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Brain edema
1. Cerebral edema occurs when there is abnormal accumulation of fluid in the brain parenchyma, increasing brain volume and intracranial pressure. 2. It can be caused by traumatic brain injury, stroke, tumors, or other conditions that disrupt the blood-brain barrier. 3. Increased intracranial pressure from cerebral edema can cause neurological deterioration and herniation if not treated. 4. Management involves controlling intracranial pressure, optimizing ventilation and oxygenation, administering osmotherapy agents like mannitol to draw water out of the brain, and in severe cases surgery may be needed.
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Brain edema
- 1. Marwa Elhady Lecturer ofpediatrics Faculty of medicine for girls. Al-Azhar University 2015
- 2. • The brainresides in a relatively rigid cranial vault with the cranial compliance ↓ with age as the skull ossification gradually replace cartilage with bone. Brain 80% CSF 10% Blood 10% • Intracranial dynamics describes the interactions of the contents—brain parenchyma, blood and CSF—within the cranium.
- 3. CPP = MAP- ICP Intracranial pressure Blood perfusion pressure Ischemic necrosis If
- 4. Cerebral blood flow •CBF is generally independent of mean arterial pressure but it is closely regulated by arterial PaCO₂ systemically and locally by regional factors such as release of endothelin and NO.
- 5. Factors affects cerebralblood flow (CBF) • Autoregulation: CBF maintaied inspite of ∆ BP • Acid-base balance of the CSF (co2 is vasodilator) • body/brain temperature: Hyperthermia→ ↑cerebral metabolic demands → cell damage • glucose utilization: Hypoglycemia →cell death • Hypoxemia as in prolonged siezures, HIE • vasoactive mediators (i.e., adenosine, NO)
- 6. Mechanisms of BBBdysfunction 1. Physical disruption by arterial hypertension →direct transmission of pressure to cerebral capillary with transudation of fluid into the extracellular fluid 2. Trauma with bleeding 3. Toxin, inflammation 4. Tumor release of vasoactive and endothelial destructive compounds eg. arachidonic acid, excitatory neurotransmitters, histamine, free radicals; vascular endothelial growth factors which weakens junctions of BBB.
- 7. • Cerebral edemais a life-threatening condition • Brain edema is defined as an abnormal accumulation of fluid within the brain parenchyma, producing a volumetric enlargement of the tissue.
- 8. Mechanism of brainedema • changes in the BBB, blood osmolality, dysregulated blood flow, or ↑ capillary pressure will influence the permeability of BBB → passive diffusion of water, ions, protiens, and other compounds in the brain. • It can be consequence of cerebral trauma, massive cerebral infarction, hemorrhages, abscess, tumor, allergy, sepsis, hypoxia, and other toxic or metabolic disorders.
- 10. 1. Cytotoxic • Permeabilityof the BBB is normal and edema results from a disturbance in ionic homeostasis. • It occurs due to a disruption in cellular metabolism that impairs ATP dependant Na/K pump in the glial cell membrane→cellular influx of Na and water. • Swollen astrocytes of both grey and white matter → loss of normal grey white matter interphase.
- 11. 2- Vasogenic • dueto a breakdown of the tight endothelial junctions → disturb BBB →↑vascular permeability → accumulation of edema fluid in the extracellular spaces • This type of edema is seen in response to trauma, tumors, focal inflammation, and late stages of cerebral ischemia.
- 12. Vasogenic (cont.) • confinedto white matter spares cortical grey matter, and pronounces the grey white matter interphase
- 13. In cytotoxic edema: influxof fluid inside the brain cells In vasogenic edema: influx of fluid into the interstitial space
- 14. involves both corticalgrey & white matter loss of normal grey white matter interphase. confined to white matter, with finger like projections extending in sub cortical white matter. Spares cortical grey matter. Grey white matter interphase is pronounced instead of loss. In vasogenic edema:In cytotoxic edema:
- 15. 3- Interstitial cerebraledema • Result from acute obstructive hydrocephalus. • CSF pushed into extracellular space in extracellular spaces of the preiventricular white matter in hydrocehalous
- 16. 4- Osmotic cerebraledema • Result from dilution of blood (↓ osmolarity) • Normally CSF and brain’s extracellular fluid osmolality is slightly lower than plasma. • If ↓ plasma osmolarity, the brain osmolality will exceed the serum osmolality creating an abnormal pressure gradient result in water influx into the brain causing edema.
- 17. Osmosis and semi-permeablecellular membrane Hypo Os Hyper Os Hypo Os Hyper Os Swelling Shrinkage
- 18. Osmotic cerebral edema(cont.) • Causes include hyponatremia, SIADH, hemodialysis, or rapid reduction of blood glucose in DKA, rapid correction of hypernatremia, infusion of hypotonic solusion.
- 19. 5-Hydrostatic • This formof cerebral edema is seen in acute, malignant hypertension. • It is thought to result from disturbance of the autoregulation of cerebral blood circulation with direct transmission of pressure to cerebral capillary with transudation of fluid into the ECF.
- 20. CYTOTOXIC VASOGENIC INTERSTITIALOSMOTIC HYDROSTATIC Pathophysi ology #cellular metabolism #Na/K pump BBB breakdown CSF leak ↑Osmotic gradient ↑Hydrostatic gradient pathology Cell swelling ↑Capillary permeability hydrocephalus ↑ blood osmolarity hypertension content Water, Na no protein Plasma high protein CSF Low protein Water no protein Water, Na no protein location Gray & white matter White matter Periventricular white matter White matter White matter ECF ↓ ↑ ↑ ↑ ↑ BBB intact disturbed intact intact intact steroid No effect effective No effect No effect No effect diuretics Transient effect Minimal effect Transient effect Minimal effect Transient effect CLASSIFICATION OF CEREBRAL EDEMA
- 21.
- 22. Clinical presentation Manifestationof ↑ICP – Headache – Vomiting – Diplopia,visual loss Cushing triad: Hypertension, Bradycardia, Papilledema Siezure Disturbed conscious level Herniation syndromes Clinical sings of brain edema start to appear when ICP exceed 30mmHg
- 23. • ICP isderived from the volume of brain components and the bony compliance. • ↑ in IC volume can result from swelling, masses, or ↑ in blood and CSF volumes • ↑ICP →↓CPP → brain ischemia • Further ↑ in ICP → cerebral herniation
- 24. cingulate herniation uncal herniation Centralherniation Cerebellar tonsillar herniation Upward cerebellar herniation
- 25. Cerebral edema Pathological increasein the water content of the brain Increased intracranial pressure Neurological deterioration Herniation Death
- 26. Management • Treatment ofcerebral edema is complex • Good prognosis only if the diagnosis and the management decision are timely.
- 27. General Measures for ManagingCerebral Edema 1. Optimizing Head and Neck Positions 2. Ventilation and Oxygenation 3. Maintain Intravascular Volume and Cerebral Perfusion 4. Seizure Prophylaxis 5. Management of Fever and Hyperglycemia 6. Nutritional Support
- 28. Optimizing Head andNeck Positions • 30 ̊elevation of the head in patients is essential for – Aim for decreasing CSF hydrostatic pressure. – But avoiding jugular compression and impedance of venous outflow from the cranium • avoid the use of restricting devices around the neck which may compress internal jugular veins. • Head position elevation may be detrimental in ischemic stroke, because it may compromise perfusion to ischemic tissue at risk.
- 29. Ventilation and Oxygenation •Hypoxia and hypercapnia are potent cerebral vasodilator • Maintaine PaCO2 > 30 mmHg to support adequate CBF or CPP to brain • mainten PaO2 at approximately 100 mmHg • Pt should be intubated in: 1. GCS scores less than or equal to 8 2. Patients with poor upper airway reflexes be intubated for airway protection. 3. Pulmonary disorder eg ARDS, aspiration pnemonia • Avoid high PEEP → # systemic venous return , ↓ COP
- 30. Maintain Intravascular Volumeand Cerebral Perfusion • Maintain CPP level >60 mmHg CPP=MAP-ICP NORMAL CPP= 70 - 90 mm of Hg • If hypertension avoid use of Potent vasodilators eg. Nitroglycerine, Nitroprusside as they may exacerbate cerebral edema via accentuated cerebral hyperemia due to their direct vasodilating effects on cerebral vs.
- 31. Seizure Prophylaxis • Phenobarband phenytoin specially in brain trauma (used for 1-2 weeks) Fever control Fever → ↑O2 consumption so worsen out come
- 32. Maintain blood glucose •Avoid hypoglycemia → brain cell damage • Avoid hyperglycemia →↑ brain injury → worse cerebral edema Nutritional Support • High caloric intake • Unless CI, enteral route is preferred • avoid free water intake →hypoosmolar state and worsen cerebral edema
- 33. Specific Measures for ManagingCerebral Edema 1. Controlled Hyperventilation 2. Osmotherapy 3. Corticosteroid Administration 4. Therapeutic Hypothermia 5. Other Adjunct Therapies
- 34. Osmotherapy • Osmotic therapydraw water out of the brain by an osmotic gradient and help to decrease blood viscosity. • These changes ↓ICP and ↑CBF. • CI of manitol ttt – Acute tubular necrosis, Anuria – Cerebral haemorrhage. – Pulmonary edema, CHF
- 35. • Osmotic diureticsare short-lasting • may be repeated provided plasma osmolarity does not exceed 320mOsm. • The osmotic effect can be prolonged by the use of loop diuretics (Furosemide) after the osmotic agent infusion.
- 36. Corticosteroid Administration • Usedin vasogenic edema • steroids decrease capillaries permeability and, in turn, stabilize the disrupted BBB, promoting the movement of Na+/K+ ions and water through the main endothelial membrane • Glucocorticoids, especially dexamethasone, are the preferred steroidal agents, due to their low mineralocorticoid activity
- 37. • Controlled hypothermia→↓ 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.
- 38. • Extended cerebraledema is treated surgically via a bilateral decompressive craniotomy, which allows the brain to expand as it continues to swell
Editor's Notes
- #3 The brain has high metabolic demands
- #4 If
- #11 In cytotoxic edema, the BBB remains intact.
- #24 The perfusion pressure of the brain (cerebral perfusion pressure [CPP]) is equal to the pressure of blood entering the cranium (mean arterial pressure [MAP]) minus the ICP, in most cases.
- #31 Labetalol Enalaprilate Nicardipine
- #34 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. Prolonged hyperventilation has been shown to result in worse outcomes in patients with TBI Overaggressive hyperventilation may actually result in cerebral ischemia.
- #35 Its long duration of action (4–6 hours) and relative stability in solution have enhanced its use over the years. The extra- osmotic properties of mannitol provide additional beneficial effects in brain injury, Decreases in blood viscosity, Resulting in increases in rCBF and CPP and a resultant cerebral vasoconstriction leading to decreased CBV free radical scavenging Inhibition of apoptosis CI Acute tubular necrosis, Anuria Pulmonary edema; Acute left ventricular failure CHF Cerebral haemorrhage. Prior to the diuresis, this leads to expansion of the extracellular volume and hyponatremia. This effect can complicate heart failure and may produce florid pulmonary edema. Headache, nausea, and vomiting are commonly observed in patients treated with osmotic diuretics.