The primary goal in cerebral edema is to optimize and regulate cerebral perfusion, oxygenation, and venous drainage, decrease cerebral metabolic demands, and to stabilize the osmolality pressure gradient between the brain and the surrounding vasculature. As cerebral edema is linked to increased intracranial pressure (ICP), many of the therapies will focus on ICP.
Treatment
Cerebral edema
Cerebral edema | Treatment
perfusion, oxygenation, and venous drainage, decrease cerebral metabolic demands, and to stabilize the osmolality pressure gradient between the brain and the surrounding vasculature. Yes. Surgically or otherwise Yes, many of the therapies will focus on ICP. many of the therapies will focus on ICP.
who is elwyn roy king?
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A fighter ace in the Australian Flying Corps (AFC) during World War I
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has he been a part of any other war?
user
Yes - World War II
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how did he die?
user
cerebral oedema
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did he get a military funeral service?
user
Yes - his funeral service was attended by hundreds of mourners from the military and civil aviation world
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did an air staff chief attend it?
user
Yes - Sir Charles Burnett
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the flying corps that king served, when was it formed?
user
1912
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do they provide trainings?
user
Yes - they conduct both pilot and mechanic training
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what are the causes of the disease king had?
user
Brain injuries from ischemic stroke, subarachnoid hemorrhage, traumatic brain injury etc
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how can we diagnose it?
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Close monitoring of a person's level of consciousness; awareness of any new or worsening focal neurological deficits; Immediate recognition of Cerebral edema and brain herniation
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can it be treated?
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Diagnosis is based on symptoms and physical examination findings and confirmed by serial neuroimaging (computed tomography scans and magnetic resonance imaging). The treatment of cerebral edema depends on the cause and includes monitoring of the person's airway and intracranial pressure, proper positioning, controlled hyperventilation, medications, fluid management, steroids. Extensive cerebral edema can also be treated surgically with a decompressive craniectomy. Cerebral edema is a major cause of brain damage and contributes significantly to the mortality of ischemic strokes and traumatic brain injuries. As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined.
Cerebral edema | Introduction
Cerebral edema is commonly present in a variety of neurological injuries. Thus, determining a definitive contribution of cerebral edema to the neurological status of an affected person can be challenging. Close bedside monitoring of a person's level of consciousness and awareness of any new or worsening focal neurological deficits is imperative but demanding, frequently requiring admission into the intensive care unit (ICU). Cerebral edema with sustained increased intracranial hypertension and brain herniation can signify impending catastrophic neurological events which require immediate recognition and treatment to prevent injury and even death. Therefore, diagnosis of cerebral edema earlier with rapid intervention can improve clinical outcomes and can mortality, or risk of death.
Cerebral edema | Diagnosis
Serial neuroimaging (CT scans and magnetic resonance imaging) can be useful in diagnosing or excluding intracranial hemorrhage, large masses, acute hydrocephalus, or brain herniation as well as providing information on the type of edema present and the extent of affected area. CT scan is the imaging modality of choice as it is widely available, quick, and with minimal risks. However, CT scan can be limited in determining the exact cause of cerebral edema in which cases, CT angiography (CTA), MRI, or digital subtraction angiography (DSA) may be necessary. MRI is particularly useful as it can differentiate between cytotoxic and vasogenic edema, guiding future treatment decisions.
Cerebral edema | Imaging
Diagnosis of cerebral edema relies on the following:
Cerebral edema | Diagnosis
Early monitoring can be used to guide medical and surgical decision making and to detect potentially life-threatening brain herniation. There was however, conflicting evidence on the threshold values of ICP that indicated the need for intervention. Researches also recommend that medical decisions should be tailored to the specific diagnosis (e.g. subarachnoid hemorrhage, TBI, encephalitis) and that ICP elevation should be used in conjunction with clinical and neuroimaging and not as an isolated prognostic marker.
Cerebral edema | Intracranial pressure monitoring
Although cerebral edema is closely related to increased intracranial pressure (ICP) and cerebral herniation and the general treatment strategies above are useful, the treatment should ultimately be tailored to the primary cause of the symptoms. The management of individual diseases are discussed separately. The following interventions are more specific treatments for managing cerebral edema and increased ICP:
Cerebral edema | Specific Measures
Finding the optimal head position in persons with cerebral edema is necessary to avoid compression of the jugular vein and obstruction of venous outflow from the skull, and for decreasing cerebrospinal fluid hydrostatic pressure. The current recommendation is to elevate the head of the bed to 30 degrees to optimize cerebral perfusion pressure and control the increase in intracranial pressure. It is also worth noting that measures should taken to reduce restrictive neck dressings or garments as these may lead to compression of the internal jugular veins and reduce venous outflow.
Cerebral edema | Positioning
The Monroe-Kellie doctrine states that the skull is a fixed and inelastic space and the accumulation of edema will compress vital brain tissue and blood vessels. Surgical treatment of cerebral edema in the context of cerebellar or cerebral infarction is typically done by removing part of the skull to allow expansion of the dura. This will help to reduce the volume constraints inside of the skull. A decompressive hemicraniectomy is the most commonly used procedure. Multiple randomized clinical trials have shown reduced risk of death with hemicraniectomy compared with medical management. However, no individual study has shown an improvement in the percentage of survivors with good functional outcomes.
Cerebral edema | Surgery
The primary goal in cerebral edema is to optimize and regulate cerebral perfusion, oxygenation, and venous drainage, decrease cerebral metabolic demands, and to stabilize the osmolality pressure gradient between the brain and the surrounding vasculature. As cerebral edema is linked to increased intracranial pressure (ICP), many of the therapies will focus on ICP.
Cerebral edema | Treatment
Cerebral edema is excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain. This typically causes impaired nerve function, increased pressure within the skull, and can eventually lead to direct compression of brain tissue and blood vessels. Symptoms vary based on the location and extent of edema and generally include headaches, nausea, vomiting, seizures, drowsiness, visual disturbances, dizziness, and in severe cases, coma and death. Cerebral edema is commonly seen in a variety of brain injuries including ischemic stroke, subarachnoid hemorrhage, traumatic brain injury, subdural, epidural, or intracerebral hematoma, hydrocephalus, brain cancer, brain infections, low blood sodium levels, high altitude, and acute liver failure.
Cerebral edema | Introduction
Cerebral edema, if associated with coma, often necessitates admission to intensive care, artificial ventilation, and close observation. The administration of fluids is slowed. The ideal treatment of cerebral edema in DKA is not established, but intravenous mannitol and hypertonic saline (3%) are used—as in some other forms of cerebral edema—in an attempt to reduce the swelling.
Diabetic ketoacidosis | Cerebral edema
However, sharp rises in blood pressure should be avoided. Maximum blood pressures tolerated are variable and controversial depending on the clinical situation.
Cerebral edema | Fluid management and cerebral perfusion
The current understanding of the pathophysiology of cerebral edema after traumatic brain injury is incomplete. Current treatment therapies aimed at cerebral edema and increased intracranial pressure are effective at reducing intracranial hypertension but have unclear impacts on functional outcomes. Additionally, cerebral and ICP treatments have varied effects on individuals based on differing characteristics like age, gender, type of injury, and genetics. There are innumerable molecular pathways that contribute to cerebral edema, many of which have yet to be discovered. Researchers argue that the future treatment of cerebral edema will be based on advances in identifying the underlying pathophysiology and molecular characteristics of cerebral edema in a variety of cases.
Cerebral edema | Research
Clinical signs of cerebral edema, such as focal neurological deficits, papilledema and decreased level of consciousness, if temporally associated with recent hemodialysis, suggest the diagnosis. A computed tomography of the head is typically done to rule-out other intracranial causes. MRI of the head has been used in research to better understand DDS.
Dialysis disequilibrium syndrome | Diagnosis
The incidence of this disorder should be considered in terms of its potential causes and is present in most cases of traumatic brain injury, central nervous system tumors, brain ischemia, and intracerebral hemorrhage. For example, malignant brain edema was present in roughly 31% of people with ischemic strokes within 30 days after onset.
Cerebral edema | Introduction
Nutritional support is necessary in all patients with acute brain injury. Enteral feeding, or through mouth via tube, is the preferred method, unless contraindicated. Additional attention must be placed on the solute concentration of the formulations to avoid free water intake, decreased serum osmolality, and worsening of the cerebral edema. Elevated blood glucose, or hyperglycemia, is associated with increased edema in patients with cerebral ischemia and increases the risk of a hemorrhagic transformation of ischemic stroke. Maintaining a normal blood glucose level of less than 180 mg/dL is suggested. However, tight glycemic control of blood glucose under 126 mg/dL is associated with worsening of stroke size.
Cerebral edema | Nutrition
Deep brain stimulation (DBS) is effective treatment for several neurological and psychiatric disorders, most notably Parkinson's disease. DBS is not without risks and although rare, idiopathic delayed-onset edema (IDE) surrounding the DBS leads have been reported. Symptoms can be mild and nonspecific, including reduction of the stimulation effect, and can be confused for other causes of edema. Thus, imaging is recommended to rule out other causes. The condition is generally self-limiting and the exact mechanism of the cause is unexplained. Early identification can help persons affected avoid unnecessary surgical procedures or antibiotic treatments.
Cerebral edema | Idiopathic delayed-onset edema
At the same time, improvement of radiographic markers, biomarkers, and analysis of clinical monitoring data is essential in treating cerebral edema. Many studies of the mechanical properties of brain edema were conducted in the 2010s, most of them based on finite element analysis (FEA), a widely used numerical method in solid mechanics. For example, Gao and Ang used the finite element method to study changes in intracranial pressure during craniotomy operations. A second line of research on the condition looks at thermal conductivity, which is related to tissue water content.
Cerebral edema | Research
The use of specific MRI techniques has allowed for some differentiation between the mechanisms.
Cerebral edema | Combined types of cerebral edema
Cerebral edema is a severe complication of acute brain injuries, most notably ischemic stroke and traumatic brain injuries, and a significant cause of morbidity and mortality.
Cerebral edema | Outcomes
Patients are usually given supplemental oxygen and dexamethasone as well. HACE can be prevented by ascending to heights slowly to allow the body more time to acclimatize. Acetazolamide also helps prevent the condition. Untreated patients usually die within 48 hours. Those who receive treatment may take weeks to fully recover. It is a rare condition, occurring in less than one percent of people who ascend to . First described in 1913, little was known about the cause of the condition until MRI studies were performed in the 1990s.
High-altitude cerebral edema | Introduction
Intracranial pressure (ICP) and its management is a fundamental concept in traumatic brain injury (TBI). The Brain Trauma Foundation guidelines recommend ICP monitoring in individuals with TBI that have decreased Glasgow-Coma Scale (GCS) scores, abnormal CT scans, or additional risk factors such as older age and elevated blood pressure. However, no such guidelines exist for ICP monitoring in other brain injuries such as ischemic stroke, intracerebral hemorrhage, cerebral neoplasm. Clinical researches have recommended ICP and cerebral perfusion pressure (CPP) monitoring in any persons with cerebral injury who are at risk of elevated intracranial pressure based on clinical and neuroimaging features.
Cerebral edema | Intracranial pressure monitoring
As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined. The incidence of this disorder should be considered in terms of its potential causes and is present in most cases of traumatic brain injury, central nervous system tumors, brain ischemia, and intracerebral hemorrhage.
Cerebral edema | Epidemiology
There are several clinical conditions in which vasogenic edema is present:
Cerebral edema | Vasogenic
Cerebral edema is frequently encountered in acute brain injuries from a variety of origins, including but not limited to:
Cerebral edema | Causes
Maintenance of cerebral perfusion pressure using appropriate fluid management is essential in patients with brain injury. Dehydration, or intravascular volume loss, and the use of hypotonic fluids, such as D5W or half normal saline, should be avoided. Blood serum ion concentration, or osmolality, should be maintained in the normo to hyperosmolar range. Judicial use of hypertonic saline can be used to increase serum osmolality and decrease cerebral edema, as discussed below. Blood pressure should be sufficient so as to sustain cerebral perfusion pressures greater than 60 mm Hg for optimal blood blow to the brain. Vasopressors may be used to achieve adequate blood pressures with minimal risk of increasing intracranial pressures.
Cerebral edema | Fluid management and cerebral perfusion
Timing of decompressive craniectomy remains controversial, but is generally suggested that the surgery is best performed before there are clinical signs of brainstem compression. Postoperative complications include wound dehiscence, hydrocephalus, infection, and a substantial proportion of patients may also require tracheostomy and gastrotomy in the early phase after surgery.
Cerebral edema | Surgery
Treatment involves removal of the etiologic mass and decompressive craniectomy. Brain herniation can cause severe disability or death. In fact, when herniation is visible on a CT scan, the prognosis for a meaningful recovery of neurological function is poor. The patient may become paralyzed on the same side as the lesion causing the pressure, or damage to parts of the brain caused by herniation may cause paralysis on the side opposite the lesion. Damage to the midbrain, which contains the reticular activating network which regulates consciousness, will result in coma. Damage to the cardio-respiratory centers in the medulla oblongata will cause respiratory arrest and (secondarily) cardiac arrest.
Brain herniation | Treatment
The most crutial aspect for recovery in patients with severe hematomas is rapid diagnosis and appropriate treatment. Once the clot has been removed the intracranial pressure is monitored for several days. Conditions which are also monitored after surgery are seizures, clot accumulation, and infection. If complications do occur, sometime the hematoma needs to be re-drained. Additional complications following a surgical or nonsurgical treatment may include temporary or permanent weakness, numbness, difficulty speaking, memory loss, dizziness, headache, anxiety, difficulty concentrating, seizures, and/or brain herniation. The most helpful predictors of the treatment outcome is the glasgow coma scale (GCS). This is a standardized pupil response assessment of the neurologic status of the patient.
Sports-related traumatic brain injury | Prognosis (short/long-term effects)
Cerebral edema has been traditional classified into two major sub-types: cytotoxic and vasogenic cerebral edema. This simple classification helps guide medical decision making and treatment of patients affected with cerebral edema. There are, however, several more differentiated types including but not limited to interstitial, osmotic, hydrostatic, and high altitude associated edema. Within one affected person, many individual sub-types can be present simultaneously. The following individual sub-types have been identified:
Cerebral edema | Classification
Pain and agitation can worsen cerebral edema, acutely increase intracranial pressure (ICP), and should be controlled. Careful use of pain medication such as morphine or fentanyl can be used for analgesia. For those persons with decreased levels of consciousness, sedation is necessary for endotracheal intubation and maintenance of a secure airway. Sedative medication used in the intubation process, specifically propofol, have been shown to control ICP, decrease cerebral metabolic demand, and have antiseizure properties. Due to a short half-life, propofol, is a quick-acting medication whose administration and removal is well tolerated, with hypotension being the limiting factor in its continued use.
Cerebral edema | Sedation
Pharmacological prophylaxis with acetazoloamide or corticosteroids can be used in non pre-acclimatized individuals. If symptoms of high-altitude cerebral edema do not resolve or worsen, immediate descent is necessary, and symptoms can be improved with administration of dexamethasone.
Cerebral edema | High Altitude Cerebral Edema
They may include antiseizure medications and hyperosmotic agents to reduce brain swelling and intracranial pressure. It is extremely rare to not require surgery. If the volume of the epidural hematoma is less than 30 mL, the clot diameter less than 15 mm, a Glasgow Coma Score above 8, and no visible neurological symptoms, then it may be possible to treat it conservatively. A CT scan should be performed, and watchful waiting should be done, as the hematoma may suddenly expand.
Epidural hematoma | Treatment
The extent and severity of the symptoms of cerebral edema depend on the exact etiology but are generally related to an acute increase of the pressure within the skull. As the skull is a fixed and inelastic space, the accumulation of cerebral edema can displace and compress vital brain tissue, cerebral spinal fluid, and blood vessels, according to the Monro-Kellie doctrine. Increased intracranial pressure (ICP) is a life-threatening surgical emergency marked by symptoms of headache, nausea, vomiting, decreased consciousness. Symptoms are frequently accompanied by visual disturbances such as gaze paresis, reduced vision, and dizziness. Increased pressures within the skull can cause a compensatory elevation of blood pressure to maintain cerebral blood flow, which, when associated with irregular breathing and a decreased heart rate, is called the Cushing reflex.
Cerebral edema | Signs and symptoms
Autoregulation of cerebral blood flow is impaired, and is associated with anaerobic glycolysis and oxidative stress. Neuronal cell astrocytes are susceptible to these changes, and they swell up, resulting in increased intracranial pressure. Inflammatory mediators also play important role. Unfortunately, signs of elevated intracranial pressure, such as papilledema and loss of pupillary reflexes, are not reliable, and occur late in the disease process. CT imaging of the brain is also unhelpful in detecting early cerebral oedema, but is often performed to rule out intra-cerebral bleeding. Invasive intracranial pressure monitoring via subdural route is often recommended; however, the risk of complications must be weighed against the possible benefit (1% fatal haemorrhage).
Acute liver failure | Encephalopathy and cerebral edema
Fever has been demonstrated to increase metabolism and oxygen demand in the brain. The increased metabolic demand results in an increase in cerebral blood flow and can increase the intracranial pressure within the skull. Therefore, maintaining a stable body temperature within the normal range is strongly recommended. This can be achieved through the use of antipyretics such as acetaminophen (paracetamol) and cooling the body, as described below.
Cerebral edema | Fever
An increase in cerebral water content is called cerebral edema and it usually results from traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), subdural hematoma, ischemic stroke, brain tumors, infectious disorders and intracranial surgery. Cerebral edema may result in compromised regional cerebral blood flow (CBF) and intracranial pressure (ICP) gradients which could lead to death of the affected. Increased ICP leads to increased intracranial volume. Unmonitored ICP leads to brain damage by global hypoxic ischemic injury due to reduction in cerebral perfusion pressure (CPP) which is found by subtracting the ICP from mean arterial pressure(MAP), cerebral blood flow, and mechanical compression of brain tissue due to compartmentalized ICP gradients.
Osmotherapy | Cerebral edema
Epidural hematoma (EDH) is a rapidly accumulating hematoma between the dura mater and the cranium. These patients have a history of head trauma with loss of consciousness, then a lucid period, followed by loss of consciousness. Clinical onset occurs over minutes to hours. Many of these injuries are associated with lacerations of the middle meningeal artery. A "lenticular", or convex, lens-shaped extracerebral hemorrhage that does not cross suture lines will likely be visible on a CT scan of the head. Although death is a potential complication, the prognosis is good when this injury is recognized and treated.
Intracranial hemorrhage | Epidural hematoma
Decreased oxygen concentration in the blood, hypoxia, and increase in the carbon dioxide concentration in the blood, hypercapnia, are potent vasodilators in the cerebral vasculature, and should be avoided in those with cerebral edema. It is recommended that persons with decreased levels of consciousness be intubated for airway protection and maintenance of oxygen and carbon dioxide levels. However, the laryngeal instrumentation involved in the intubation process is associated with a acute, brief rise in intracranial pressure. Pretreatment with a sedative agent and neuromuscular blocking agent to induce unconsciousness and motor paralysis has been recommended as part of standard Rapid Sequence Intubation (RSI).
Cerebral edema | Ventilation and oxygenation
This can lead to cerebral edema, potentially resulting in seizures, permanent brain damage, or death. Therefore, significant hypernatremia should be treated carefully by a physician or other medical professional with experience in treatment of electrolyte imbalance. Specific treatments such as thiazide diuretics (e.g., chlorthalidone) in congestive heart failure or corticosteroids in nephropathy also can be used.
Hypernatremia | Treatment
With the rise of sophisticated treatment modalities such as gamma knife, cyber knife, and intensity modulated radiotherapy, a large number of individuals with brain tumors are treated with radiosurgery and radiotherapy. Radiation-induced brain edema (RIBE) is a potentially life threatening complication of brain tissue radiation and is characterized radiation necrosis, endothelial cell dysfunction, increased capillary permeability, and breakdown of the blood brain barrier. Symptoms include headache, seizure, psychomotor slowing, irritability, and focal neurological deficits. Options for management of RIBE are limited and include corticosteroids, anti platelet drugs, anticoagulants, hyperbaric oxygen therapy, multivitamins, and bevacizumab.
Cerebral edema | Radiation-Induced Brain Edema
Posterior reversible encephalopathy syndrome (PRES) is a rare clinical disease characterized by cerebral edema. The exact pathophysiology, or cause, of the syndrome is still debated but is hypothesized to be related to the disruption of the blood-brain barrier. The syndrome features acute neurological symptoms and reversible subcortical vasogenic edema predominantly involving the parieto-occipital areas on MR imaging. PRES in general has a benign course, but PRES-related intracranial hemorrhage has been associated with a poor prognosis.
Cerebral edema | Posterior Reversible Encephalopathy Syndrome
If the swelling is untreated, it causes death by brain herniation. The brain swelling is likely a result of vasogenic edema, the penetration of the blood–brain barrier by fluids. This process has been observed in MRI studies. Hypoxia increases extracellular fluid, which passes through the vasogenic endothelium in the brain. The leaking may be caused by increased pressure, or it may be caused by inflammation that makes the endothelium vulnerable to leaking. An MRI study found microhemorrhages in the corpus callosum of HACE patients, and hypoxia may also cause microvascular permeability. It has been hypothesized that vascular endothelial growth factor may cause the vascular permeability at the root of HACE.
High-altitude cerebral edema | Cause and mechanism
Cerebral edema is a present with many common cerebral pathologies and risk factors for development of cerebral edema will depend on the cause. The following were reliable predictors for development of early cerebral edema in ischemic strokes.
Cerebral edema | Risk Factors
It is important to note that prolonged hyperventilation in those with traumatic brain injuries has been shown to worsen outcomes.
Cerebral edema | Hyperventilation
Cerebral edema is mainly classified into cytotoxic edema, vasogenic edema and interstitial edema. Cytotoxic edema affects both the white and gray matter and results from the swelling of cellular elements such as neurons, glia and endothelial cells. Vasogenic edema affects white matter and results from blood brain barrier (BBB) breakdown. Interstitial edema results from lack of proper cerebrospinal fluid (CSF) absorption.
Osmotherapy | Cerebral edema
The Cushing reflex often indicates compression of the brain on brain tissue and blood vessels, leading to decreased blood flow to the brain and eventually death.
Cerebral edema | Signs and symptoms
Interstitial edema can be best characterized by in noncomunnicating hydrocephalus where there is an obstruction to the outflow of cerebrospinal fluid within the ventricular system. The obstruction creates a rise in the intraventricular pressure and causes CSF to flow through the wall of the ventricles into the extracellular fluid within brain. The fluid has roughly the same composition of CSF. Other causes of interstitial edema include but are not limited to communicating hydrocephalus, and normal pressure hydrocephalus.
Cerebral edema | Interstitial (Hydrocephalic)
Depending on the individual and the location of the stenosis there are multiple treatments that can be undertaken. These include angioplasty, stent insertion, or bypass the blocked area.
Cerebral atherosclerosis | Treatment
Identification of the underlying cause plays an important role in treatment. Brain abscesses or tumors can be—at least temporarily or partially, if not fully and permanently—surgically treated and chemotherapy and/or radiotherapy is given to the patient. If seizures do continue, various anticonvulsant medication regimens that can be tolerated by the patient can be tested and if need be, administered, either orally, or in emergency conditions such as status epilepticus after tonic-clonic (grand mal) seizures, intravenously. If stroke or other similar, transient disorders occur (cerebrovascular accident, or transient ischemic attack, TIA), then neurological imaging of the affected lobes or hemispheres of the brain can be performed (CT, MRI, PET, etc.) and, if not absolutely contraindicated, antithrombolytic therapy might be given if it can be tolerated due to the seizures; if a hemorrhagic stroke has occurred and surgery can be performed to cauterize the vessel or otherwise stop the bleeding, it will be attempted if it can be done safely.
Epilepsia partialis continua | Treatment
Direct superficial temporal artery (STA) to middle cerebral artery (MCA) bypass is considered the treatment of choice, although its efficacy, particularly for hemorrhagic disease, remains uncertain. Multiple burr holes have been used in frontal and parietal lobes with good neovascularisation achieved. The EDAS (encephaloduroarteriosynangiosis) procedure is a synangiosis procedure that requires dissection of a scalp artery over a course of several centimeters and then making a small temporary opening in the skull directly beneath the artery. The artery is then sutured to a branch of the middle cerebral artery on the surface of the brain and the bone is replaced.
Moyamoya disease | Treatment
If a lumbar puncture is performed, it will show normal cerebral spinal fluid and cell counts but an increase in pressure. In one study, CT scans of patients with HACE exhibited ventricle compression and low density in the cerebellum. Only a few autopsies have been performed on fatal cases of HACE; they showed swollen gyri, spongiosis of white matter, and compressed sulci. There was some variation between individuals, and the results may not be typical of HACE deaths.
High-altitude cerebral edema | Signs and symptoms
The diagnosis is usually made by brain scan (MRI) on which areas of swelling can be identified. The treatment for PRES is supportive: removal of the cause or causes and treatment of any of the complications, such as anticonvulsants for seizures. PRES may be complicated by intracranial hemorrhage, but this is relatively rare. The majority of people recover fully, although some may experience some residual symptoms. PRES was first described in 1996.
Posterior reversible encephalopathy syndrome | Introduction
Brain herniation frequently presents with abnormal posturing, a characteristic positioning of the limbs indicative of severe brain damage. These patients have a lowered level of consciousness, with Glasgow Coma Scores of three to five. One or both pupils may be dilated and fail to constrict in response to light. Vomiting can also occur due to compression of the vomiting center in the medulla oblongata. Severe headaches and seizures as a result of increased intracranial pressure are not uncommon. Cardiovascular and pulmonary symptoms may also be present as the brain loses function, but might also be associated with bleeding. They can include: hypertension, respiratory depression, arrhythmia and in severe cases cardiac arrest.
Brain herniation | Signs and symptoms
Seizures, including subclinical seizure activity, can complicate clinical courses and increase progression of brain herniation in persons with cerebral edema and increased intracranial pressure. Anticonvulsants can be used to treat seizures caused by acute brain injuries from a variety of origins. However, there are no clear guidelines on the use of anticonvulsants for prophylactic use. Their use may be warranted on depending on the clinical scenario and studies have shown that anticonvulsants such as phenytoin can be given prophylactically without a significant increase in drug-related side effects.
Cerebral edema | Seizure prophylaxis
An AVM diagnosis is established by neuroimaging studies after a complete neurological and physical examination. Three main techniques are used to visualize the brain and search for AVM: computed tomography (CT), magnetic resonance imaging (MRI), and cerebral angiography. A CT scan of the head is usually performed first when the subject is symptomatic. It can suggest the approximate site of the bleed. MRI is more sensitive than CT in the diagnosis of AVMs and provides better information about the exact location of the malformation. More detailed pictures of the tangle of blood vessels that compose an AVM can be obtained by using radioactive agents injected into the blood stream.
Cerebral arteriovenous malformation | Diagnosis
Research studies are going on to find more efficient mechanisms to treat cerebral edema. Combining osmotherapy with other treatment mechanisms has a greater potential to treat cerebral edema and its serious pathological effects more effectively.
Osmotherapy | Future
Patients with HACE should be brought to lower altitudes and provided supplemental oxygen, and rapid descent is sometimes needed to prevent mortality. Early recognition is important because as the condition progresses patients are unable to descend without assistance. Dexamethasone should also be administered, although it fails to ameliorate some symptoms that can be cured by descending to a lower altitude. It can also mask symptoms, and they sometimes resume upon discontinuation. Dexamethasone's prevention of angiogenesis may explain why it treats HACE well. Three studies that examined how mice and rat brains react to hypoxia gave some credence to this idea.
High-altitude cerebral edema | Treatment and prognosis
Epidural hematoma is a surgical emergency. Delayed surgery can result in permanent brain damage or death. Without surgery, death usually follows, due to enlargement of the hematoma, causing a brain herniation. As with other types of intracranial hematomas, the blood almost always must be removed surgically to reduce the pressure on the brain. The hematoma is evacuated through a burr hole or craniotomy. If transfer to a facility with neurosurgery is unavailable, prolonged trephination (drilling a hole into the skull) may be performed in the emergency department. Large hematomas and blood clots may require an open craniotomy. Medications may be given after surgery.
Epidural hematoma | Treatment
Since cerebral swelling presents a danger to the patient, treatment of cerebral contusion aims to prevent swelling. Measures to avoid swelling include prevention of hypotension (low blood pressure), hyponatremia (insufficient sodium), and hypercapnia (increased carbon dioxide in the blood). Due to the danger of increased intracranial pressure, surgery may be necessary to reduce it. People with cerebral contusion may require intensive care and close monitoring.
Cerebral contusion | Treatment
Treatment depends on the location and size of the AVM and whether there is bleeding or not. The treatment in the case of sudden bleeding is focused on restoration of vital function. Medical management
Cerebral arteriovenous malformation | Treatment
The goal of osmotic therapy is to create a higher concentration of ions within the vasculature at the blood-brain barrier. This will create an osmotic pressure gradient and will cause the flow of water out of the brain and into the vasculature for drainage elsewhere. An ideal osmotic agent produces a favorable osmotic pressure gradient, is nontoxic, and is not filtered out by the blood-brain barrier. Hypertonic saline and mannitol are the main osmotic agents in use, while loop diuretics can aid in the removal of the excess fluid pulled out of the brain.
Cerebral edema | Osmotic Therapy
When possible, treatment involves resolving the underlying cause. Many cases of heart or kidney disease, are treated with diuretics. Treatment may also involve positioning the affected body parts to improve drainage. For example, swelling in feet or ankles may be reduced by having the person lie down in bed or sit with the feet propped up on cushions. Intermittent pneumatic compression can be used to pressurize tissue in a limb, forcing fluids—both blood and lymph—to flow out of the compressed area.
Edema | Treatment
Additionally, the use of nondepolarizing neuromusclar blocking agents (NMBA), such as doxacurium or atracurium, have been indicated to facilitate ventilation and manage brain injuries but there are no controlled studies on the use of NMBAs in the management of increased intracranial pressure. Depolarizing neuromuscular blocking agents, most notably succinylcholine, can worsen increased ICP due to induction of muscle contraction within the body.
Cerebral edema | Sedation
Cytotoxic, osmotic, and vasogenic edema exist on a continuum. The mechanism of the cause of cerebral edema can often overlap between these types. In most instances, cytotoxic and vasogenic edema occur together. When the two edema types evolve simultaneously, the damage of one type reaches a limit and will bring about the other type of injury. For example, when cytotoxic edema occurs in the endothelial cells of the blood-brain barrier, oncotic cell death contributes to loss of integrity of the blood-brain barrier and promotes the progression to vasogenic edema. When brain edema types are combined, there is typically a primary form and the edema type and context of the cause must be determined in order to start appropriate medical or surgical therapy.
Cerebral edema | Combined types of cerebral edema
Sometimes the lesion appearance imaged by MRI remains inconclusive. Consequently, neurosurgeons will order a cerebral angiogram or magnetic resonance angiogram (MRA). Since CCMs are low flow lesions (they are hooked into the venous side of the circulatory system), they will be angiographically occult (invisible). If a lesion is discernible via angiogram in the same location as in the MRI, then an arteriovenous malformation (AVM) becomes the primary concern.
Central nervous system cavernous hemangioma | Diagnosis
Cerebral contusion is bruising of the brain tissue. The piamater is not breached in contusion in contrary to lacerations. The majority of contusions occur in the frontal and temporal lobes. Complications may include cerebral edema and transtentorial herniation. The goal of treatment should be to treat the increased intracranial pressure. The prognosis is guarded.
Head injury | Cerebral contusion
If the appearances are not typical, other causes for the symptoms and the imaging abnormalities need to considered before PRES can be diagnosed conclusively. In many cases there is evidence of constriction of the blood vessels (if angiography is performed), suggesting a possible overlap with reversible cerebral vasoconstriction syndrome (RCVS). Diffusion MRI may be used to identify areas of cytotoxic edema caused by poor blood flow (ischemia) but it is not clear if this prognostically relevant. Abnormal apparent diffusion coefficient is seen in about 20% of cases. In 10–25% of cases of PRES there is evidence of hemorrhage on neuroimaging.
Posterior reversible encephalopathy syndrome | Diagnosis
In ionic edema, the solute concentration (osmolality) of the brain exceeds that of the plasma and the abnormal pressure gradient leads to accumulation of water intake into the brain parenchyma through the process of osmosis. The blood-brain barrier is intact and maintains the osmotic gradient. The solute concentration of the blood plasma can be diluted by several mechanisms: Ionic brain edema can also occur around the sites of brain hemorrhages, infarcts, or contusions due to a local plasma osmolality pressure gradient when compared to the high osmolality in the affected tissue.
Cerebral edema | Ionic (Osmotic)
According to the "autoregulation breakthrough" conception, cerebral arterioles are forced to dilate, leading to vasogenic edema. Cerebral edema can be generalized or focal. Brain ventricles are compressed, cortical gyri flattened.
Hypertensive encephalopathy | Pathogenesis
The risk of developing HACE is diminished if acetazolamide or dexamethasone are administered. Generally, the use of acetazolamide is preferred, but dexamethasone can be used for prevention if there are side effects or contraindications. Some individuals are more susceptible to HACE than others, and physical fitness is not preventive. Age and sex do not by themselves affect vulnerability to HACE.
High-altitude cerebral edema | Diagnosis and prevention
Subjects are exposed to a substantial amount of radiation with this procedure, so their use is limited.
Cerebral atherosclerosis | Diagnosis
Investigation is underway regarding the use of neuroprotective agents during the prolonged post-traumatic period of brain hypersensitivity associated with the syndrome.
Brain herniation | Treatment
In severe cases, dobutamine should be used to support the right ventricular failure. Frequent Glasgow coma scale (GCS) charting is required to assess the neurological progression of a person with FES. A placement of intracranial pressure monitor may be helpful to direct the treatment of cerebral odema.
Fat embolism syndrome | Treatment
Hydrostatic extracellular brain edema is typically caused by severe arterial hypertension. A difference in the hydrostatic pressure within the arterial system relative to the endothelial cells allows ultrafiltration of water, ions, and low molecular weight substances (such as glucose, small amino acids) into the brain parenchyma. The blood-brain barrier is intact usually and the extent of the edema depends on the arterial pressure. The regulatory processes of the brain circulation can function up to systolic arterial pressures of 150 mm Hg and will have impaired function at higher blood pressures.
Cerebral edema | Hydrostatic
Diagnosis can be confirmed by CT Scan or MRI for advanced investigations.
Middle cerebral artery syndrome | Diagnosis
Successful treatment depends on control of the underlying cause. Severe swelling can cause permanent damage to nerves, resulting in peripheral neuropathy. Many cases from temporary or minor causes resolve on their own, with no lasting damage.
Peripheral edema | Prognosis
MRI scans of patients with HACE showed increased T2 in the corpus callosum, although grey matter was unchanged. This demonstrated that the blood-brain barrier was broken by cerebral blood vessels, thus interfering with white matter metabolism. Another study looked at the brains of HACE sufferers several months after their recovery; it showed hemosiderin deposits in the corpus callosum, evidence of vascular permeability. While there is strong evidence that vasogenic edema plays a major role in HACE, cytotoxic edema, cellular retention of fluids, may contribute as well. Cytotoxic edema may be caused by the failure of cellular ion pumps, which results from hypoxia.
High-altitude cerebral edema | Cause and mechanism
Amyloid-related imaging abnormalities (ARIA) are abnormal differences seen in neuroimaging of Alzheimer's disease patients given targeted amyloid-modifying therapies. Human monoclonal antibodies such as aducanumab, solanezumab, and bapineuzumab have been associated with these neuroimaging changes and additionally, cerebral edema. These therapies are associated with dysfunction of the tight endothelial junctions of the blood-brain barrier, leading to vasogenic edema as described above. In addition to edema, these therapies are associated with microhemorrhages in the brain known as ARIA-H. Familiarity with ARIA can aid radiologists and clinicians in determining optimal management for those affected.
Cerebral edema | Amyloid-Related Imaging Abnormalities - Edema
Progressive cerebral edema may also occur. The increase of blood and brain volume within the skull causes a rapid and severe increase in intracranial pressure, which can in turn cause uncal and cerebellar brain herniation, a disastrous and potentially fatal condition in which the brain is squeezed past structures within the skull. Studies on animals have shown that the brain may be more vulnerable to a second concussive injury administered shortly after a first. In one such study, a mild impact administered within 24 hours of another one with minimal neurological impairment caused massive breakdown of the blood brain barrier and subsequent brain swelling.
Second-impact syndrome | Pathophysiology
Sometimes, multiple modalities are used on the same lesion. Surgery (by craniotomy, open brain surgery) may be offered based on the risks of treatment as determined by the Spetzler–Martin scale (grade I-V); this score is higher in larger lesions that are close to important brain structures and have deep venous drainage. High grade lesions (IV and V) have an unacceptably high risk and surgery is not typically offered in those cases. Radiosurgery (using targeted radiation therapy such as by a gamma knife) may be used if the lesion is small but close to vital structures. Finally, embolization may be used on small lesions that have only a single feeding vessel.
Hereditary hemorrhagic telangiectasia | Brain AVMs
The swelling of the individual cells of the brain is the main distinguishing characteristic of cytotoxic edema, as opposed to vasogenic edema, wherein the influx of fluid is typically seen in the interstitial space rather than within the cells themselves. Researchers have proposed that "cellular edema" may be more preferable to the term "cytotoxic edema" given the distinct swelling and lack of consistent "toxic" substance involved. There are several clinical conditions in which cytotoxic edema is present:
Cerebral edema | Cytotoxic
Treatments are focused on the underlying cause of hyponatremia and include When EAH is treated early, complete recovery is expected. In addition to the above treatments, athletes experiencing EAH encephalopathy may also receive high-flow oxygen and a rapid infusion of 100 ml of 3% NaCl to reduce brain edema.
Exercise-associated hyponatremia | Treatment
Currently, the only effective treatment for encephaloceles is reparative surgery, generally performed during infancy. The extent to which it can be corrected depends on the location and size of the encephaloceles; however, large protrusions can be removed without causing major disability. Surgery repositions the bulging area back into the skull, removes the protrusions, and corrects the deformities, typically relieving pressure that can delay normal brain development. Occasionally, shunts are placed to drain excess cerebrospinal fluid from the brain. The goals of treatment include:
Encephalocele | Treatment
There are various neuroimaging investigations that may detect cerebral sinus thrombosis. Cerebral edema and venous infarction may be apparent on any modality, but for the detection of the thrombus itself, the most commonly used tests are computed tomography (CT) and magnetic resonance imaging (MRI), both using various types of radiocontrast to perform a venogram and visualise the veins around the brain. Computed tomography, with radiocontrast in the venous phase ("CT venography" or CTV), has a detection rate that in some regards exceeds that of MRI. The test involves injection into a vein (usually in the arm) of a radioopaque substance, and time is allowed for the bloodstream to carry it to the cerebral veins - at which point the scan is performed.
Cerebral venous sinus thrombosis | Imaging
The aim is to maintain intracranial pressures below 25 mm Hg, and cerebral perfusion pressures above 50 mm Hg.
Acute liver failure | Encephalopathy and cerebral edema
As mentioned previously, hypoxia and hypercapnia are potent vasodilators in the cerebral vasculature, leading to increased cerebral blood flow (CBF) and worsening of cerebral edema. Conversely, therapeutic hyperventilation can be used to lower the carbon dioxide content in the blood and reduce ICP through vasoconstriction. The effects of hyperventilation, although effective, are short-lived and once removed, can often lead to a rebound elevation of ICP. Furthermore, overaggressive hyperventilation and vasoconstriction and lead to severe reduction in CBF and cause cerebral ischemia, or strokes. As a result, standard practice is to slowly reverse hyperventilation while more definitive treatments aimed at the primary cause are instituted.
Cerebral edema | Hyperventilation
Then intracellular sodium and osmolarity increase, and there is an influx of water that causes cellular swelling. After the failure of the ATPase pumps, free radicals form and cause damage that complicates the edema. Evidence against cytotoxic edema includes the high levels of hypoxemia (low bloodstream oxygen) needed to cause it.
High-altitude cerebral edema | Cause and mechanism
There are various classification systems for a cerebral infarction, some of which are described below.
Cerebral infarction | Classification
Computed tomography (CT) and MRI scanning will show damaged area in the brain, showing that the symptoms were not caused by a tumor, subdural hematoma or other brain disorder. The blockage will also appear on the angiogram.
Cerebral infarction | Diagnosis
In the treatment of traumatic brain injury (TBI), there are 4 examination methods that have proved useful: skull x-ray, angiography, computed tomography (CT), and magnetic resonance imaging (MRI). The skull x-ray can detect linear fractures, impression fractures (expression fractures) and burst fractures. Angiography is used on rare occasions for TBIs i.e. when there is suspicion of an aneurysm, carotid sinus fistula, traumatic vascular occlusion, and vascular dissection. A CT can detect changes in density between the brain tissue and hemorrhages like subdural and intracerebral hemorrhages. MRIs are not the first choice in emergencies because of the long scanning times and because fractures cannot be detected as well as CT.
Coma | Imaging and testing
Some research focuses on identifying novel targets that prevents formation of cerebral edema. In order to develop strategies that prevent cerebral edema, it's important understand cerebral edema at a molecular level. Targets identified includes: NKCC1, SUR1/ TRPM4 channel, Vasopressin receptor antagonist.
Osmotherapy | Novel targets
Traumatic brain injury: Sedation, ICP monitoring and management, Decompressive Craniectomy, Hyperosmolar therapy and maintain hemodynamic stability. Stroke: Airway management, Maintenance of blood pressure and cerebral perfusion, intravenous fluid management, Temperature control, prophylaxis against seizures, nutrition, ICP management and treatment of medical complications. Subarachnoid hemorrhage: Find the cause of hemorrhage, treat aneurysm or arteriovenous malformation if necessary, monitor for clinical deterioration, manage systemic complications and maintain cerebral perfusion pressure and prevent vasospasm and bridge patient to angiographic clipping. Status epilepticus: Termination of seizures, prevention of seizure recurrence, treatment of cause of seizure, management of complications, monitoring of hemodynamic stability and continuous Electroencephalography(EEG).
Neurointensive care | Common neurointensive care illnesses and treatments
Subdural and epidural hematomas are serious conditions and should be immediately diagnosed and treated by a physician. Hematomas may not show the full extent of the problem initially after the head injury, but it may be revealed after comprehensive medical evaluation and diagnostic test. Diagnostic test may include: blood test, x-ray, computed tomography scan (CT/CAT scan), electroencephalogram (EEG), and magnetic resonance imaging (MRI). The two most important diagnostic tests are the CT scan and the MRI. The CT scan reveals evidence of blood within the skull, fractures, and signs of compression on the brain from the hematoma. The MRI is a more thorough evaluation of injuries to the brain tissue.
Sports-related traumatic brain injury | Diagnosis in sports
High-altitude cerebral edema (HACE) is a medical condition in which the brain swells with fluid because of the physiological effects of traveling to a high altitude. It generally appears in patients who have acute mountain sickness and involves disorientation, lethargy, and nausea among other symptoms. It occurs when the body fails to acclimatize while ascending to a high altitude. It appears to be a vasogenic edema (fluid penetration of the blood–brain barrier), although cytotoxic edema (cellular retention of fluids) may play a role as well. Individuals with the condition must immediately descend to a lower altitude or coma and death can occur.
High-altitude cerebral edema | Introduction
Elevated blood glucose levels, known as hyperglycemia, can exacerbate brain injury and cerebral edema and has been associated with worse clinical outcomes in persons affected by traumatic brain injuries, subarachnoid hemorrhages, and ischemic strokes.
Cerebral edema | Hyperglycemia
This is shown by cases of cerebral metastases where the initial complaint was of a mass in the breast.
Neurological examination | Patient's history
Glucocorticoids, such as dexamethasone, have been shown to decrease tight-junction permeability and stabilize the blood-brain barrier. Their main use has been in the management of vasogenic cerebral edema associated with brain tumors, brain irradiation, and surgical manipulation. Glucocorticoids have not been shown to have any benefit in ischemic stroke and have been found to be harmful in traumatic brain injury. Due to the negative side effects (such as peptic ulcers, hyperglycemia, and impairment of wound healing), steroid use should be restricted to cases where they are absolutely indicated.
Cerebral edema | Glucocorticoids
Cerebral hyperperfusion syndrome is a dysregulated state of cerebral blood flow following the restoration of arterial blood flow to the brain, usually following treatment of carotid artery stenosis. Risk factors include hypertension, particularly high blood pressures in the first few days following revascularization, and bilateral stenosis. The first symptom is usually severe headache, and a headache in the setting of recent carotid endarterectomy or carotid stenting should prompt a return to the hospital and close attention by clinicians. Symptoms may progress to seizures and coma in severe cases. Treatment is control of the blood pressure, often with continuous intravenous antihypertensives medicines in the intensive care setting.
Cerebral hyperperfusion syndrome | Introduction
Dexamethasone (a potent glucocorticoid) in doses of 16 mg/day may reduce edema around the lesion and protect the cord from injury. It may be given orally or intravenously for this indication. Surgery is indicated in localised compression as long as there is some hope of regaining function. It is also occasionally indicated in patients with little hope of regaining function but with uncontrolled pain. Postoperative radiation is delivered within 2–3 weeks of surgical decompression. Emergency radiation therapy (usually 20 grays in 5 fractions, 30 grays in 10 fractions or 8 grays in 1 fraction) is the mainstay of treatment for malignant spinal cord compression.
Spinal cord compression | Treatment and prognosis