STUDY - Technical - New Dacian's Medicine
The
Edema (3)
Translation Draft
Idiopathic edema, which occurs almost exclusively in women, is characterized by periodic episodes of edema (not related to the menstrual cycle) frequently accompanied by abdominal distension. Daylight weight alterations occur by orthostatic retention of sodium and water, so that the patient can weigh a few extra pounds after being in the orthostatic position for several hours. Such large diurnal changes in weight suggest an increase in capillary permeability, the severity of which appears to fluctuate and is aggravated by warm weather.
There is evidence that a reduction in plasma volume occurs in those states, with secondary RAA activity and inhibition of impaired AVP release. Idiopathic edema should be particularly cyclic or premenstrual, in which sodium and water retention may be secondary to excessive estrogen stimulation. There are other situations where edema appears to be "diureticly induced".
It has been postulated that in these patients, chronic administration of diuretics leads to a mild deplation of blood volume, which causes chronic hyperthermia and juxtaglomerular hyperplasia. The mechanisms of sodium retention seem to compensate excessively for the direct effects of diuretics. Sudden discontinuation of diuretics can leave sodium retention forces unopposed, leading to fluid retention and edema.
Low dopaminergic activity and reduced urinary excretion of kalikrein and kinin in this situation have been described and may also be of pathogenetic importance. Treatment of cyclic idiopathic edema includes a reduction in salt consumption, rest in clinostatism for several hours a day, wearing elastic socks (which are put in the morning before getting out of bed) and an understanding of any emotional problems.
A variety of pharmacological agents, including ACE inhibitors, progesterone, dopamine receptor agonists (bromocriptine and sympathomimetic amines) dextroamphetamine have been shown to be useful when administered to patients who do not respond to simple measures. Diuretics may initially be useful, but they can lose their effectiveness through continuous use (they should be administered rationally). Discontinuation of diuretics paradoxically leads to diuresis in the "diuretic-induced" edema described above.
From the point of view of differential diagnosis, localized edema can be easily differentiated from generalized edema. The vast majority of patients with generalized edema suffer from advanced heart, kidney, liver or nutritional diseases. Consequently, the differential diagnosis of generalized edema should be directed towards the identification or exclusion of these few causes.
To come as support to differential diagnosis, let's talk a little about several forms of edema, starting with localized edema. Edema resulting from inflammation or hypersensitivity is easy to highlight. Localized edema due to venous or lymphatic obstruction can be caused by thrombophlebitis, chronic lymphangitis, resection of regional lymph nodes, fkeratosis, etc. Lymphedema is usually non-resorbable, because the restriction of lymph flow causes an increased concentration of proteins in the interstitial flow, a circumstance that aggravates fluid retention.
It's the turn of edema from heart failure. The presence of heart disease, manifested by cardiomegaly and galloping rhythm, along with symptoms of heart failure, such as dyspnea, basal crepitating rals, venous distension and hepatomegaly are usually indications provided by the clinical examination that edema results from heart failure. Non-invasive tests, such as echocardiography and radioisotopic angiography, can be helpful in establishing the diagnosis of heart failure.
In the case of edema from nephrotic syndrome, marked proteinuria, severe hypoalbuminemia and, in some situations, hypercholesterolemia are present. This syndrome can occur during kidney diseases including glomerulonephritis, diabetic glomerulosclerosis and hypersensitivity reactions. There may or may not be a history of previous kidney disease.
Let's talk about edema from acute glomerulonephritis and other forms of renal failure. Edema occurring in the acute phase of glomerulonephritis is typically associated with hematuria, proteinuria and hypertension. Although some evidence shows that fluid retention is due to increased capillary permeability, in most cases, edema from this disease results from primary retention of sodium and water by the kidneys due to renal failure.
This condition differs from congestive heart failure in that it is characterized by a normal (or sometimes even increased) cardiac output and arteriovenous difference in normal oxygen. Patients with renal failure edema show signs of pulmonary congestion on chest X-rays before cardiomegaly is observed, but usually do not show ortopnea. Patients with chronic impairment of renal function may also develop edema due to primary sodium and water retention.
Let's move on to the cirrhosis edema. Ascita and clinical and biochemical evidence of liver disease (collateral venous circulation, jaundice, star angiomas), characterize edema of hepatic origin. Ascita is refractory to treatment, because it occurs as a result of the association of lymphatic circulation obstruction, portal hypertension and hypoalbuminemia. Edema can also occur in other regions of the body as a result of hypoalbuminemia. Furthermore, the noticeable accumulation of ascites fluid may increase intraabdominal pressure and prevent venous circulation from the lower extremities, thus favouring the accumulation of fluids in these regions as well.
As for the edema of nutritional origin... High protein deficiencies in the diet over a longer period of time can produce hypoproteinemia and edema. The latter can be intensified by the development of beri-beri heart disease, also of nutritional origin, in which multiple peripheral arteriovenous fistulas, cause the reduction of the effective systemic infusion and the volume of effective arterial blood, thus intensifying the formation of edema.
Fluid build-up can indeed be intensified when these patients initially receive a proper diet. An increased intake of food can increase the amount of salt ingested, which is then retained along with water. The so-called "refueling oedema" may also be related to the discharge of insulin which directly increases tubular sodium rearbsorption. In addition to hypoalbuminemia, hypopotasemia and caloric deficiency can be prevented in the edema of inaniation.
Other causes of edema include hypothyroidism, in which edema (mixedema) can be typically located in the pretibial region and which may also be associated with periorbital swelling. Exogenous hyperadrenocorticism, pregnancy and administration of estrogens and vasodilators, in particular calcium antagonist, nifedipine, may also cause edema.
The distribution of edema is an important guide to finding out the cause. Thus, edema of a lower limb or one or both arms is generally the result of venous and/ or lymphatic obstruction. Edema resulting from hypoproteinemia is characteristically generalized, but it is especially evident in the soft tissues of the eyelids and face and tends to be more pronounced in the morning because of nighttime clinostatism. Uncommon causes for facial edema include trichinosis, allergic reactions and mixedema.
Edema associated with heart failure, on the other hand, tends to be more pronounced in the lower limbs and more pronounced in the evening, a characteristic also determined in large part by posture. When patients with heart failure lie in bed, edema may be more pronounced in the pressed region. Unilateral edema occasionally results from damage to the central nervous system, affecting vasomotor fibers on one side of the body, with paralysis also reducing venous and lymphatic drainage on the affected side.
Other significant clues for the orientation of the diagnosis are the color, consistency and sensitivity of the skin. Local cyanosis may be significant for venous obstruction. in an individual who has repeated episodes of prolonged edema, the skin can be thickened, endured and often reddish. Measuring or estimating venous pressure is important to assess edema. Its increases in an isolated part of the body generally reflect the presence of venous obstruction.
Generalized increase in systemic venous pressure indicates the presence of congestive heart failure. Typically, significant increase in venous pressure can be recognized after the level at which cervical vein collapse occurs. In patients with upper vena vein obstructions, edema is localized in the face, neck and upper limbs, where venous pressure is increased compared to the lower limbs.
Measuring venous pressure in the upper limbs is also useful in patients with massive edema of the lower limbs and ascites, it is increased when edema has cardiac origin (e.g. constrictive pericarditis or tricuspid stenosis), but is normal when it is secondary to cirrhosis. Severe heart failure can cause ascites, which can be differentiated from ascites from cirrhosis of the liver by jugular venous pressure, which is generally increased in heart failure and normal in cirrhosis.
Determining serum albumin concentration is particularly important for identifying those patients whose edema is due, at least in part, to the decrease in intravascular colloid-oncotic pressure. The presence of proteinuria also provides useful data. The total absence of proteins in the urine is proof that kidney disease is not the cause of edema. Reduced to moderate proteinuria usually occurs in patients with heart failure, as massive and persistent proteinuria is a characteristic of nephrotic syndrome.
I will complete this post with some elements about the patient's approach. An important first question is whether edema is localized or generalized. if it's located, we'll focus on those phenomena that may be responsible. Localized edema includes hydrothorax and ascites. Each may be the consequence of local venous or lymphatic obstruction, as in an inflammatory or neoplastic disease.
If edema is generalized, it must first be determined whether hypoalbuminemia is significant, i.e. the concentration of serum albumins is below 2,5 g/dl. if so, history, physical examination, urine tests and other laboratory data will help assess the diagnosis of cirrhosis, severe malnutrition, gastroenteropathy with loss of protein or nephrotic syndrome, as the underlying disease. If hypoalbuminemia is not present, the existence of signals of severe congestive heart failure leading to edema should be sought. Finally, it should be seen whether the patient has an adequate diuresis, or if significant oliguria or even anuria is present.
On May 26th we'll start the shock posts... Don't forget that I only started posting in the odd days!
Idiopathic edema, which occurs almost exclusively in women, is characterized by periodic episodes of edema (not related to the menstrual cycle) frequently accompanied by abdominal distension. Daylight weight alterations occur by orthostatic retention of sodium and water, so that the patient can weigh a few extra pounds after being in the orthostatic position for several hours. Such large diurnal changes in weight suggest an increase in capillary permeability, the severity of which appears to fluctuate and is aggravated by warm weather.
There is evidence that a reduction in plasma volume occurs in those states, with secondary RAA activity and inhibition of impaired AVP release. Idiopathic edema should be particularly cyclic or premenstrual, in which sodium and water retention may be secondary to excessive estrogen stimulation. There are other situations where edema appears to be "diureticly induced".
It has been postulated that in these patients, chronic administration of diuretics leads to a mild deplation of blood volume, which causes chronic hyperthermia and juxtaglomerular hyperplasia. The mechanisms of sodium retention seem to compensate excessively for the direct effects of diuretics. Sudden discontinuation of diuretics can leave sodium retention forces unopposed, leading to fluid retention and edema.
Low dopaminergic activity and reduced urinary excretion of kalikrein and kinin in this situation have been described and may also be of pathogenetic importance. Treatment of cyclic idiopathic edema includes a reduction in salt consumption, rest in clinostatism for several hours a day, wearing elastic socks (which are put in the morning before getting out of bed) and an understanding of any emotional problems.
A variety of pharmacological agents, including ACE inhibitors, progesterone, dopamine receptor agonists (bromocriptine and sympathomimetic amines) dextroamphetamine have been shown to be useful when administered to patients who do not respond to simple measures. Diuretics may initially be useful, but they can lose their effectiveness through continuous use (they should be administered rationally). Discontinuation of diuretics paradoxically leads to diuresis in the "diuretic-induced" edema described above.
From the point of view of differential diagnosis, localized edema can be easily differentiated from generalized edema. The vast majority of patients with generalized edema suffer from advanced heart, kidney, liver or nutritional diseases. Consequently, the differential diagnosis of generalized edema should be directed towards the identification or exclusion of these few causes.
To come as support to differential diagnosis, let's talk a little about several forms of edema, starting with localized edema. Edema resulting from inflammation or hypersensitivity is easy to highlight. Localized edema due to venous or lymphatic obstruction can be caused by thrombophlebitis, chronic lymphangitis, resection of regional lymph nodes, fkeratosis, etc. Lymphedema is usually non-resorbable, because the restriction of lymph flow causes an increased concentration of proteins in the interstitial flow, a circumstance that aggravates fluid retention.
It's the turn of edema from heart failure. The presence of heart disease, manifested by cardiomegaly and galloping rhythm, along with symptoms of heart failure, such as dyspnea, basal crepitating rals, venous distension and hepatomegaly are usually indications provided by the clinical examination that edema results from heart failure. Non-invasive tests, such as echocardiography and radioisotopic angiography, can be helpful in establishing the diagnosis of heart failure.
In the case of edema from nephrotic syndrome, marked proteinuria, severe hypoalbuminemia and, in some situations, hypercholesterolemia are present. This syndrome can occur during kidney diseases including glomerulonephritis, diabetic glomerulosclerosis and hypersensitivity reactions. There may or may not be a history of previous kidney disease.
Let's talk about edema from acute glomerulonephritis and other forms of renal failure. Edema occurring in the acute phase of glomerulonephritis is typically associated with hematuria, proteinuria and hypertension. Although some evidence shows that fluid retention is due to increased capillary permeability, in most cases, edema from this disease results from primary retention of sodium and water by the kidneys due to renal failure.
This condition differs from congestive heart failure in that it is characterized by a normal (or sometimes even increased) cardiac output and arteriovenous difference in normal oxygen. Patients with renal failure edema show signs of pulmonary congestion on chest X-rays before cardiomegaly is observed, but usually do not show ortopnea. Patients with chronic impairment of renal function may also develop edema due to primary sodium and water retention.
Let's move on to the cirrhosis edema. Ascita and clinical and biochemical evidence of liver disease (collateral venous circulation, jaundice, star angiomas), characterize edema of hepatic origin. Ascita is refractory to treatment, because it occurs as a result of the association of lymphatic circulation obstruction, portal hypertension and hypoalbuminemia. Edema can also occur in other regions of the body as a result of hypoalbuminemia. Furthermore, the noticeable accumulation of ascites fluid may increase intraabdominal pressure and prevent venous circulation from the lower extremities, thus favouring the accumulation of fluids in these regions as well.
As for the edema of nutritional origin... High protein deficiencies in the diet over a longer period of time can produce hypoproteinemia and edema. The latter can be intensified by the development of beri-beri heart disease, also of nutritional origin, in which multiple peripheral arteriovenous fistulas, cause the reduction of the effective systemic infusion and the volume of effective arterial blood, thus intensifying the formation of edema.
Fluid build-up can indeed be intensified when these patients initially receive a proper diet. An increased intake of food can increase the amount of salt ingested, which is then retained along with water. The so-called "refueling oedema" may also be related to the discharge of insulin which directly increases tubular sodium rearbsorption. In addition to hypoalbuminemia, hypopotasemia and caloric deficiency can be prevented in the edema of inaniation.
Other causes of edema include hypothyroidism, in which edema (mixedema) can be typically located in the pretibial region and which may also be associated with periorbital swelling. Exogenous hyperadrenocorticism, pregnancy and administration of estrogens and vasodilators, in particular calcium antagonist, nifedipine, may also cause edema.
The distribution of edema is an important guide to finding out the cause. Thus, edema of a lower limb or one or both arms is generally the result of venous and/ or lymphatic obstruction. Edema resulting from hypoproteinemia is characteristically generalized, but it is especially evident in the soft tissues of the eyelids and face and tends to be more pronounced in the morning because of nighttime clinostatism. Uncommon causes for facial edema include trichinosis, allergic reactions and mixedema.
Edema associated with heart failure, on the other hand, tends to be more pronounced in the lower limbs and more pronounced in the evening, a characteristic also determined in large part by posture. When patients with heart failure lie in bed, edema may be more pronounced in the pressed region. Unilateral edema occasionally results from damage to the central nervous system, affecting vasomotor fibers on one side of the body, with paralysis also reducing venous and lymphatic drainage on the affected side.
Other significant clues for the orientation of the diagnosis are the color, consistency and sensitivity of the skin. Local cyanosis may be significant for venous obstruction. in an individual who has repeated episodes of prolonged edema, the skin can be thickened, endured and often reddish. Measuring or estimating venous pressure is important to assess edema. Its increases in an isolated part of the body generally reflect the presence of venous obstruction.
Generalized increase in systemic venous pressure indicates the presence of congestive heart failure. Typically, significant increase in venous pressure can be recognized after the level at which cervical vein collapse occurs. In patients with upper vena vein obstructions, edema is localized in the face, neck and upper limbs, where venous pressure is increased compared to the lower limbs.
Measuring venous pressure in the upper limbs is also useful in patients with massive edema of the lower limbs and ascites, it is increased when edema has cardiac origin (e.g. constrictive pericarditis or tricuspid stenosis), but is normal when it is secondary to cirrhosis. Severe heart failure can cause ascites, which can be differentiated from ascites from cirrhosis of the liver by jugular venous pressure, which is generally increased in heart failure and normal in cirrhosis.
Determining serum albumin concentration is particularly important for identifying those patients whose edema is due, at least in part, to the decrease in intravascular colloid-oncotic pressure. The presence of proteinuria also provides useful data. The total absence of proteins in the urine is proof that kidney disease is not the cause of edema. Reduced to moderate proteinuria usually occurs in patients with heart failure, as massive and persistent proteinuria is a characteristic of nephrotic syndrome.
I will complete this post with some elements about the patient's approach. An important first question is whether edema is localized or generalized. if it's located, we'll focus on those phenomena that may be responsible. Localized edema includes hydrothorax and ascites. Each may be the consequence of local venous or lymphatic obstruction, as in an inflammatory or neoplastic disease.
If edema is generalized, it must first be determined whether hypoalbuminemia is significant, i.e. the concentration of serum albumins is below 2,5 g/dl. if so, history, physical examination, urine tests and other laboratory data will help assess the diagnosis of cirrhosis, severe malnutrition, gastroenteropathy with loss of protein or nephrotic syndrome, as the underlying disease. If hypoalbuminemia is not present, the existence of signals of severe congestive heart failure leading to edema should be sought. Finally, it should be seen whether the patient has an adequate diuresis, or if significant oliguria or even anuria is present.
On May 26th we'll start the shock posts... Don't forget that I only started posting in the odd days!
A soothing and restful
weekend. I don't really have that, I have to spend at the party
of my major, Mariuca!
Dorin, Merticaru