Management Of Brain Edema Research Articles

Role of decompressive craniectomy in the management of acute ischemic stroke (Review).

The application of decompressive craniectomy (DC) is thoroughly documented in the management of brain edema, particularly following traumatic brain injury. However, an increasing amount of concern is developing among the universal medical community as regards the application of DC in the treatment of other causes of brain edema, such as subarachnoid hemorrhage, cerebral hemorrhage, sinus thrombosis and encephalitis. Managing stroke continues to remain challenging, and demands the aggressive and intensive consulting of a number of medical specialties. Middle cerebral artery (MCA) infarcts, which consist of 1-10% of all supratentorial infarcts, are often associated with mass effects, and high mortality and morbidity rates. Over the past three decades, a number of neurosurgical medical centers have reported their experience with the application of DC in the treatment of malignant MCA infarction with varying results. In addition, over the past decade, major efforts have been dedicated to multicenter randomized clinical trials. The present study reviews the pertinent literature to outline the use of DC in the management of malignant MCA infarction. The PubMed database was systematically searched for the following terms: 'Malignant cerebral infarction', 'surgery for stroke', 'DC for cerebral infarction', and all their combinations. Case reports were excluded from the review. The articles were categorized into a number of groups; the majority of these were human clinical studies, with a few animal experimental clinical studies. The surgical technique involved was DC, or hemicraniectomy. Other aspects that were included in the selection of articles were methodological characteristics and the number of patients. The multicenter randomized trials were promising. The mortality rate has unanimously decreased. As for the functional outcome, different scales were employed; the Glasgow Outcome Scale Extended was not sufficient; the Modified Rankin Scale and Bathel index, as well as other scales, were applied. Other aspects considered were demographics, statistics and the very interesting radiological ones. There is no doubt that DC decreases mortality rates, as shown in all clinical trials. Functional outcome appears to be the goal standard in modern-era neurosurgery, and quality of life should be further discussed among the medical community and with patient consent.

Basic principle in the management of brain edema and elevated intracranial pressure

Background: Brain edema is a well-recognized pathophysiological secondary change after primary brain injury. The mechanism of brain edema may differ based on the types of brain edema. However, numerous ion channels are involved in its development and are therefore currently a hot target for anti-edema therapy. Here, this paper reviews the clinically important differences among the types of brain edema and a step-wise management strategy for brain edema and elevated intracranial pressure (ICP).Current Concepts: Brain edema can be classified as cytotoxic, ionic, vasogenic, and interstitial edema. Although the underlying mechanisms may differ among the various types of brain edema, multiple ion channels and the integrity of tight junctions are associated with the development of brain edema. If brain edema aggravates, the intracranial volume expands and leads to an elevation of ICP. A basic principle in the management of ICP includes proper positioning, screening for a need for extraventricular drainage, proper sedation, transient hyperventilation, assessing the intracranial water status with the serum sodium level, optimization of cerebral perfusion pressure, hyperosmolar therapy, targeted temperature management, and induction of a pharmacological coma with sedatives.Discussion and Conclusion: Stepwise treatment strategies are recommended in the management of patients with ICP crisis. Based on the principle, detailed management plans need to be adjusted based on the status of an individual patient.

Prospects of immune checkpoint blockade and vaccine-based immunotherapy for glioblastoma

AbstractGlioblastoma multiforme (GBM) is the most prevalent primary brain tumor endowed with a dismal prognosis. Nowadays, immunotherapy in a particular immune checkpoint blockade and therapeutic vaccines are being extensively pursued. Yet, several characteristics of GBM may impact such immunotherapeutic approaches. This includes tumor heterogeneity, the relatively low mutational load of primary GBM, insufficient delivery of antibodies to tumor parenchyma and the unique immunosuppressive microenvironment of GBM. Moreover, standard treatment of GBM, comprising temozolomide chemotherapy, radiotherapy and in most instances the application of glucocorticoids for management of brain edema, results in a further increased immunosuppression. This review will provide a brief introduction to the principles of vaccine-based immunotherapy and give an overview of the current clinical studies, which employed immune checkpoint inhibitors, oncolytic viruses-based vaccination, cell-based and peptide-based vaccines. Recent experiences as well as the latest developments are reviewed. Overcoming obstacles, which limit the induction and long-term immune response against GBM when using vaccination approaches, are necessary for the implementation of effective immunotherapy of GBM.

The Pathophysiology of Brain Edema and Intracranial Hypertension

Brain edema is defined as an increase in brain volume resulting from abnormal accumulation of fluid within the brain parenchyma. Brain edema is a potentially life-threatening complication of neurocritical illness as it raises the intracranial pressure and may progress to brain herniation and death. The management of brain edema and increased intracranial pressure is a significant challenge in neurocritical care. The purpose of this review is to describe the pathophysiology of diverse types of brain edema. Key Words: Brain edema; Vasogenic edema; Cytotoxic edema; Interstitial edema; Intracranial hypertension

PRO

Two different main concepts for the treatment of severe traumatic brain injury have been established during the last 15 years, namely the more conventional concept recommended in well-established guidelines (eg, the US Guideline, European Guideline, Addelbrook's Guideline from Cambridge) on the one hand, and the Lund concept from the University Hospital of Lund, Sweden on the other. Owing to the lack of well-controlled randomized outcome studies comparing these 2 main therapeutic approaches, we cannot conclude that one is better than the other. This study is the PRO part in a PRO-CON debate on the Lund concept in the present journal. Although the Lund concept is based on a physiology-oriented approach dealing with hemodynamic principles of brain volume and brain perfusion regulation, traditional treatments are primarily based on a meta-analytic approach from clinical studies. High cerebral perfusion pressure has been an essential goal in the conventional treatments (the cerebral perfusion pressure-guided approach), even though it has been modified in a recent update of US guidelines. The Lund concept has instead concentrated on management of brain edema and intracranial pressure, simultaneously with improvement of cerebral perfusion and oxygenation (the intracranial pressure and perfusion-guided approach). Although conventional guidelines are restricted to clinical data from meta-analytic surveys, the physiological approach of the Lund therapy finds support in both experimental and clinical studies. It offers a wider base and can also give recommendations regarding fluid therapy, lung protection, optimal hemoglobin concentration, temperature control, the use of decompressive craniotomy, and ventricular drainage. This study puts forward arguments in support of the Lund therapy.

Prevention and management of brain edema in patients with acute liver failure

1. Intracranial pressure is the pressure exerted by the cranial contents on the dural envelope and consists of the partial pressures of the brain, blood, and cerebrospinal fluid. 2. Severe cases of acute liver failure are frequently complicated by brain edema (due to cytotoxic edema) and an increase in cerebral blood flow while the cerebrospinal fluid volume remains constant. 3. The development of intracranial hypertension in patients with acute liver failure may be controlled by manipulation of the position, body temperature, plasma tonicity, arterial carbon dioxide tension, and arterial pressure. 4. If intracranial hypertension evolves despite these first-tier interventions, increased sedation, induction of hypothermia (body temperature of 33 degrees C to 34 degrees C), and the use of anti-inflammatory drugs may help secure brain viability.

Treatment of medical complications in patients with brain tumors

Patients with primary brain tumors and those with cerebral metastases are at risk throughout their illness for several major medical problems, including vasogenic edema, seizures, and symptomatic venous thrombosis. In turn, the corticosteroids, anti-epileptic drugs, and anticoagulants used to treat these problems may produce significant adverse effects and result in important drug-drug interactions that may complicate chemotherapy. Although few Class I studies address any of these issues, guidelines can be offered to maximize quality of life and minimize hospital readmissions. Optimal management of brain edema involves minimizing corticosteroid use and tapering the steroid dose slowly to avoid steroid withdrawal symptoms. Prophylaxis of Pneumocystis pneumonia is necessary for patients requiring corticosteroids for more than 1 month. Anti-epileptic drugs (AEDs) should be avoided unless patients experience seizures. If possible, non-CTY (P450) enzyme-inducing drugs should be chosen. AED levels should be obtained frequently during corticosteroid taper. Multimodality venous thrombosis prophylaxis should begin at the time of the original surgery with external leg compression and unfractionated subcutaneous heparin or a low molecular weight heparin (LMWH). Brain tumor patients with symptomatic venous thrombosis or pulmonary embolism can be anticoagulated safely with warfarin or with LMWH, and LMWHs are preferable from the standpoints of efficacy, safety, and convenience for long-term outpatient treatment of venous thrombosis. Clinicians should be aware of potential drug-drug interactions between prescribed AEDs and chemotherapy and possible interactions with complementary and alternative therapies chosen by their patients. They also should be aware of interventions to minimize late sequelae of brain tumors and their treatment, including cognitive decline, depression, and increased stroke risk.

MRI Assessment of Peritumoral Brain Edema in Human Astrocytomas: Correlation with Angiogenesis Biomarkers

Mass effect due to peritumoral brain edema (PTBE) is one of the most common imaging characteristics encountered in glial tumors. The severity and variety of the PTBE may increase the difficulties of cancer treatment. However, its pathogenesis is not well documented. Recently, more attention has been paid to vascular endothelial growth factor (VEGF), the polypeptides mediating tumor angiogenesis and microvascular permeability. The purpose of this study was to investigate PTBE index in astrocytomas obtained from MRI and its correlation with angiogenesis biomarkers, VEGF and microvessel density. Our results demonstrated that PTBE in human astrocytomas correlated with both VEGF expression and vessel density. The relationship of PTBE with angiogenesis biomarkers allows a better understanding its molecular mechanisms, and may have implications for clinical management of brain edema associated with human astrocytomas.

The management of brain edema in brain tumors

This review focuses on pathophysiology, clinical signs, and imaging of brain edema associated with intracranial tumors and its treatment. Brain edema in brain tumors is the result of leakage of plasma into the parenchyma through dysfunctional cerebral capillaries. The latter type of edema (ie, vasogenic edema) and the role of other types in brain tumors is discussed. Vascular endothelial growth factor-induced dysfunction of tight junction proteins probably plays an important role in the formation of edema. Corticosteroids are the mainstay of treatment of brain edema. When possible, corticosteroids should be used in a low dose (eg, 4 mg dexamethasone daily) to avoid serious side effects such as myopathy or diabetes. Higher doses of dexamethasone (16 mg/day or more), sometimes together with osmotherapy (mannitol, glycerol) or surgery, may be used in emergency situations. On tapering, one should be aware of the possible development of corticosteroid dependency or withdrawal effects.Novel therapies include vascular endothelial growth factor receptor inhibitors and corticotropin releasing factor, which should undergo further clinical testing before they can be recommended in practice.

Management of Brain Edema Complicating Stroke

Management of Brain Edema Complicating Stroke

Management of Brain Edema Complicating Stroke

Ischemic brain edema, the accumulation of fluid within the brain parenchyma following stroke, is a predictable consequence of both ischemic and hemorrhagic strokes. Its development is the result of injury to both brain parenchyma and the blood vessels supplying the parenchyma. Ischemic stroke produces both cytotoxic (intracellular) edema, which develops when cells are damaged, and vasogenic (extracellular) edema, which arises from injury to structures essential to blood-brain barrier integrity. An understanding of the distinction between cytotoxic and vasogenic edema is essential in preventing secondary brain injury, since the treatments for the two entities differ. The development of new brain imaging technologies has advanced our understanding of brain edema. Both computed tomography (CT) and magnetic resonance imaging (MRI) can detect edema. Specific MRI sequences such as diffusion-weighted imaging can distinguish cytotoxic and vasogenic subtypes, and thereby detect ischemic cell injury within minutes of the onset of symptoms. Brain edema causes neurologic deterioration predominantly through its mass effect, which leads to distortion of the intracranial contents and impairment of both regional and global cerebral blood flow (CBF). Edema may also cause local tissue dysfunction. Management of the intracranial hypertension and tissue shifts caused by ischemic brain swelling is based on the fundamental relationship between pressure, flow, and resistance. Interventions are directed at preserving CBF and preventing secondary brain injury. Strategies include reducing intracranial blood volume with hypocapnia, reducing brain volume with osmotic agents, reducing cerebral metabolism with hypothermia and barbiturates, reducing resistance with rheologic agents, increasing blood pressure with vasoconstrictors, and expanding the cranial vault with decompressive surgery. All individual therapies must be used as part of a structured approach that involves frequent serial neurologic assessments, quantitative measures of pressure, flow, and resistance, and prespecified protocols for intervention.

Antitumor effect and peritumoral brain edema formation in relation to MX2, ACNU, and doxorubicin therapy: A comparative analysis using rodent models of gliomas

The potential antitumor effect of MX2, a new lipophilic morpholino anthracycline, was compared with those of ACNU or doxorubicin (DOX) using two different rodent glioma models. A mouse subcutaneous glioma model (203 glioma) was used to measure the effect of each drug on reducing the glioma size and a rat 9L intracerebral glioma model (9L glioma) was used to assess the antitumor effect on survival rate in a clinically similar fashion. Treatment with ACNU inhibited tumor growth by 94.6% ip ˂ 0.0001) and complete regression of the tumor was observed in 3 of 25 (12.0%) of the ACNU-treated cases. Tumor growth was inhibited by 32.4% with DOX despite a tendency (p˂0.16) and by 59.4% with MX-2 7p ˂ 0.001); neither of these drugs resulted in complete tumor regression. In the intracerebral glioma rats, only ACNU tended to ameliorate survival rate, but there was no statistical significance. These results suggest that ACNU has the most potent effect but MX2 can be an option for chemotherapy of malignant gliomas. Interestingly, all three drugs significantly elevated the brain water content on both the ipsilateral and contralateral sides of the tumor, although they did not induce brain edema in the normal rat brains. Careful management of brain edema might be required regardless of the drug used during chemotherapy to maximize the prognosis of glioma patients. [Neurol Res 2000; 22: 819-824]

Regulation of brain water and electrolyte contents: the possible involvement of central atrial natriuretic factor.

The intraventricular administration of 0.2 or 2 micrograms of synthetic rat atrial natriuretic factor (syn rANF), sequence 101-126 of the precursor, prevented the water accumulation elicited in rat brain by a systemic hypoosmolar fluid load and led to a statistically significant sodium loss from the nervous tissue, while the potassium content remained unaltered. Similar syn rANF administration to rats not treated with a hypoosmolar fluid load caused no significant change in the water, potassium, and sodium content of the hemispheres. In this experiment, a primary systemic action of centrally administered syn rANF with ensuing secondary changes in brain ion and water homeostasis seems unlikely, as the serum osmolality and sodium and potassium concentrations remained unaltered. Thus, a central influence of the intraventricularly administered hormone upon the water and ion balances of the nervous tissue can be hypothesized. The significant loss of sodium may reflect the primary role of volume regulation of the nervous tissue, i.e., the loss of extracellular osmols such as Na+ in response to a hypoosmolar environment. These data lend further support to the concept that a central neuroendocrine system regulates brain ion and volume homeostasis. The possible role of ANF in the management of brain edema should be considered.