Edema is an atypical accumulation of fluid in the ISF leading to tissue swelling and it can be caused by any event that steps up the flow of fluid out of the blood or hinders its return. Therefore, without considering the dehydration and hypotension problems, can a doctor treat a patient with ascites, pleural effusion, or pericardial effusion by merely restricting the salt and water intake ( without therapeutic paracentesis ) ?
can ascites result from excess water intake and reduced water loss?
Yes, removal is indicated when the fluid is too big for the normal resorption process. The usual thing to do is to first try salt restriction with diuretics. Then if no response and if the accumulation big and causing a distress...parasynthesis.
can ascites result from excess water intake and reduced water loss? this question does not seem like very practical. if a patient has reduced water loss usually water intake also decreases. but, serene, if you try to understand the mechanism behind ascites, it is secondary hyperaldostronism due to volume depletion. at the begining reduced plasma proteins and a decrease in plasma oncotic pressure starts ascites in a patient with cirrhsis but after that volume depletion makes the scenario worse by stimulating renin-ang-ald system. please correct me if i'm wrong, it's an interesting discussion
hipp, you are right if we concern the RAA system.
But in this case,we are considering that the patient is developing an ascites as he drinks a lot of water before he sleeps for several days or a patient drinks a lot of water but he has problem in any of the fluid loss mechanisms like passing urine
( as in some diseases ) or sweating (ie, staying in cold places or having some diseases ), will the fluid start accumulating in the peritoneal cavity and start developing an ascites ???
serene, a normal person does not develop ascites because he had lots of water before going to bed. about your other examples could you be more specific?? which disease or condition is that when you say problem with fluid loss mechanism ?
i am not good with diseases but i think there must be some diseases that can cause the problem in passing urine and lead to accummulation of water in the urinary system. Anyway, disease like stones in gallbaldder may occlude the outflow tract of urine, causing the urine production come to a halt as the hydrostatic pressure in the Bowman's capsule is higher than that in glomerular capillaries. hence...
1. fluid accumulated in the blod vessel (from excess water intake)
2. hydrostatic pressure in blood vessel increased
3. increase in tissue perfussion
4. increase in ISF
5. result in edema
6. ascites developed if accumulation takes place in the peritoneal cavity
am i rite ??
Hi serene, your pathogenesis doesn't look correct to me. Urinary obstruction can't result in ascities. Urinary obstruction has a pressure effect which in the long damages the kidney paranchyma. But what type of obstruction are you thinking of: bilateral or unilateral? I can explain each for you!
zuzuethflorida ,
I am just thinking of if the the pathogenesis can be correct ?? :
1. problem in fluid loss ( as in, for instance, obstruction in urinary tract ).
2. accumulation of water in the blood vessels.
3. increase in hydrostatic pressure in the blood vessel.
.
.
.
or
1. obstruction in UI
2. fluid keep accumulating in UI as the production of urine keeps going on
3. UIT bulges
4. UIT bursts
or like what zuzuethflorida said, it will only cause impairment to the kidney
anyway, I would like to hear your explanation for both bilateral and unilateral, zuzuethflorida .
zuzuethflorida ,
thank you very much for your reply as I am quite satisfied with your explanation, but it will be better if someone can tell me what's wrong in my assumptions.
Thanks^^
in ascites there has to be liver cirrhosis. the hypoproteinemia starts the ascites that i know for sure. also the liver is where the hormones of our body get deactivated and so hormones like estrogen and aldosterone do not get inactivated with a resultant rise in their plasma levels. so the secondary hyperaldosteronism is a s a result of the inability of the liver to get rid of it! that causes hypertension ----> increased hydrostatic pressure of the blood and increased filtration into the IS SPACE adding to the ascites. and so it becomes a vicious cycle! thats why ascites is incurable unless the patient gets a liver transplant. the only treatment is asymptomatic with diuretics, reducing salt intake and paracentesis in severe cases.