T2WI are typical feature of MR imaging in patients with RIBI. Ringlike or irregular enhancement in the bilateral temporal lobes are also frequently seen on T1WI enhanced MR imaging while haemorrhage with heterogeneous signals is relative rare. Proton magnetic Resonance Spectroscopy (MRS)MRS is used to display metabolite changes in normal appearing white matter after fWBI in the brain. Brain metabolites are quanti?ed including choline(Cho), creatine(Cr), glutamate(Glu), glutamine(Gln), N-acetyl-aspartate (NAA) and lactate. It is reported that NAA, Cr and Cho change regularly from the center of the visible lesions.

In the visible lesions, the levels of NAA increase slightly, while the contents of Cr and Cho decreased obviously. Certain extent away from the visible lesions, the contents of NAA decrease and the levels of Cr and Cho increase. Diffusion Tensor Imaging (DTI)DTI is a novel way to assess tissue microstructure by measuring the diffusion of water molecules in three-dimensional (3D) space.
It is often applied to distinguish demyelination from axonal injury within white matter bundle.
In a DTI study of childhood survivors after fWBI for acute lymphoblastic leukemia, fractional anisotropy (FA) decreases signi?cantly in the frontal and parietal lobes related to declines in intelligence quotient [47]. In another study of adult survivors post fWBI for acute leukemia, FA values reduced obviously in normal appearing cerebral white matter of the temporal lobe, hippocampus, and thalamus [48].
DTI is thought to be a promising technique to detect early changes in white matter integrity before image evidence of radiation-induced demyelination or necrosis.
Treatment strategiesUp to now, there has been no proven effective treatment to reverse or terminate the pathogenesis brain irradiation injury, which could be particularly devastating to patients and caregivers since the exact mechanisms of RIBI is unclear.
A large number of experimental and clinical studies have confirmed its polyvalent efficacy of narrowing lesions, relieving symptoms as well as improving their prognosis by counteracting the radiation-induced vascular endothelial damage and inflammatory cascade [49].
Many a researchers recommend maintenance therapy with regular dose for more than 3 months while some others affirm the effect of early large dosage of corticosteroids for shorter periods [49]. Some patients may be weaned off after a period of symptomatic exacerbation while in some cases symptoms can return after steroid cessation and lead to necessitating long-term steroid use. Antiplatelets and anticoagulationRadiation induced vascular endothelial injury may lead to subsequent mural thrombosis, thus antiplatelets may play a crucial part in preventing the RIBI. Currently exsisted antiplatelet drugs mainly include cyclooxygenase(COX) inhibitors and adenosine diphosphate (ADP) receptor antagonists. Phosphodiesterase inhibitors, a new type of antiplatelet agents, have been proved to be protective for intravascular thrombosis after radiation [2].Another kind of drug to control thrombosis is anticoagulation drugs.
It’s reported that the use of heparin and warfarin lead to partial recovery of function in five of eight patients with cerebral radiation necrosis when they were proved to be unresponsive to steroid therapy [50]. One case concerning a patient experienced a recurrence of symptoms following discontinuation of anticoagulation therapy and was reversed again by resuming anticoagulation treatment [50] demonstrated the limited success of anticoagulation drug. Reactive Oxygen Species (ROS) scavengersEdaravone, a new agent of ROS scavenger, has been verified effective in reducing the vascular endothelial cell injury, inhibiting brain encephaledema and preventing neuronal cell necrosis [51]. After a 4-week treatment, the lesion volume on MRI was smaller than before in edaravone group, and the scores of 6 domains, 19 aspects and the overall quality of life in edaravone group were significantly higher than those in non-edaravone group [52]. However, ROS scavengers have received not so much attention because they are likely to protect brain tumors to the same extent as they protect normal brain [2]. The administration of Vitamin E significantly reduced the severity of radiation-induced brain damages and increased the activity of superoxide dismutase and catalase enzymes in the brain. Refactoring microcirculationThe butyl-phthalide, a neotype of drugs reforming the microcirculation, has multiple effects of increasing the perfusion in the ischemia area, protecting the mitochondria from hypoxic injury, and also reducing neuronal apoptosis.
Reconstructing the nerve functionRadiation injury could destroy the nerve structure and then lead to loss of neuron function. Therefore neural plasticity is thought to play a vital role in the comprehensive treatment for RIBI. As our data from animals and humans shows that gangliosides is helpful in promoting the recovery of nerve function in lesioned brain, spinal cord and also peripheral nerve.
A host of in vivo and in vitro studies also demonstrated that neurotrophic factors are neuroprotective in radiation-induced nouropathy.
Renin–Angiotensin System(RAS) inhibitorsThe RAS has been viewed as a classical systemic hormonal system. Both angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) have been proved effective in treating experimental radiation nephropathy and pneumopathy [56, 57]. Symptomatic treatmentDehydration medicine such as mannitol and albumin should be given to patients with high cranial pressure. Serotonin (5-HT) reuptake inhibitors and psychological therapies might be preferred when anxiety and depression are the cardinal symptoms.It should be mentioned that there has been no known preventive medications for radiation-induced cognitive impairment in humans, although several pharmacologic agents have been assessed for symptomatic management [2]. Memantine, an NMDA receptor antagonist being able to block ischemia-induced NMDA excitation, was proven to be effective in vascular dementia. Thus it is supposed to be conducive to radiation-induced cognitive impairment if radiation-induced ischemia occurs after fWBI. Other potential pharmacological mediators based on preclinical researches suggesting that anti-in?ammatory agents could prevent or ameliorate radiation-induced cognitive function. Surgical managementSurgical resection can be considered when the patient’s necrosis are symptomatic and have no take a turn for the better after medical treatments. For example, when suffering from large area-cerebral edema, and the condition progressively exacerbated active medications although has been given, patients should also be recommended to surgically remove the focal brain lesions in time when the location is in a region that is surgically accessible. During this process, the surgeon should avoid incurring additional significant neurologic morbidity. Neural Stem Cells(NSCs) therapiesIn addition to drug therapeutics, there has been increased interest in the use of various NSCs therapies.
Pioneering researchers directly inject NSCs into rodent brains after WBI and found it partially restores cognitive function [62, 63]. Interestingly, these NSCs not only differentiate into neurons, but also oligodendrocytes, astrocytes and endothelial cells that can alter the hippocampal microenvironment [63]. Organ-sparing approachTo date, one of the strategies to prevent RIBI in the clinic involves organ-sparing approach which is based on neuroanatomical target theory. Technology has evolved to potentially allow for selective avoidance of the regions of adult neurogenesis, including the hippocampus and neural stem cell niche in the periventricular regions. With the help of advanced radiation techniques, such as 3D conformal image guidance [64], inverse-planned intensity modulated radiotherapy (IMRT) [65] and proton beam radiotherapy [66], it is expected to reduce the occurrence of RIBI by limiting the dose to critical organs and possibly increasing locoregional tumor control.
Anti-VEGF antibodyAs is mentioned above, the necrosis is partly due to increasing capillary permeability which is caused by cytokine release leading to extracellular edema. The edema is the most common pathology of RIBI is just sustained by endothelial dysfunction, tissue hypoxia as well as subsequent necrosis.
Consequently, it is a logical option to block the vascular endothelial growth factor (VEGF) at an early stage to reduce the development of radiation necrosis and thus decrease the vascular permeability. Hyperbaric Oxygen Treatment (HBOT)HBOT is proven to be able to stimulate angiogenesis and restore the regional blood supply by reaching the goal of increasing parenchymal oxygen concentration.
HBOT treatment has been demonstrated to be beneficial in pediatric patients with radiation necrosis [69]and in smaller series and case reports [70, 71].
As single institution studies vary widely due to patient selection bias, it would be necessary to conduct more randomized trials to delineate the true benefit of HBOT. Problems and prospectsAlthough a great many treatment strategies have eliminated acute and early delayed brain injury as well as most delayed demyelination and white matter necrosis, radiotherapy is still carries a risk of RIBI which may seriously affect the life quality of survivors. This risk is further exacerbated while the patient need to use chemotherapeutic agents at the same time [2].To get more knowledge about the mechanism of RIBI is the key to the solution.
Although many theories have been proposed, it is likely that the pathogenesis in long term survivors of various tumors like small cell lung cancer, NPC, low-grade glioma, non-parenchymal tumors, primary brain tumors and metastatic brain tumors are different just because they were treated differently. There is not a solely theory that can be used to fully answer this question.As a result, it is imperative to detect the pathological change non-invasively as early as possible. It is explicit that the most important issue is to differentiate radiation necrosis and tumor progression. Fortunately, there are multiple radiological and nuclear medicine techniques available to help us even these anatomic and metabolic imaging techniques all have inherent limitations in sensitivity and specificity.Researchers all over the world have tried hard but have had only modest success in modulating RIBI to date. However, the future looks promising since we have attached importance to RIBI and find some innovative treatments such as the NECs or anti-VEGF therapy which can be the alternative offer [72].Over the next decade, we will continue paying more attention to the investigation that how radiation-induced brain injury develops and how it can be treated [2]. AcknowledgementsWe are grateful for support from the National Natural Science Foundation of China (no.

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