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Cerebral Edema

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Cerebral Edema

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Cerebral Edema

  2. 2. • Brain tissue, which is composed of 80% water, is separated from the systemic circulation by a complex series of interfaces. • The major site is the endothelial cells that are a component of the neurovascular unit • Cells that form these interfaces have specialized proteins that form tight junctions; some have carrier proteins that shuttle essential molecules, and multiple electrolyte pumps on cell membranes. • Cellular membranes preserve the compartmental structure with water in extracellular and intracellular spaces. INTRODUCTION Bradley’s Neurology in Clinical Practice,6th
  3. 3. THE NEURO-VASCULAR UNIT Bradley’s Neurology in Clinical Practice,6th
  4. 4. Interface Tight-Junction Location Functional Aspects Blood-CSF Choroid plexus cell Active secretion of CSF via ATPase and carbonic anhydrase CSF-blood Arachnoid membrane Arachnoid granulations absorb CSF by one-way valve mechanism Blood-brain Capillary endothelial cell Active transport of ISF via ATPase; increased mitochondria and glucose transporters in capillary endothelial Bradley’s Neurology in Clinical Practice,6th ATPase, Adenosine triphosphatase; CSF, cerebrospinal fluid; ISF, interstitial fluid.
  5. 5. • Brain edema is a common term to describe events related to brain insults. • When shifts in water from one compartment to another occur under pathological conditions, swelling in the various compartments leads to increased intracranial pressure (ICP). • Edema represents a serious, often life threatening consequence of many common brain disorders including stroke, trauma, tumors, and infection. • Cerebral edema is the end result of many neurological diseases. Excess fluid can accumulate in the intracellular or extracellular spaces. Bradley’s Neurology in Clinical Practice,6th
  6. 6. CLASSIFICATION • A convenient (though simplified) classification separates brain edema into Cytotoxic or cellular swelling , and Vasogenic or vascular leakage (Klatzo, 1967). • Another proposed category is Interstitial edema , which represents the accumulation of fluid in interstitial spaces in hydrocephalus (Fishman,1975). Bradley’s Neurology in Clinical Practice,6th
  7. 7. ETIOLOGY Type Cause Cytotoxic Ischemia, trauma, toxins, metabolic diseases Vasogenic Infections, brain tumors, hyperosmolar states, inflammation Interstitial Hydrocephalus with transependymal flow Bradley’s Neurology in Clinical Practice,6th
  8. 8. MOLECULAR CASCADE IN INJURY • Cytotoxic edema, which results from pathological processes that damage cell membranes, constricts the extracellular spaces, constraining movement of fluid between the cells. • Disruption of the BBB leads to vasogenic edema, which expands the extracellular space. Vasogenic edema moves more readily in between the linearly arranged fibers that form the white matter. The gray matter restricts water movement because of the dense nature of the neuropil. • Because of the lack of cell damage in vasogenic edema, once the damage to the blood vessel resolves, there may be a return to normal in the edematous tissue. This is generally not the case in cytotoxic edema, which is due to direct injury to cells. Bradley’s Neurology in Clinical Practice,6th
  9. 9. MOLECULAR CASCADE IN INJURY Bradley’s Neurology in Clinical Practice,6th
  10. 10. CYTOTOXIC EDEMA • Stroke, trauma, and toxins induce cytotoxic edema. After a stroke, brain water increases rapidly owing to energy failure and loss of ATP. Cytotoxic edema is seen between 24 and 72 hours after the stroke, when the danger of brain herniation is greatest. • Damage to the blood vessels, resulting in vasogenic edema, occurs at multiple times after the insult. In brain trauma, there is an early opening of the BBB along with extensive damage to the brain tissue, and a mixture of cytotoxic and vasogenic edema leads to severe brain edema in the early stages after injury. • Greater damage occurs in transient ischemia, because the restoration of blood flow returns oxygen and white blood cells to the region, enhancing the damage. Reperfusion injury particularly damages the capillary, with disruption of the BBB. Bradley’s Neurology in Clinical Practice,6th
  11. 11. VASOGENIC EDEMA • Occurs when there is damage to the capillary and subsequent disruption of the BBB. • Tight junctions in the endothelial cells are the first line of protection. • Protein and blood products enter brain tissue, increasing the oncotic pressure in the brain and exposing brain cells to toxic products from the blood. • Bacterial meningitis initiates an inflammatory response in the meninges caused by the invading organisms and by the secondary release of cytokines and chemokines. The secondary inflammatory response may aggravate the infection. Bradley’s Neurology in Clinical Practice,6th
  12. 12. BLOOD PRESSURE AND OSMOLALITY CHANGES ON BRAIN EDEMA • Cerebral blood pressure is tightly regulated in the waking state to ensure adequate flow to the brain. Loss of autoregulation occurs at both the lower and upper extremes of blood pressure, with resulting syncope and hypertensive encephalitis, respectively. • Rapid elevation of blood pressure causes hypertensive encephalopathy. In experimental animals, hyperemia is present, suggesting that the blood vessels are dilated and have increased permeability, • MRI shows vasogenic edema, primarily in the posterior white matter of the brain, a condition referred to by some as reversible posterior leukoencephalopathy syndrome, Bradley’s Neurology in Clinical Practice,6th
  13. 13. BLOOD PRESSURE AND OSMOLALITY CHANGES ON BRAIN EDEMA • Another cause of cerebral edema is a rapid change in serum osmolality. • Rapid reduction of plasma glucose and sodium puts patients treated for diabetic ketoacidosis at risk for edema secondary to water shifts into the brain. • Cerebral edema is a complication of acute mountain sickness, which in rare circumstances may be life threatening. Cerebral symptoms are prominent, and there is an increase in cerebral blood volume related to the hypoxia. Bradley’s Neurology in Clinical Practice,6th
  14. 14. EDEMA IN VENOUS OCCLUSION AND INTRACEREBRAL HEMORRHAGE • Occlusion of the venous sinuses draining the brain can cause increased ICP and venous hemorrhagic infarction. • Intracerebral hemorrhage (ICH) causes brain edema around the hemorrhagic mass. • This edema is both cytotoxic and vasogenic. • Blood contains coagulation cascade enzymes such as thrombin and plasmin which can damage cells both directly by their toxic effects and indirectly by activation of other proteases. Bradley’s Neurology in Clinical Practice,6th
  15. 15. GENERAL MEASURES FOR MANAGING CEREBRAL EDEMA 1. Optimizing Head and Neck Positions 2. Ventilation and Oxygenation 3. Intravascular Volume and Cerebral Perfusion 4. Seizure Prophylaxis 5. Management of Fever and Hyperglycemia 6. Nutritional Support Neurosurg Focus 22 (5):E12,2007
  16. 16. OPTIMIZING HEAD AND NECK POSITIONS • 30 ̊elevation of the head in patients is essential for 1. avoiding jugular compression and impedance of venous outflow from the cranium 2. for decreasing CSF hydrostatic pressure.. • Head position elevation may be detrimental in ischemic stroke, because it may compromise perfusion to ischemic tissue at risk. Neurosurg Focus 22 (5):E12,2007
  17. 17. VENTILATION AND OXYGENATION • Hypoxia and hypercapnia are potent cerebral vasodilator • Patient should be intubated in: 1. GCS scores less than or equal to 8 2. Patients with poor upper airway reflexes be intubated preemptively for airway protection. 3. Aspiration pneumonitis 4. Pulmonary contusion 5. Acute respiratory distress syndrome. Neurosurg Focus 22 (5):E12,2007
  18. 18. INTRAVASCULAR VOLUME AND CEREBRAL PERFUSION • Maintenance of CPP using adequate fluid management in combination with vasopressors is vital in patients with brain injury • Hypotonic fluids should be avoided at all cost • Euvolemia or mild hypervolemia with the use of isotonic fluids (0.9% saline) should always be maintained through rigorous attention to daily fluid balance, body weight, and serum electrolyte monitoring. Neurosurg Focus 22 (5):E12,2007
  19. 19. TREATING HYPERTENSION • Judicious use of antihypertensives 1. Labetalol 2. Enalapril 3. Nicardipine is recommended for treating systemic hypertension. • Potent vasodilators are to be avoided • Nitroglycerine • Nitroprusside • as they may exacerbate cerebral edema via accentuated cerebral hyperemia and CBV due to their direct vasodilating effects on cerebral vasculature. Neurosurg Focus 22 (5):E12,2007
  20. 20. CONTROLLED HYPERVENTILATION • A decrease in PaCO2 by 10 mmHg produces proportional decreases in CBF resulting in rapid and prompt ICP reduction. • The vasoconstrictive effect of respiratory alkalosis on cerebral arterioles has been shown to last for 10 to 20 hours • Beyond which vascular dilation may result in exacerbation of cerebral edema and rebound elevations in ICP. Neurosurg Focus 22 (5):E12,2007
  21. 21. TREATMENT Cerebral Edema Medical Osmotherapy Diuretics Corticosteroids Hyperventilation Other Agents Surgical
  22. 22. OSMOTHERAPY • The most rapid and effective means of decreasing tissue water and brain bulk. • Decrease ICP and increase cerebral blood flow. • Mannitol is the most popular osmotic agent, MOA is unclear, • IV Mannitol is given in the dosage of 0.25-1.0 g/kg. • Glycerol is another useful agent given in oral doses of 30 ml every 4-6 hour or daily IV 50 g in 500 ml of 2.5% saline solution. Used in a dose of 0.5-1.0 g/kg body weight.
  23. 23. CONTRAINDICATIONS FOR MANNITOL 1. Acute tubular necrosis, 2. Anuria 3. Pulmonary edema; 4. Acute left ventricular failure 5. CHF 6. Cerebral haemorrhage. SIDE EFFECTS: DEHYDRATION, HYPERKALEMIA, AND HYPERNATREMIA Neurosurg Focus 22 (5):E12,2007
  24. 24. THERAPEUTIC BASIS AND GOAL OF OSMOTHERAPY • Fundamental goal of osmotherapy is to create an osmotic gradient to cause egress of water from the brain extracellular (and possibly intracellular) compartment into the vasculature • The goal of using osmotherapy is to maintain a euvolemic or a slightly hypervolemic state. • A serum osmolality in the range of 300 to 320 mOsm/L has traditionally been recommended for patients with acute brain injury Neurosurg Focus 22 (5):E12,2007
  25. 25. HYPERTONIC SALINE • Unique extraosmotic properties of hypertonic saline 1. Modulation of CSF production resorption 2. Accentuation of tissue oxygen delivery. 3. May modulate inflammatory response. 4. Following brain injury that may act together to ameliorate cerebral edema. • FORMULATIONS OF HYPERTONIC SALINE • 2% • 3% NaCl has 513 mEq/L of Na and Cl. • 5% NaCl has 856 mEq/L of Na and Cl. • 7% (1200 mEq/L) and • 7.5% • 10% • 23.4% (approx 4000 mEq/L), Neurosurg Focus 22 (5):E12,2007
  26. 26. DIURETICS • The osmotic effect can be prolonged by the use of loop diuretics (Furosemide) after the osmotic agent infusion. Loop diuretics (Furosemide) can be used as an adjunct. Furosemide (0.7 mg/kg) has been shown to prolong the reversal of blood brain osmotic gradient established with the osmotic agents by preferentially excreting water over solute. Neurosurg Focus 22 (5):E12,2007
  27. 27. CORTICOSTEROIDS • Lower intracranial pressure primarily in vasogenic edema because of their beneficial effect on the blood vessel, • Less effective in cytotoxic edema, and are not recommended in treatment of edema secondary to stroke or haemorrhage. • Inj. Dexamethasone 4-6 mg IM every 4-6 hours. • Management of malignant brain tumours, either primary or secondary, as adjuvant chemotherapy of some CNS tumours and perioperatively in brain surgery Neurosurg Focus 22 (5):E12,2007
  28. 28. OTHER AGENTS • Barbiturates, Procaine derivatives, Indomethacin, Propofol and THAM (Tromethamine), are some other agents which have been tried and used in the past ,not being used routinely in present practice,
  29. 29. PHARMACOLOGICAL COMA -BARBITURATES • Barbiturates lower ICP, principally via a reduction in cerebral metabolic activity, resulting in a coupled reduction in CBF and CBV. • In patients with TBI, barbiturates are effective in reducing ICP but have failed to show evidence of improvement in clinical outcome. • Agents used • Pentobarbital : a barbiturate with an intermediate physiological half life (approximately 20 hours) is the preferred agent • Phenobarbital : which has a much longer half- life (approximately 96 hours) • Thiopental : which has a much shorter half-life (approximately 5 hours) Neurosurg Focus 22 (5):E12,2007
  30. 30. ANALGESIA, SEDATION AND PARALYSIS. • Pain and agitation can worsen cerebral edema and raise ICP significantly, and should always be controlled. • Judicious intravenous doses of • bolus morphine (2–5 mg) • fentanyl (25– 100 mcg) • continuous intravenous infusion of fentanyl (25–200 mcg/hour) can be used for analgesia. • A NEUROMUSCULAR BLOCKADE: • can be used as an adjunct to other measures when controlling refractory ICP. • Nondepolarizing agents should be used, because a depolarizing agent (such as succinylcholine) can cause elevations in ICP due to induction of muscle contraction. Neurosurg Focus 22 (5):E12,2007
  31. 31. THERAPEUTIC HYPOTHERMIA • Hyperthermia is deleterious to brain injury, achieving normothermia is a desirable goal in clinical practice. • External cooling devices • air-circulating cooling blankets • iced gastric lavage • surface ice packs Neurosurg Focus 22 (5):E12,2007
  32. 32. OTHER ADJUNCT THERAPIES • HYPERBARIC OXYGEN: • For the treatment of cerebral edema, based on a clinical trial (100% oxygen at 1.5 atmospheres for 1 hour every 8 hours) that demonstrated enhanced survival in patients with TBI • INDOMETHACIN: • Although the mechanisms are poorly understood, indomethacin treatment has been shown to attenuate increases in ICP in Traumatic Brain Injury and fever prevention Neurosurg Focus 22 (5):E12,2007
  33. 33. SURGERY • Surgical treatment is occasionally recommended for large hemispherical infarcts with edema and life threatening brain-shifts. • Temporary ventriculostomy or craniectomy may prevent deterioration and may be lifesaving. • Decompressive craniectomy in the setting of acute brain swelling from cerebral infarction is a life saving procedure and should be considered in younger patients who have a rapidly deteriorating neurological status. • Severe Hydrocephaus- Ventriculo Peritoneal shunt. Bradley’s Neurology in Clinical Practice,6th
  34. 34. REFERENCES • Bradley’s Neurology in clinical practice 6th Edition • Medical Journal Of Armed Forces Of India • Brain Trauma Foundation Guidelines • Neurosurg Focus 22 (5):E12,2007
  35. 35. THANK YOU
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