Brain edema, cerebral edema or cerebral œdema is an excess accumulation of fluid in the intracellular or extracellular spaces of the brain.
At present, the following types of cerebral edema are differentiated:
The vasogenic edema resulting from an increased permeability of the endothelium of cerebral capillaries to albumin and other plasma proteins
The cytotoxic edema resulting from the exhaustion of the energy potential of cell membranes without damage to the barrier;
The hydrostatic cerebral edema resulting from disturbance of the autoregulation of cerebral blood circulation
The osmotic cerebral edema resulting from dilution of blood; and the interstitial cerebral edema resulting from acute hydrocephalus.
Simard et al. suggest a new theory suggesting that ischaemia-induced capillary dysfunction can be attributed to de novo synthesis of a specific ensemble of proteins that determine osmotic and hydraulic conductivity in Starling's equation, and whose expression is driven by a distinct transcriptional program 1).
The risk of brain swelling after dural opening is high in patients with midline shift undergoing supratentorial tumor surgery. Brain swelling may result in increased intracranial pressure, impeded tumor exposure, and adverse outcomes.
Massive brain swelling may occur in up to 10% of cerebral ischemic strokes 2).
Cerebral edema is a life-threatening condition that develops as a result of an inflammatory reaction. Most frequently, this is the consequence of cerebral trauma, massive cerebral infarction, hemorrhages, abscess, meningitis or encephalitis, tumor, allergy, sepsis, hypoxia, and other toxic or metabolic factors.
The blood–brain barrier (BBB) or the blood–cerebrospinal fluid (CSF) barrier may break down, allowing fluid to accumulate in the brain's extracellular space.
Altered metabolism may cause brain cells to retain water, and dilution of the blood plasma may cause excess water to move into brain cells.
Fast travel to high altitude without proper acclimatization can cause high-altitude cerebral edema (HACE).
Previous studies have shown that female mice have less brain edema and better recovery in neurological deficits after intracerebral hemorrhage (ICH) and that 17β-estradiol treatment in male mice markedly reduces ICH-induced brain edema.
Some authors have reported a rare unexplained complication of sudden death in association with massive cerebral edema immediately after cranioplasty. Sviri reports on 4 patients who underwent cranioplasty after decompressive craniectomy (DC) between January 2005 and August 2010 at his department and died because of massive cerebral edema immediately after uneventful surgery and anesthesia. All 4 of the new cases reported involved young male patients who underwent decompressive hemicraniectomy after traumatic brain injury. They developed massive cerebral swelling immediately after uneventful cranioplasty (3 patients) or after removal of an epidural hematoma several hours after surgery (1 patient). All 4 patients had a large skull defect and significantly sunken craniotomy site, and all were treated with a closed vacuum suction system that was placed under the scalp and kept open at the end of the cranioplasty procedure. After surgery, the patients' pupils became fixed and dilated, and brain CT scans showed massive brain edema. Despite emergency DC, the patients did not recover, and all 4 died. A MEDLINE search showed 8 similar cases that were reported previously. Fatal cerebral swelling after uneventful cranioplasty is a distinct clinical entity, although it is unpredictable. It is postulated that a negative pressure difference from the elimination of atmospheric pressure that had been chronically applied on the injured sinking brain in combination with the negative pressure applied by the closed subgaleal suction drain may lead to a massive brain shift toward the cranioplasty site and initiate a fatal vasomotor reaction 3).
A retrospective chart review was performed on all patients who underwent DBS electrode implantation over a 3-year period. Routine CT imaging on postoperative day (POD) 1 was negative. Patients were identified based on clinical neurological changes, leading to imaging and subsequent diagnosis.
Five of 145 patients (3.4%) presented with new neurological symptoms from POD 1 to 14, which were confirmed by CT imaging to show perilead and/or subcortical edema around 6 of 281 electrodes (2.1%). Four of 5 patients had unilateral edema despite bilateral implantation. Clinical presentations varied widely. Two patients presenting on POD 1 with deteriorating conditions required longer inpatient stays with supportive measures than those presenting later (p = 0.0002). All patients were treated with corticosteroids and returned to baseline by 3 months after surgery.
Acute instances of DBS lead edema may occur as early as POD 1 and can rapidly progress into profound deficits. Treatment with supportive care and corticosteroids is otherwise identical to those cases presenting later 4).
Certain changes in morphology are associated with cerebral edema: the brain becomes soft and smooth and overfills the cranial vault, gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed.
Symptoms include nausea, vomiting, blurred vision, faintness, and in severe cases, seizures and coma. If brain herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory centers in the pons and medulla oblongata.
Since brain edema presents a danger to the patient, treatment of cerebral contusion aims to prevent swelling. Measures to avoid swelling include prevention of hypotension, hyponatremia, and hypercapnia.
The early massive edema caused by severe cerebral contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24-72 h post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration.
Contusions are likely to heal on their own without medical intervention.
Despite decades of research into the pathogenesis of cerebral edema, nonsurgical therapy for brain swelling has advanced very little after more than half a century. Recent advancements in our understanding of molecular water transport have generated interest in new targets for edema therapy.
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Monitoring of the patient's condition in the intensive care unit is a necessity. It is important to ensure proper positioning of the patient–the head should be tilted at 30 degrees in order to optimize the cerebral perfusion pressure and control of the increase in intracranial pressure. Hyperventilation should be applied. Controlled hypothermia decreases the rate of metabolism in the brain. Slightly positive fluid balance should be maintained using crystalloid or colloid (hypertonic-hyperoncotic) solutions, at the same time maintaining cerebral perfusion pressure exceeding 70 mmHg. The treatment includes administration of antihypertensive medications, nonsteroidal antiinflammatory drugs, and barbiturates. Steroids decrease the permeability of capillaries and the hemato-encephalic barrier, promoting the movement of Na(+)/K(+) ions and water through the main endothelial membrane, and therefore they are used in the treatment of vasogenic cerebral edema as well as edema caused by a cerebral tumor. Glutamate and N-methyl-D-aspartate receptor antagonists improve cerebral microcirculation and metabolism. Trometamol corrects cerebral acidosis. Extended cerebral edema is treated surgically via a bilateral decompressive craniotomy, sometimes including craniotomy of lateral and posterior fossae. The treatment of cerebral edema is complex, and positive results may be expected only if the diagnosis and the provision of assistance are timely 5).
Mannitol is recommended as a first-line dehydration treatment to reduce brain edema and enable brain relaxation during neurosurgery. Research has indicated that mannitol enhanced brain relaxation in patients undergoing supratentorial tumor surgery; however, these results need further confirmation, and the optimal mannitol dose has not yet been established. We propose to examine whether different doses of 20% mannitol improve brain relaxation in a dose-dependent manner when administered at the time of incision. We will examine patients with preexisting mass effects and midline shift undergoing elective supratentorial brain tumor surgery.
Evidence suggests low molecular weight heparin reduces brain edema and improves neurological recovery following stroke and traumatic brain injury (TBI), through blunting of cerebral leukocyte (LEU) recruitment. It remains unknown if unfractionated heparin (UFH) similarly affects brain inflammation and neurological recovery post TBI.
Prophylaxis was associated with decreased risk of pulmonary embolism and deep vein thrombosis, but no increase in risk of late neurosurgical intervention or death. Early prophylaxis may be safe and should be the goal for each patient in the context of appropriate risk stratification 7).
Unfractionated heparin (UFH) after TBI reduces LEU recruitment, microvascular permeability and brain edema to injured brain. Lower UFH doses concurrently improve neurological recovery while higher UFH may worsen functional recovery. Further study is needed to determine if this is due to increased bleeding from injured brain with higher UFH doses 8).
Mirroring Enoxaparin (ENX), HMGB1 signaling blockade reduces LEU recruitment, cerebrovascular permeability, and brain edema following TBI. ENX further reduced lung edema indicating a multifaceted effect beyond HMGB1 blockade. Further study is needed to determine how ENX may play a role in blunting HMGB1 signaling in brain injury patients 9).
Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury (TBI) as it increases intracranial pressure, impairs cerebral perfusion pressure and oxygenation, and contributes to additional ischemic injuries.
In this book, leading world authorities on brain edema and neurological disorders/injuries and experts in preconditioning join forces to discuss the latest progress in basic sciences, translational research, and clinical management strategies relating to these conditions. The range of topics covered is wide, including microglia, energy metabolism, trace metals and ion channels, vascular biology, cellular treatment, hemorrhagic stroke, novel technological advances, anesthesia and medical gases, pediatric brain edema, neuroimaging, behavioral assessment, clinical trials, peripheral to central signaling pathways, preconditioning translation, and animal models for preconditioning and brain edema research. The book comprises presentations from Brain Edema 2014, the joint meeting of the 16th International Conference on Brain Edema and Cellular Injury and the 3rd Symposium on Preconditioning for Neurological Disorders, held in Los Angeles on September 27–30, 2014.