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Cerebral Edema
Other namesBrain Edema [1]

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General measures for managing cerebral edema

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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.[1] As cerebral edema is linked to increased intracranial pressure (ICP), many of the therapies will focus on ICP.[1]

Positioning

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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.[1] 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.[1]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.[1]

Ventilation and oxygenation

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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.[1] It is recommended that persons with decreased levels of consciousness be intubated for airway protection and maintenance of oxygen and carbon dioxide levels.[1] However, the laryngeal instrumentation involved in the intubation process is associated with a acute, brief rise in intracranial pressure.[2] 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).[2] Intravenous lidocaine prior to RSI has been suggested to reduce the rise in ICP but there is no supporting data at this time.[2]

Additionally, ventilation with use of positive pressure (PEEP) can improve oxygenation with the deleterious effect of decreasing cerebral venous drainage and increasing intracranial pressure (ICP), and thus, must be used with caution.[1]

Fluid management and cerebral perfusion

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Maintenance of cerebral perfusion pressure using appropriate fluid management is essential in patients with brain injury.[1] Dehydration, or intravascular volume loss, and the use of hypotonic fluids, such as D5W or half normal saline, should be avoided.[1][3] Blood serum ion concentration, or osmolality, should be maintained in the normo to hyperosmolar range.[1] Judicial use of hypertonic saline can be used to increase serum osmolality and decrease cerebral edema, as discussed below.[1]

Blood pressure should be sufficient so as to sustain cerebral perfusion pressures greater than 60 mm Hg for optimal blood blow to the brain.[1] Vasopressors may be used to achieve adequate blood pressures with minimal risk of increasing intracranial pressures.[1] However, sharp rises in blood pressure should be avoided.[1] Maximum blood pressures tolerated are variable and controversial depending on the clinical situation.[1][4]

Seizure prophylaxis

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Seizures, including subclinical seizure activity, can complicate clinical courses and increase progression of brain herniation in persons with cerebral edema and increased intracranial pressure.[1][5] Anticonvulsants can be used to treat seizures caused by acute brain injuries from a variety of origins.[1] However, there are no clear guidelines on the use of anticonvulsants for prophylactic use.[1] 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.[1]

Fever

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Fever has been demonstrated to increase metabolism and oxygen demand in the brain.[1] The increased metabolic demand results in an increase in cerebral blood flow and can increase the intracranial pressure within the skull.[6] Therefore, maintaining a stable body temperature within the normal range is strongly recommended.[1] This can be achieved through the use of antipyretics such as acetaminophen (paracetamol) and cooling the body, as described below.[1]

Hyperglycemia

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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.[1]

Sedation

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Pain and agitation can worsen cerebral edema, acutely increase intracranial pressure (ICP), and should be controlled.[1] Careful use of pain medication such as morphine or fentanyl can be used for analgesia.[1] For those persons with decreased levels of consciousness, sedation is necessary for endotracheal intubation and maintenance of a secure airway.[1] Sedative medication used in the intubation process, specifically propofol, have been shown to control ICP, decrease cerebral metabolic demand, and have antiseizure properties.[1] Due to a short half-life, propofol, is a quick-acting medication thats administration and removal is well tolerated, with hypotension being the limiting factor in its continued use.[1] 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.[1][7] Depolarizing neuromuscular blocking agents, most notably succinylcholine, can worsen increased ICP due to induction of muscle contraction within the body.[1]

Nutrition

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Nutrtional support is necessary in all patients with acute brain injury.[1] Enteral feeding, or through mouth via tube, is the preferred method, unless contraindicated.[1] 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.[1]

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.[4] Maintaining a normal blood glucose level of less than 180 mg/dL is suggested.[4] However, tight glycemic control of blood glucose under 126 mg/dL is associated with worsening of stroke size.[4]

Specific Measures

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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.[8] The management of individual diseases are discussed separately.

The following interventions are more specific treatments for managing cerebral edema and increased ICP

Osmotic Therapy

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The goal of osmotic therapy is to create a higher concentration of ions within the vasculature at the blood-brain barrier.[1] 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.[1] An ideal osmotic agent produces a favorable osmotic pressure gradient, is nontoxic, and is not filtered out by the blood-brain barrier.[1] 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.[1][9][10][11]

  • Hypertonic saline is a highly concentrated solution of sodium chloride in water and is administered intravenously.[1] It has a rapid-onset, with reduction of pressures within 5 minutes of infusion, lasting up to 12 hours in some cases, and with negligible rebound pressure.[12] The exact volume and concentration of the hypertonic saline varies between clinical studies.[1][12][13] Bolus doses, particularly at higher concentrations, for example 23.4%, are effective at reducing ICP and improving cerebral perfusion pressure.[12][14] In traumatic brain injuries, a responsiveness to hypertonic saline lasting greater than 2 hours was associated with decreased chance of death and improved neurologic outcomes.[12] The effects of hypertonic saline can be prolonged with combination to agents such as dextran or hydroxyethyl starch, although their use is currently controversial.[12] When compared to mannitol, hypertonic saline has been shown to be as effective as mannitol in decreased ICP in neurocritical care and is more effective in many cases.[12] Hypertonic saline may be preferable to mannitol in persons with hypovolemia or hyponatremia.[12]
  • Mannitol is an alcohol derivative of simple sugar mannose, and is historically the most commonly used osmotic diuretic.[1] Mannitol acts as an inert solute in the blood, decreasing ICP through osmosis as discussed above.[12] Additionally, mannitol decreases ICP and increased cerebral perfusion pressure by increasing reabsorption of cerebrospinal fluid, dilutes and decreased the viscosity of the blood, and can cause cerebral vasoconstriction.[12] Furthermore, mannitol acts in a dose-dependent manner and will not lower ICP if it is not elevated.[12] However, the common limitation of the use of mannitol is its tendency to cause low blood pressure hypotension.[12] Compared to hypertonic saline, mannitol may be more effective at increasing cerebral perfusion pressures and may be preferable in those with hypoperfusion.[12]
  • Loop diuretics, commonly furosemide, act within kidney to increase excretion of water and solutes.[1] Combination with mannitol produces a profound diuresis and increases the risk of systemic dehydration and hypotension.[1] Their use remains controversial.[1]
  • Acetazolamide, a carbonic anhydrase inhibitor, acts as a weak diuretic and modulates CSF production but has not role in the management of cerebral edema from acute brain injuries.[1] It can be used in the outpatient management of cerebral edema caused by idiopathic intracranial hypertension (pseudotumor cerebrii).[1]

Glucocorticoids

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Glucocorticoids, such as dexamethasone, have been shown to decrease tight-junction permeability and stabilize the blood-brain barrier.[1] Their main use has been in the management of vasogenic cerebral edema associated with brain tumors, brain irradiation, and surgical manipulation.[1][11][15] Glucocorticoids have not been shown to have any benefit in ischemic stroke and have been found to be harmful in traumatic brain injury.[1] 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.[1]

Hyperventilation

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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.[1] Conversely, therapeutic hyperventilation can be used to lower the carbon dioxide content in the blood and reduce ICP through vasoconstriction.[1] The effects of hyperventilation, although effective, are short-lived and once removed, can often lead to a rebound elevation of ICP.[1] Furthermore, overaggressive hyperventilation and vasoconstriction and lead to severe reduction in CBF and cause cerebral ischemia, or strokes.[1] As a result, standard practice is to slowly reverse hyperventilation while more definitive treatments aimed at the primary cause are instituted.[1]

It is important to note that prolonged hyperventilation in those with traumatic brain injuries has been shown to worsen outcomes.[1]

Barbiturates

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Induction of a coma via the use of barbiturates, most notably pentobarbital and thiopental, after brain injury is used for secondary treatment of refractory ICP.[12] Yet their use is not without controversy and it is not clear whether barbiturates are favored over surgical decompression.[1] In patients with traumatic brain injuries, babiturates are effective in reducing ICP but have failed to show benefit to clinical outcomes.[1] Evidence is limited for their use in cerebral disease that include tumor, intracranial hypertension, and ischemic stroke.[1] There are several adverse effects of barbiturates that limit their use, such as lowering of systemic blood pressure and cerebral perfusion pressure, cardiodepression, immunosuppression, and systemic hypothermia.[1]

Hypothermia

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As discussed previously in the treatment of fever, temperature control has been shown to decrease metabolic demand and reduce further ischemic injury.[16] In traumatic brain injury, induced hypothermia may reduce the risks of mortality, poor neurologic outcome in adults.[17] However, outcomes varied greatly depth and duration of hypothermia as well as rewarming procedures.[16][17] In children with traumatic brain injury, there was no benefit to therapeutic hypothermia and increased the risk of mortality and arrhythmia.[18] The adverse effects of hypothermia are serious and require clinical monitoring including increased chance of infection, coagulopathy, and electrolyte derangement.[1] The current consensus is that adverse effects outweigh the benefits and its use restricted to clinical trials and refractory increased ICP to other therapies.[1][4][17]

Surgery

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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.[4][19] 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.[4] This will help to reduce the volume constraints inside of the skull.[4] A decompressive hemicraniectomy is the most commonly used procedure.[4] Multiple randomized clinical trials have shown reduced risk of death with hemicraniectomy compared with medical management.[4][20][21] However, no individual study has shown an improvement in the percentage of survivors with good functional outcomes.[4]

Timing of decompressive craniectomy remains controversial, but is generally suggested that the surgery is best performed before there are clinical signs of brainstem compression.[4] 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.[4]

Outcomes

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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.[1][22][23]

  • Cerebral edema is the cause of death in 5% of all patients with cerebral infarction and mortality after large ischemic strokes with cerebral edema is roughly 20 to 30% despite medical and surgical interventions.[4][24] Cerebral edema usually occurs between the second after fifth day after onset of symptoms.[24] Large territory ischemic strokes can lead to the rapid development of malignant brain edema and increased intracranial pressure.[25] Cerebral edema in the context of a malignant middle cerebral artery (MCA) infarct has a mortality of 50 to 80% if treated conservatively.[24] Individuals with cerebral edema had a worse 3-month functional outcome than those without edema.[24] These effects were more pronounced with increasing extent of cerebral edema and were independent of the size of the infarct.[24]
  • Mild traumatic brain injury (TBI) represents 70 to 90% of all reported head injuries.[23] The presence of brain edema on the initial CT scan of those with traumatic brain injuries is an independent prognostic indicator of in-hospital death.[23] The association of brain edema with increased in hospital risk of death was observed in TBI across all level of severity.[23] Edema in the acute and chronic phases were associated with a worse neurologic and clinical outcome.[23] Children with TBI and cerebral edema have worse clinical outcomes as well.[23]

Epidemiology

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As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined.[26] 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.[26]

  • In one study, cerebral edema was found in 28% of those individuals with thrombolysis-treated ischemic strokes, 10% of which occurred in severe forms.[27] A further study detected cerebral edema in 22.7% of cerebral ischemic strokes.[24] A meta-analysis of current studies showed that 31% of those affected by ischemic strokes developed cerebral edema in 31% of cases.[22]
  • In traumatic brain injuries, cerebral edema occurred in greater than 60% of those with mass lesions, and in 15% of those with initial normal CT scans.[28]

Research

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The current understanding of the pathophysiology of cerebral edema after traumatic brain injury is incomplete.[29] Current treatment therapies aimed at cerebral edema and increased intracranial pressure are effective at reducing intracranial hypertension but have unclear impacts on functional outcomes.[28] Additionally, cerebral and ICP treatments have varied effects on individuals based on differing characteristics like age, gender, type of injury, and genetics.[28] There are innumerable molecular pathways that contribute to cerebral edema, many of which have yet to be discovered.[29] 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.[28][29] At the same time, improvement of radiographic markers, biomarkers, and analysis of clinical monitoring data is essential in treating cerebral edema.[28]

References

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  1. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl Raslan A, Bhardwaj A (2007). "Medical management of cerebral edema". Neurosurgical Focus. 22 (5): E12. doi:10.3171/foc.2007.22.5.13. PMID 17613230.
  2. ^ a b c Robinson, N.; Clancy, M. (November 2001). "In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature". Emergency medicine journal: EMJ. 18 (6): 453–457. doi:10.1136/emj.18.6.453. ISSN 1472-0205. PMC 1725712. PMID 11696494.
  3. ^ Schmoker, J. D.; Shackford, S. R.; Wald, S. L.; Pietropaoli, J. A. (September 1992). "An analysis of the relationship between fluid and sodium administration and intracranial pressure after head injury". The Journal of Trauma. 33 (3): 476–481. doi:10.1097/00005373-199209000-00024. ISSN 0022-5282. PMID 1404521.
  4. ^ a b c d e f g h i j k l m n Wijdicks, Eelco F. M.; Sheth, Kevin N.; Carter, Bob S.; Greer, David M.; Kasner, Scott E.; Kimberly, W. Taylor; Schwab, Stefan; Smith, Eric E.; Tamargo, Rafael J.; Wintermark, Max; American Heart Association Stroke Council (April 2014). "Recommendations for the management of cerebral and cerebellar infarction with swelling: a statement for healthcare professionals from the American Heart Association/American Stroke Association". Stroke. 45 (4): 1222–1238. doi:10.1161/01.str.0000441965.15164.d6. ISSN 1524-4628. PMID 24481970.
  5. ^ Gabor, A. J.; Brooks, A. G.; Scobey, R. P.; Parsons, G. H. (June 1984). "Intracranial pressure during epileptic seizures". Electroencephalography and Clinical Neurophysiology. 57 (6): 497–506. doi:10.1016/0013-4694(84)90085-3. ISSN 0013-4694. PMID 6202480.
  6. ^ Busija, D. W.; Leffler, C. W.; Pourcyrous, M. (August 1988). "Hyperthermia increases cerebral metabolic rate and blood flow in neonatal pigs". The American Journal of Physiology. 255 (2 Pt 2): H343–346. doi:10.1152/ajpheart.1988.255.2.H343. ISSN 0002-9513. PMID 3136668.
  7. ^ Murray, Michael J.; Cowen, Jay; DeBlock, Heidi; Erstad, Brian; Gray, Anthony W.; Tescher, Ann N.; McGee, William T.; Prielipp, Richard C.; Susla, Greg; Jacobi, Judith; Nasraway, Stanley A. (January 2002). "Clinical practice guidelines for sustained neuromuscular blockade in the adult critically ill patient". Critical Care Medicine. 30 (1): 142–156. doi:10.1097/00003246-200201000-00021. ISSN 0090-3493. PMID 11902255.
  8. ^ Koenig, Matthew A. (December 2018). "Cerebral Edema and Elevated Intracranial Pressure". Continuum (Minneapolis, Minn.). 24 (6): 1588–1602. doi:10.1212/CON.0000000000000665. ISSN 1538-6899. PMID 30516597.
  9. ^ Adukauskiene, Dalia; Bivainyte, Asta; Radaviciūte, Edita (2007). "[Cerebral edema and its treatment]". Medicina (Kaunas, Lithuania). 43 (2): 170–176. ISSN 1648-9144. PMID 17329953.
  10. ^ Witherspoon, Briana; Ashby, Nathan E. (June 2017). "The Use of Mannitol and Hypertonic Saline Therapies in Patients with Elevated Intracranial Pressure: A Review of the Evidence". The Nursing Clinics of North America. 52 (2): 249–260. doi:10.1016/j.cnur.2017.01.002. ISSN 1558-1357. PMID 28478873.
  11. ^ a b Leinonen, Ville; Vanninen, Ritva; Rauramaa, Tuomas (2018), "Raised intracranial pressure and brain edema", Handbook of Clinical Neurology, vol. 145, Elsevier, pp. 25–37, doi:10.1016/b978-0-12-802395-2.00004-3, ISBN 978-0-12-802395-2, retrieved 2020-04-06
  12. ^ a b c d e f g h i j k l m Alnemari, Ahmed M.; Krafcik, Brianna M.; Mansour, Tarek R.; Gaudin, Daniel (October 2017). "A Comparison of Pharmacologic Therapeutic Agents Used for the Reduction of Intracranial Pressure After Traumatic Brain Injury". World Neurosurgery. 106: 509–528. doi:10.1016/j.wneu.2017.07.009. ISSN 1878-8769. PMID 28712906.
  13. ^ Thompson, Mary; McIntyre, Lauralyn; Hutton, Brian; Tran, Alexandre; Wolfe, Dianna; Hutchison, Jamie; Fergusson, Dean; Turgeon, Alexis F.; English, Shane W. (August 17, 2018). "Comparison of crystalloid resuscitation fluids for treatment of acute brain injury: a clinical and pre-clinical systematic review and network meta-analysis protocol". Systematic Reviews. 7 (1): 125. doi:10.1186/s13643-018-0790-x. ISSN 2046-4053. PMC 6097326. PMID 30115113.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  14. ^ Lazaridis, Christos; Neyens, Ron; Bodle, Jeffrey; DeSantis, Stacia M. (May 2013). "High-osmolarity saline in neurocritical care: systematic review and meta-analysis". Critical Care Medicine. 41 (5): 1353–1360. doi:10.1097/CCM.0b013e31827ca4b3. ISSN 1530-0293. PMID 23591212.
  15. ^ Simjian, Thomas; Muskens, Ivo S.; Lamba, Nayan; Yunusa, Ismaeel; Wong, Kristine; Veronneau, Raymond; Kronenburg, Annick; Brouwers, H. Bart; Smith, Timothy R.; Mekary, Rania A.; Broekman, Marike L. D. (July 2018). "Dexamethasone Administration and Mortality in Patients with Brain Abscess: A Systematic Review and Meta-Analysis". World Neurosurgery. 115: 257–263. doi:10.1016/j.wneu.2018.04.130. ISSN 1878-8769. PMID 29705232.
  16. ^ a b Madden, Lori Kennedy; DeVon, Holli A. (August 2015). "A Systematic Review of the Effects of Body Temperature on Outcome After Adult Traumatic Brain Injury". The Journal of Neuroscience Nursing: Journal of the American Association of Neuroscience Nurses. 47 (4): 190–203. doi:10.1097/JNN.0000000000000142. ISSN 1945-2810. PMC 4497869. PMID 25951311.
  17. ^ a b c McIntyre, Lauralyn A.; Fergusson, Dean A.; Hébert, Paul C.; Moher, David; Hutchison, James S. (2003-06-11). "Prolonged therapeutic hypothermia after traumatic brain injury in adults: a systematic review". JAMA. 289 (22): 2992–2999. doi:10.1001/jama.289.22.2992. ISSN 1538-3598. PMID 12799408.
  18. ^ Zhang, Bin-Fei; Wang, Jiao; Liu, Zun-Wei; Zhao, Yong-Lin; Li, Dan-Dong; Huang, Ting-Qin; Gu, Hua; Song, Jin-Ning (April 2015). "Meta-analysis of the efficacy and safety of therapeutic hypothermia in children with acute traumatic brain injury". World Neurosurgery. 83 (4): 567–573. doi:10.1016/j.wneu.2014.12.010. ISSN 1878-8769. PMID 25514616.
  19. ^ Jha, Ruchira M.; Kochanek, Patrick M. (November 7, 2018). "A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?". Current Neurology and Neuroscience Reports. 18 (12): 105. doi:10.1007/s11910-018-0912-9. ISSN 1534-6293. PMC 6589108. PMID 30406315.
  20. ^ Hofmeijer, Jeannette; Kappelle, L. Jaap; Algra, Ale; Amelink, G. Johan; van Gijn, Jan; van der Worp, H. Bart; HAMLET investigators (April 2009). "Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial". The Lancet. Neurology. 8 (4): 326–333. doi:10.1016/S1474-4422(09)70047-X. ISSN 1474-4422. PMID 19269254.
  21. ^ Das, Suparna; Mitchell, Patrick; Ross, Nicholas; Whitfield, Peter C. (March 2019). "Decompressive Hemicraniectomy in the Treatment of Malignant Middle Cerebral Artery Infarction: A Meta-Analysis". World Neurosurgery. 123: 8–16. doi:10.1016/j.wneu.2018.11.176. ISSN 1878-8769. PMID 30500591.
  22. ^ a b Wu, Simiao; Yuan, Ruozhen; Wang, Yanan; Wei, Chenchen; Zhang, Shihong; Yang, Xiaoyan; Wu, Bo; Liu, Ming (December 2018). "Early Prediction of Malignant Brain Edema After Ischemic Stroke". Stroke. 49 (12): 2918–2927. doi:10.1161/STROKEAHA.118.022001. ISSN 1524-4628. PMID 30571414.
  23. ^ a b c d e f Tucker, Brian; Aston, Jill; Dines, Megan; Caraman, Elena; Yacyshyn, Marianne; McCarthy, Mary; Olson, James E. (July 2017). "Early Brain Edema is a Predictor of In-Hospital Mortality in Traumatic Brain Injury". The Journal of Emergency Medicine. 53 (1): 18–29. doi:10.1016/j.jemermed.2017.02.010. ISSN 0736-4679. PMID 28343797.
  24. ^ a b c d e f Thorén, Magnus; Azevedo, Elsa; Dawson, Jesse; Egido, Jose A.; Falcou, Anne; Ford, Gary A.; Holmin, Staffan; Mikulik, Robert; Ollikainen, Jyrki; Wahlgren, Nils; Ahmed, Niaz (September 2017). "Predictors for Cerebral Edema in Acute Ischemic Stroke Treated With Intravenous Thrombolysis". Stroke. 48 (9): 2464–2471. doi:10.1161/STROKEAHA.117.018223. ISSN 1524-4628. PMID 28775140.
  25. ^ Brogan, Michael E.; Manno, Edward M. (January 2015). "Treatment of malignant brain edema and increased intracranial pressure after stroke". Current Treatment Options in Neurology. 17 (1): 327. doi:10.1007/s11940-014-0327-0. ISSN 1092-8480. PMID 25398467.
  26. ^ a b Leinonen, Ville; Vanninen, Ritva; Rauramaa, Tuomas (2018), "Raised intracranial pressure and brain edema", Handbook of Clinical Neurology, vol. 145, Elsevier, pp. 25–37, doi:10.1016/b978-0-12-802395-2.00004-3, ISBN 978-0-12-802395-2, retrieved 2020-04-06
  27. ^ Strbian, Daniel; Meretoja, Atte; Putaala, Jukka; Kaste, Markku; Tatlisumak, Turgut; Helsinki Stroke Thrombolysis Registry Group (October 2013). "Cerebral edema in acute ischemic stroke patients treated with intravenous thrombolysis". International Journal of Stroke: Official Journal of the International Stroke Society. 8 (7): 529–534. doi:10.1111/j.1747-4949.2012.00781.x. ISSN 1747-4949. PMID 22405327.
  28. ^ a b c d e Jha, Ruchira M.; Kochanek, Patrick M.; Simard, J. Marc (February 2019). "Pathophysiology and treatment of cerebral edema in traumatic brain injury". Neuropharmacology. 145 (Pt B): 230–246. doi:10.1016/j.neuropharm.2018.08.004. ISSN 1873-7064. PMC 6309515. PMID 30086289.
  29. ^ a b c Jha, Ruchira M.; Kochanek, Patrick M. (2018-11-07). "A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?". Current neurology and neuroscience reports. 18 (12): 105. doi:10.1007/s11910-018-0912-9. ISSN 1528-4042. PMC 6589108. PMID 30406315.
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