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Cellular edema / cellular swelling ???? Rapid correction of chronic hypernatremia Rapid / Acute onset hyponatremia Rapid correction of hypertonic dehydration Rapid correction of chronic hyperglycemia ( D KA) Rapid D ialysis for the 1 st time (renal failure) Na-K pump d ysfunction e.g. due to ischemia (no ATP) Mitochondrial d ysfunction e.g. due to toxins (no ATP)

Normal Cells Blood vessels Cytotoxic (cellular) edema Cells Blood vessels

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Urea distributes rapidly across cell membranes and equilibrates throughout total-body water and is, with one exception, an ineffective osmole. Equilibration of urea across the blood-brain barrier can take several hours and in this circumstance urea may function as a “transiently effective” osmole. If urea is rapidly removed from the ECF with initiation of hemodialysis in a patient with end-stage renal disease, the potential exists for the development of “dialysis disequilibrium syndrome.” As urea concentration falls during hemodialysis; a transient osmotic gradient for water movement into brain is established. This results in brain edema ; (headache, nausea, vomiting, and, in some cases, generalized seizures). Dialysis disequilibrium can be minimized by initiating hemodialysis with low blood flow rates and for short periods of time.

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Increased BBB permeability Capillary BBB Intact Normal Water movement is tightly controlled. Balance t*tween fluid in extracellular and intracellular spaces. Normal ICP 5-15m m Hg BBB Intact Cells in Size Cytotoxic Edema Failure of the NA+/K+ ATPase pump results in loss of ion homeostatis. Na• flcxxls into cells and water follows leading to ællular swelling. No Change in ICP as no in brain volume •t@30 Plasma • protein Fluid No in cell size volume of extracellular space Vasogenic Edema Breakdown Of the BBB the movement of plasma proteins (i.e albumin) into the brain tissue. Water is obligated to follow and accumulates within the extracellular spaæ. t ICP due to in brain volume

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Safety factors prevent edema ???

Tissue glycoproteins (act as tissue sponges)

Glycocalyx Interstitium

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Safety factors prevent edema ???

Tight cell – cell interactions which provide no space for anything to accumulate

nucleus

Intercellular space

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Safety factors prevent edema ???

Residual capacity of lymphatics which can compensate (10 – 50 times potential lymphatic capacity), due to increase interstitial HP if any fluid accumulates in interstitium

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Safety factors prevent edema ???

Continuous wash down of interstitial tissue proteins (through lymphatics) i.e. deproteination of ISF

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Safety factors prevent edema ???

Tissue glycoproteins (act as tissue sponges) Tight cell – cell interactions which provide no space for anything to accumulate Residual capacity of lymphatics which can compensate (10 – 50 times potential lymphatic capacity); The most important safety factor ??? Continuous wash down of interstitial tissue proteins (through lymphatics) i.e. deproteination of ISF

Within limits…..above these limits, edema develops

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Safety factors prevent edema ???

Tissue glycoproteins (act as tissue sponges) Tight cell – cell interactions which provide no space for anything to accumulate Residual capacity of lymphatics which can compensate (10 – 50 times potential lymphatic capacity); The most important safety factor ??? Continuous wash down of interstitial tissue proteins (through lymphatics) i.e. deproteination of ISF

Within limits…..above these limits, edema develops

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ifL]utld soculy nymphatjcc: captUUaoy Élood (D ctrcu)atocty 000 q;jCö aal[s fluÜd

EDEMA to be formed due to increase CHP or decrease COP or increase capillary permeability , or even lymphatic obstruction, excess fluid must be greater than compensatory lymphatic potential capacity