Scene 1

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

Scene 2

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.

Scene 3

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

Scene 4

Tissue glycoproteins  (act as tissue sponges)

Scene 5

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

Scene 6

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

Scene 7

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

Scene 8

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

Scene 9

Scene 10

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

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