notes by dr Claudio Italiano
Putting aside the many crap that are heard in TV commercials, where we talk about water
retention and a thousand other crimes, to those of us who did not happen,
instead, to run into a patient who really has fluid retention and peripheral
edema , what to understand with your feet and swollen legs, that breathes badly?
The appearance of peripheral edema indicates the accumulation of interstitial
fluid.
The mechanisms that determine it are multiple.
In the normal subject, the volume of the interstitial fluid, that is, the volume contained in the spaces between the cells, is regulated by forces that promote the passage of liquids in the interstitium, and others that tend to reabsorb excess fluid. An alteration of the balance can give rise to peripheral edema.
Substantially they can be traced back to the intimate mechanisms that regulate the perfusion of interstitial fluids in the periphery and which also cause the reabsorption, due to substances that, so to speak, magnetize the liquids towards the inside of the lumen, to the venous pole.
The causes of peripheral edema are:
1) increase of the capillary hydrostatic pressure, that is, increases the
arterial pressure or an obstacle to the venous outflow.
2) Difficulty of lymphatic drainage (for example in tumors that infiltrate the
lymphatic pathways)
3) Reduction of colloid-osmotic plasma presion due to hypoproteinemia. In fact,
proteins of plasma, albumin and hemoglobin contained in red blood cells exert a
kind of "action magnet" for water, bringing liquids back to the bloodstream.
a) Congestive heart failure
because myocardial pump deficiency is shock, ie the
body understands that the low flow rate and the low pressure are due to loss of
volemia, i.e. circulating fluid, and activates the sodium-retention mechanism.
This happens mainly because the filtration rate of the glomerule is reduced, the
renin-angiotensin-aldosterone system is stimulated and the neurohypophysis with
increased sodium and water retention and edema appear. If you do not intervene
immediately with diuretic therapy of the loop and antialdosterone, in short the
patient, in the most severe forms of decompensation, it goes to dyspnoea and
respiratory insufficiency.
b) patient with cirrhosis.
The patient with cirrhosis presents a whole series of edemigenous factors that have been the result of study and research and for
which there are still no news of extreme certainty. What is certain is that in
the cirrhotic there is a subversion of the entero-hepatic circle with an
increase in the pressure of the portal system due to the altered histology of
the hepatic microcirculation, which, as we know, is mainly represented by the
portal circle and its branches. the hepatic artery contributes only partially to
this circle. The obstacle to blood flow through the hepatic filter is
responsible, as it were, for a chronic oozing of the liquid that collects in the
abdominal cavity. Also in this case, the low volemia, ie the lack of circulating
liquids, is responsible for the activation of the renin-angiotensin-aldosterone
system, with sodium and water retention, also due to the increase in ADH. The
treatment of the hepatopatient becomes very difficult, since the hepatologist is
fought by the right dosage of loop diuretic therapy, by the anti-ddosterones, by
the low arterial pressure, by the hypoalbuminemia. These are all factors that
hinder the treatment that sometimes, if you exaggerate with the dosage of loop
diuretics, leads to portosystemic encephalopathy.
c) nephropathy with nephrotic syndrome and glomerulonephritis.
The patient may have fever, malaise and headache, hypertension and haematuria, proteinuria as signs of damage to the glomerular filter of the kidney. This results in a reduction in the glomerular filtration rate with sodium retention.
The patient
will be edematous, first in the face and periorbital, then the edema will go to
the lower limbs and, finally, will be generalized as anasarca state with pleural
effusions and therefore pericardial and even accumulation in the abdominal
cavity (hydrothorax and ascites)
d) states of anemia
e) m. thromboembolic and tromflebite or peripheral venous insufficiency
f) in traumas, fractures and burns due to damage to the microcirculation and
lymphatic circuit
g) under conditions of surgical lymphoedema, for example after demolition surgery
h) iatrogenic edema from drugs, for example estrogen, testosterone, corticosteroids, etc.
i) conditions of hypothyroidism with mixedema, ie hard edema not improntabile,
therefore without the sign of the fovea.
j) Severe hypertension, although it is rare for severe hypertension to cause
peripheral edema
k) menstrual cycle with water retention near menstruation and mammary edema
l) states of hypoalbuminemia, for example in the cirrhotic and in the
nephropathy that loses albumine with the glomerular filter.
In this case the colloid-osmotic pressure exerted by the albumin is reduced and, therefore, the liquids are not recalled in the circle. With similar mechanisms as described, hypovolaemia ultimately causes sodium and water retention, aggravating the state of edema.