---start path.lec.04.22.97---

dr chacko again

yesterday we got up to shock. will discuss shock on friday
today, we'll discuss fluid exchange and edema

see handout for list of important things.

remember, there are arterial and venous sides to the circulation, 
connected by the capillaries and the heart. all of the system is lined by 
endothelium and all the fluid exchange occurs at the capillary end. all 
the fluid that goes out also needs to come back in. we're talking about 
tissue/fluid exchange.

this is occuring all the time. any time the fluid doesn't return to 
venous side, there is accumulation of fluid outside the vasculature, in 
the interstitium. that is what we call "edema"

the fluid is in the intercellular spaces then, and also in the body 
cavities. eg, thorax, pertioneum, pericardial cavity, etc. any time there 
is accumulation of fluid in the interstitium we call it edema. this is 
only a clinical sign. it's not a diagnosis. need to find out what is 
causing the edema, figure otu the pathogenesis and design tx.

when fluid accumulates, where does it go? it stays in interstitium and 
causes separation - eg, if in connective tissue, causes separation of 
fibers; causes separation of cells, etc. if lots of fluid in 
interstitium, there is a lot of edema, we see swelling, and if you press 
it, you can see "pitting". we call this "pitting edema" (in a surprise 
move... :)). if animal has a generalized edema, eg not just in one 
extremity or something, the clinician may use the term "anasarca" which 
means generalized edema. the best way to understand pathogenesis of edema 
is to review knowledge of tissue/fluid exchange. then it is easy to 
understand why this happens.

review major factors regulating fluid exhange:

hydrostatic pressure - arterial and venous
interstitial fluid pressure
plasma colloid oncotic pressure

say you have a hydrostatic pressure of 30 mmHg on arterial end, and 15 
mmHg on venous end. the tissue fluid pressure is about 8 mmHg. so on 
arterial side, effective hydrostatic pressure is about 22 mmHg, and about 
7 mmHg on the venous side.

the plasma oncotic pressure/osmotic pressure, which is due mainly to 
albumin, is about 25 mmHg. tissue fluid oncotic pressure is about 10. so 
effective plasma oncotic pressure is about 15 mmHg - and therefore the 
filtration pressure is about 7 mmHg (22-15). on the venous side, the 
effective absorption pressure is about 15 (oncotic) -7 (hydrostatic) = 8. 
so, any fluid that is filtered OUT is absorbed back in on the venous 
side, and anything that isn't is picked up by lymphatics.

what if something isn't normal? eg, hydrostatic pressure. say that blood 
pressure is increased. we have right heart failure, so heart isn't able 
to pump blood and it's backing up on venous side. this causes hydrostatic 
pressure to increase - say it's now 20 on the venous side, instead of 15. 
now, the effective pressure is 12 instead of 7, and the absorption 
pressure is only 3 instead of 8. so now, fluid will accumulate 
(filtration pressure is 7, absorption only 3...) you will get edema.

ok, so blood backs up on venous side. central vein will be engorged. 
animal will have chronic passive congestion of liver. this will also 
affect edema. 

so - animal w/right heart failure can have edema due to increased 
hydrostatic pressure.

similarly, we can figure out a situation where there is left heart 
failure.
the cardiac output is decreased. there is decreased renal perfusion. 
there is activation of renin/angiotensin system. more aldosterone is 
released. more sodium and water are retained. so in this case, you are 
increasing the total blood volume. this will contribute to hydrostatic 
pressure, causing an increase. again we will see edema.

when edema is caused by heart failure, often called "cardiac edema" - 
doesn't mean there is edema in or on the heart!

the fluid accumulating due to heart failure has low protein - the 
endothelium is intact. the SG is less than 1.004 . this is a transudate 
type fluid. we will also see ascites - fluid in abd cavity. and 
hydropericardium, etc.

edema caused by change in osmotic pressure: reduced plasma protein. can 
be secondary to starvation, parasitism, malabsorption, protein losing 
renal process eg amyloidosis, etc. say plasma oncotic pressure is reduced 
to 20...the filtration pressure goes up to 12 mmHg. then on venous side, 
the absorption pressure drops to 3 mmHg. again we develop edema. can be 
called "parasitic edemA" if secondary to parasite. could be called "renal 
edema" if due to kidney problem. these are both caused by reduced plasma 
oncotic pressure. also "hunger edema"

now...
endothelial lining - let's talk about it.  inflammation can damage 
endothelial lining, and permeability increases, so protein can be lost - 
this will reduce the plasma oncotic pressure. we call this "inflammatory 
edema" and this will produce edema fluid high in protein - sometimes 
fibrinous. this edema fluid is called an exudate since it is high in 
protein. we see this secondary to any inflammation, from toxin, injury, 
venom, bacteria, etc. anything that increases vascular permeability...

important role of lymphatics...
normally all filtered plasma fluid is reabsorbed or taken up by 
lymphatics. sometimes lymphatic is obstructed - by parasite, tumor, etc. 
if lymphatics aren't draining an area, we may see edema. we call this 
lymphedema. this is called lymphedema only because it is due to problem 
with lymphatics. isn't because it is pure lymph accumulating. seen in 
pregnancy in women in legs due to uterus pressing on lymphatics. dogs can 
have congenital lymphedema, where some regional lymph nodes do not 
develop, so as lymphatics pick up fluid, there is a lot of subcutaneous 
edema. actually was very similar to mildroid's dz in people.

grossly edema shows up as swelling, maybe pitting.
but histologically, how does it appear? well. you can't really see it, 
unless edema fluid is proteinaceous eg in alveoli or skin, if we see a 
lot of protein, we can say yes, this is edema. otherwise, we just see 
separation of fibers or cells. 

edema in an organ, eg kidney - might notice tense capsule due to swollen 
kidney - maybe ruptured capsule. if you make cut section, would see 
tissue bulging out. can squeeze out fluid, like from sponge. in lung in 
particular, lung will be very heavy and if you press it, will get 
frothing. froth will ooze out on cut section. also will not float in 
water like it should.

edema fluid puts pressure on nearby cells. this can affect cell function. 
cells may atrophy. in lung, if edema is present for a couple of days, you 
can suffocate and die. if fluid is very minimal, eg pulmonary edema 
present with CHF, and not that extensive, may stay ther eand stimulate 
fibrosis in the lung, so you will get fibrosis occuring in the lung. 
presence of fluid for a long time stimulates fibroblasts to proliferate.

now we'll see slides, and go to lab, and review slides.

slide: a yucky lung. it is dark red/maroon. it is very solid, if you cut 
it lots of blood oozes out. it is a torsion of a lung lobe. the lobe is 
congested. it is a passive hyperemia.

another lung - mottled red/yellow. is heavy and if cut oozes fluid. 
chronic passive congestion of lung. CHF animal.

congestion of liver. when there is more blood in there, organ is 
enlarged. edges are rounded - he said SHARPER yesterday, but he didn't 
mean it. edges will be ROUNDED like with fatty change. when there is 
fibrosis, edges will be sharper, though.

long standing CHF produces hyperemia and a proteinaceous type edema in 
the lung. this is secondary to endothelial damage from longstanding fluid 
accumulation. early stages will have transudate type fluid only. still 
not an inflammatory edema though. 

hemorrhage: can be due to rhexis, diapedesis. can appear as petechia, 
pinpoints; or ecchymosis, larger areas, or purpura - both ecchymosis and 
petechia. hematoma is hemorrhage into tissue. hemothorax and 
hemopericardium are obvious. hemopericardium can cause cardiac tamponade 
- prevents filling of heart during diastole. hemoperitoneum, hemarthrosis 
are obvious.

important things: rate of loss, volume of loss, site of hemorrhage. eg, 
in the brain, is much more serious than in skin.

sometimes when you look at sections it is very difficult to decide what's 
going on. you see a lot of blood, could be hyperemia or hemorrhage. need 
to see if RBCs are in vessels or not. if hemorrhage, will see blood all 
over, in tissue, not just in vessels. in very vascular area can be hard 
to tell. in recent hemorrhage, can still see rbcs, if old, harder to make 
them out. 

when we discuss tissue fluid exchange...we have capillaries that are not 
always OPEN. usually, most of them are closed. they open up when there is 
hyperemia, or if you are using a particular tissue. probably they open up 
in response to vasoactive amines or whatever. but usually, a lot of 
capillaries are closed.
hydrostatic pressure and interstitial fluid osmotic pressure pull fluid 
OUT of vessels, and plasma oncotic pressure and interstitial pressure 
push it in.

look over pictures in handout. friday when we discuss shock etc handout 
will be helpful.

edema: transudate sg 1.012, exudate more than 1.018. just know that 
transudate is very low in protein, exudate high in protein.

ok, we go to lab now :)

 
---end---