Anasarka is a diffuse puffiness of soft tissues with predominant localization in the lower half of the trunk, which appears as a consequence of other diseases and has a progressive course. Excess of the liquid component in the ansarck is observed not only in the form of a subcutaneous localized fluid, but also intracavitary accumulation of exudate with the development of ascites, pericarditis and pleurisy.
Establishing the conclusion of "anasark", doctors imply an extremely serious condition of the patient, which needs immediate application of medical correction of this pathology.
Causes of anasarca
The pathogenetic mechanisms of the development of anasarca are as follows:
- increased hydrostatic type of blood pressure circulating in the lumen of the vessel with a simultaneous decrease in oncotic plasma pressure;
- stagnant changes in blood in the vessels of the venous bed;
- the appearance of increased permeability of the vessel wall and the ability to pass the liquid component of blood into extravascular interstitial tissues;
- redistribution of ions in the blood and an increase in the propensity to accumulate sodium, which retards water in all tissues.
Thus, all diseases, accompanied by the above pathogenetic links, can become background for the development of anasarca.
Thus, a large category of patients suffering from chronic pathology of cardiac abnormalities followed by decompensated heart failure are at risk for complications such as anasarca. Progressing ischemic myocardial damage, dilated type of cardiomyopathy and hypertension are direct background diseases provoking an anasarku, provided there are no measures taken either by the patient or by the attending physician.
Anasarka with heart failure has a tendency to slow progression for several years and rapid leveling of symptoms when using medication.
Severe diseases of the urinary system with concomitant nephrotic syndrome are the second most frequent pathology, accompanied by a massive anasarka. Unlike generalized edema observed in cardiac decompensation, the anasarka of this type has a malignant aggressive course and system hemodialysis must be used to eliminate it. The mechanism of development of this type of anasarka is a violation of the excretory function of the kidneys and accompanying disorders of mineral metabolism.
Isolated thyroid damage and prolonged hypothyroidism is accompanied by a rapid loss of albumin from the plasma and a sharp decrease in the oncotic type of pressure in the lumen of the vessels, resulting in a progressive accumulation of fluid in the cavities and soft tissues, which has the nosological name "myxedema."
The aldosterone produced by the adrenal cortex is of great importance in the regulation of metabolic electrolyte processes, in connection with which, any endocrine pathology accompanied by increased production of mineralocorticoids becomes a provocateur for the development of anasarca.
The only pathological condition provoking the development of the acute form of the anasarka, is Quincke's edema , which is observed when the allergic factor is affected.
Symptoms of anasarca
The clinical symptomatology and intensity of the progression of anasarca directly depends on the background disease, of which it is a complication, but in most cases a slowly progressing current with a long latent period is observed.
The debut of anasarca is the appearance of persistent edematous syndrome, which initially has a limited, and then generalized character. The localization of edema in various pathologies has its own characteristics. So, if the patient makes complaints about the marked swelling of the eyelids and neck in the morning hours, one should assume the kidney nature of the anasarca, while the cardiac pathology is accompanied by the accumulation of fluid in the subcutaneous tissue of the distal limbs in the evening. Subsequently, soft tissue edema progressively increases and does not disappear without the use of drug correction.
At an objective examination of the patient with an ansarca, first of all, it is necessary to determine the primary localization of the edematous syndrome and the depth of its manifestation, for which a compression test is used.
In addition to visual changes in soft tissues, a patient with a prolonged course of anasarca is disturbed by progressive dyspnea, which is a consequence of impregnation of fluid in the interalveolar spaces and accumulation in the lower parts of the pleural cavities. As a rule, hydrothorax in this case has a two-sided character and is accompanied by pronounced respiratory disorders due to compression of the main structures of the mediastinum. Thus, the appearance of symptoms of impaired ventilation indicates a massive accumulation of fluid in the pleural cavities.
The terminal degree of anasarka is accompanied by severe hemodynamic disorders due to impaired cardiac activity. In a situation where there is an excessive accumulation of exudate in the pericardial cavity, an extremely serious condition of the patient comes, requiring urgent medical measures aimed at preserving the life of the patient.
A separate clinical form of edematous syndrome is fetal anasarca, observed with a frequency of 1 case per 1000 episodes of childbirth. The appearance of this terrible disease in the child is due to immune and non-immune mechanisms (hemolytic disease of the newborn, severe intrauterine infection of the fetus, gross cardiac malformations with severe cardiohemodynamics).
Diagnosis of this condition is not difficult, because immediately after birth, the child has marked visual changes in the form of total edema of soft tissues. Due to the fact that the anasarka in a newborn child has a lightning course and is accompanied by gross respiratory disorders, the mortality rate of this category of patients is very high. Due to the fact that at the present time high technologies of instrumental visualization are used in medicine, which allow to diagnose this pathology early in the early stages and begin medical correction before the onset of labor, in the pediatric practice the cases of complete recovery of the child with an anasarka began to occur more.
Treatment of anasarca
In a situation where there is moderate anasarca, consisting of a small puffiness in the soft tissues of the limbs, no active medical therapy is needed, but only a correction of eating behavior with limited consumption of salty foods, as well as a systematic use of compression knitwear items. If the fact of the renal nature of the anasarca is excluded from the laboratory, it is recommended to introduce into the diet of the patient food containing a large percentage of proteins.
If the patient's anasarca is a consequence of heart failure and affects all organs and systems, the patient is shown bed rest and use of drugs of the cardiac glycoside group (digoxin at the maximum initial daily dose of 0.0005 g, followed by a transition to a maintenance therapeutic dosage of 0.00015 g for life). In this case, it is expedient and pathogenetically justified to use drugs that have a dilating effect on the wall of venous vessels (Nitroglycerin in a single dose of 5 mg long course). In order to eliminate metabolic disturbances in the cardiac muscle, the patient should prescribe medications of a group of cardiotropic metabolites (Mildronate in a daily dose of 500 mg intravenously with a course of 10 injections).
The most effective for stopping the signs of anasarca by a group of medicines are diuretics, and when prescribing a medication, one must take into account the background disease. Thus, the anasarka in chronic heart pathology is well treatable with a combination of Furosemide in a daily dose of 40 mg with Veroshpiron in a dosage of 0.025 mg under the mandatory control of the volume of diuresis daily, which should be 800 ml higher than the amount of liquid consumed per day.
If the patient has a progressive course that is not treated with diuretics with concomitant signs of respiratory failure, it is necessary to decide on surgical removal of excess fluid from the pleural and abdominal cavities using thoraco- and pleurocentesis. These activities in this category of patients are classified as palliative interventions and in the future these activities should be supplemented by active diuretic therapy.
When anasarka occurs as a complication of severe hypothyroidism, the only pathogenetically justified treatment is substitution therapy with L-thyroxine at a daily dose of 1.6 μg per kg of body weight, as well as infusion of plasma preparations.
If the anasarka has a kidney origin, often resort to the appointment of glucocorticosteroids (Dexamethasone 4 mg 2 times a day intramuscularly).