Signs and treatment of abdominal ascites in liver cirrhosis

Abdominal ascites - symptoms and treatment options, prognosis for life Ascites (abdominal dropsy) is a condition characterized by the accumulation of free fluid in the abdominal cavity (more than 25 ml), which can be either inflammatory (exudate) or non-inflammatory (transudate) in nature . The disease is manifested by an increase in abdominal circumference, difficulty breathing, pain in the peritoneum, a feeling of heaviness and distension.

Most often (in 80% of cases) ascites occurs against the background of liver cirrhosis, which has reached the final stage of decompensation. This stage is characterized by depletion of liver resources, serious disturbances of the hepatic and abdominal circulation, that is, the emergence of favorable conditions for the accumulation of fluid.

Causes

The causes of ascitic disease are unexpected, the most common among them are presented below. This:

• malignant neoplasms and metastases;
• liver cirrhosis and increased blood pressure in the portal system;
• thrombosis (narrowing of the hepatic, inferior vena cava and portal veins);
• acute and chronic inflammatory kidney diseases;
• nephrotic syndrome (protein begins to be excreted in the urine);
• chronic renal failure;
• inflammatory lesion of the serous membrane of the heart;
• acute and chronic heart failure;
• some infectious and inflammatory bowel diseases, in which diarrhea and protein loss are observed;
• inflammation of the pancreas;
• tuberculosis;
• pseudomyxoma (mucus accumulation);
• anasrka.

This disease is a complication of liver cirrhosis and more. It progresses gradually in the body; at first it does not manifest itself in any way. Abdominal ascites is difficult to treat successfully. However, healing occurs if the main pathogenic factor is eliminated.

Diagnostic tests

The patient consults a doctor with characteristic signs of pathology in the body. After a visual examination, palpation of the abdomen, listening with a phonendoscope and taking an anamnesis, the specialist prescribes a diagnostic examination. It will not be difficult for a doctor to determine the problem, since the pathology is manifested by “wave” fluctuations when palpating the peritoneum.

To confirm the diagnosis, the following instrumental methods are prescribed:

• ultrasound to detect increased fluid accumulation;
• laparoscopy to assess changes in the condition of internal organs;
• laparocentesis (a puncture is made to remove free water);
• CT scan;
• chest x-ray;
• Magnetic resonance imaging;
• angiography (if the cause is vascular problems).

In severe cases, diagnosis and treatment of liver cirrhosis with ascites is carried out in a hospital setting. A biochemical blood test is prescribed, which allows you to determine the level of protein, creatine, urea and potassium. After the study, based on the results of the protocol, the doctor makes a decision on choosing one or another tactic.

Symptoms of ascites

The formation of abdominal ascites in most patients with cancer occurs gradually, over several weeks or even months. Therefore, the first signs of this formidable complication remain unattended.

Clinically, ascites begins to manifest itself after a sufficiently large amount of fluid has accumulated in the abdominal cavity; this complication manifests itself:

1. Feeling of fullness in the stomach.
2. Abdominal pain of different nature and duration.
3. Belching and heartburn.
4. Nausea.

You can visually pay attention to the gradually increasing belly; in a vertical position it hangs down, and in a horizontal position it spreads out to the sides. Stretching the skin of the abdominal wall allows you to see the network of blood vessels and the protruding navel.

Pressure on the chest causes shortness of breath and irregular heart function. With ascites, it is difficult for a person to bend over, fasten shoes, or put on trousers.

Possible complications

The answer to the question of how long a patient will live with ascites against the background of liver cirrhosis largely depends on the timeliness of seeing a doctor.

The disease itself is decompensation, that is, a complication of an existing pathology, so the lack of competent care often leads to death.

Possible consequences are:

• The appearance of bleeding of different localization.
• Development of hepatic encephalopathy.
• Blood clots in the spleen or collar vein.
• Inflammatory processes in the peritoneum.
• Hepotoreanal syndrome.

It is important to know! The disease threatens the patient, so seeing a doctor at the primary stage is extremely important. This will allow the specialist to prescribe the necessary therapy, eliminate complications and increase life expectancy.

Stages

Depending on the amount of accumulated exudate, three stages of ascites are distinguished:

Pathogenetic approaches to diuretic therapy of ascites in patients with liver cirrhosis

Ascites is one of the most significant complications of liver cirrhosis, occurring in approximately 40–50% of patients within a 10-year period from diagnosis. The development of ascites is considered an important unfavorable prognostic sign of disease progression, as it is associated with 50% mortality over the next two years [23, 26].

To date, the mechanisms of ascites formation in liver cirrhosis remain unclear. How does fluid accumulate in the abdominal cavity, what is the physiological essence of this process, what is its connection with central hemodynamics, the condition of the kidneys and peritoneum? Why is this particular syndrome a turning point in the lives of patients with cirrhosis and, regardless of the etiology of the disease, determines the further survival and quality of life of these patients?

In addition, the progressive growth of the pharmacological market is almost not noticeable in hepatology. Whereas in other areas of medicine, for example, in cardiology, consensus documents on the treatment of patients with heart failure (HF) are annually adopted, which include new diuretic drugs, and optimize regimens and approaches to therapy. Treatment of edematous-ascitic syndrome in a cardiac patient has been clearly established, while discussion of the principles of supervision of a hepatological patient entails a number of disputes and disagreements.

These and many other questions already require resolution today, primarily for medical specialists who are involved every day in the treatment of patients with chronic liver diseases.

Mechanisms of ascites in patients with liver cirrhosis

The development of ascites is caused by increased lymph production in the liver due to the blockade of the outflow of venous blood from it, but its occurrence begins from the moment of damage to hepatocytes, i.e., from the stage of hepatitis.

The main mechanisms for the development of edematous-ascitic syndrome are (

):

1. liver dysfunction (hepatoprivate syndrome);
2. release of vasodilators and cytokines by damaged hepatocytes;
3. activation of the sympathoadrenal (SAS) and renin-angiotensin-aldesterone system (RAAS) with subsequent dysfunction of the cardiovascular system (CVS) and kidneys;
4. formation of portal hypertension (PH): • due to activation of cells of the sinusoidal compartment with the development of functional PH; • activation of fibrogenesis processes in the liver with disruption of its vascular bed and the development of organic PG;
5. blockade of venous and lymphatic drainage from the liver.

Let us take a closer look at these provisions.

Development of hepatic cell failure syndrome (HCF) in patients with liver cirrhosis. Characterized by:

• disruption of protein synthesis and the development of hypoalbuminemia, which leads to a decrease in the oncotic pressure of the blood plasma, while the release of fluid from the vascular bed increases, the volume of intravascular fluid decreases, the filling of the central arterial bed decreases (effective circulating blood volume (BCV)), which compensatory increases the activity of the RAAS and increases the level of aldosterone, which causes fluid retention. However, in conditions of persistent liver pathology, the compensatory mechanism (activation of the RAAS) becomes pathological, contributing to further fluid retention in the body, the formation of ascites and edema;
• disruption of the detoxifying function of the liver, which is accompanied by a disorder of hormone catabolism, an increase in the content of estrogens in the blood, which have an antidiuretic effect and stimulate fluid retention and activation of the RAAS.

Release of vasodilators and cytokines by damaged hepatocytes. Impairment of the detoxifying function of the liver, the development of PCN and porta-caval shunting contribute to the penetration into the blood from damaged hepatocytes of vasodilators, such as glucagon, nitric oxide, prostaglandin E2α, atrial natriuretic hormone, vasointestinal peptide, prostacyclin, which leads to generalized vasodilation and a decrease in overall peripheral vascular resistance (PVR). At the same time, powerful vasoconstrictors, in particular endothelin-1, are synthesized in the endothelium of liver vessels, under the influence of endotoxins and cytokines, which causes vasospasm. That is, there is a disconnection of local and general blood flow associated with an imbalance of vasodilating and vasoconstrictive substances, which leads to:

• to the activation and transformation of Ito sinusoidal cells into myofibroblasts, which contract, narrow the lumen of the sinusoids, forming a functional PG, together with Kupffer cells they synthesize collagen and vasoactive substances that stimulate the SAS and RAAS;
• to inadequate peripheral vasodilation, causing compensatory activation of the SAS and RAAS, and an increase in the level of antidiuretic hormone (ADH).

Activation of SAS and RAAS. Activated SAS and RAAS affect the main targets:

• CVS: the consequence of peripheral vasodilation is an increase in blood volume, stroke volume (SV), minute volume of blood flow (MCV) and the formation of a hyperkinetic type of blood circulation. The hyperkinetic state of central hemodynamics initially has a compensatory nature, aimed at increasing the central effective volume of circulating blood and intrahepatic blood flow, which prevents a decrease in portal pressure with the development of portosystemic collaterals. However, already in the early stages, this type of hemodynamics leads to functional overload of the myocardium, contributing to the development of diastolic and subsequently systolic dysfunction, realizing systemic manifestations of the disease in the form of heart failure and ascites [20, 22, 24, 37];

The main factors affecting the CVS in liver cirrhosis are blood shunting with a direct toxic effect on the myocardium of biologically active substances (adrenaline, histamine, serotonin), dysmetabolic disorders associated with impaired liver function, autonomic disorders, prolonged hyperactivation of the SAS and RAAS [7, 35, 38 ]. A combination of metabolic disorders of biologically active substances leads to the development of so-called metabolic cardiomyopathy with dilatation of the heart cavities and heart failure. This condition is aggravated by chronic functional overload of the heart against the background of a hyperkinetic type of blood circulation [2, 4, 6]. That is, with the development of liver disease, a systemic reaction develops, which is realized through the involvement of the cardiovascular system in the process, forming methods of compensation and decompensation similar to heart failure with the occurrence of edematous-ascitic syndrome [11, 12, 34].

• Kidneys: decreased blood flow in the cortex against the background of a hyperdynamic type of blood circulation, which leads to vasoconstriction, release of renin and increased aldosterone levels. Compensatory for the restoration of bcc, these systems stimulate an increase in the reabsorption of sodium and water, causing the transition of fluid into the intercellular space, which leads to the formation of ascites and edema [5, 8].

The main factors of kidney damage in liver cirrhosis are:

• • reduction in renal blood flow and perfusion of the renal cortex as a result of blood shunting through anastomoses in the subcortical layer;
• • decrease in effective BCC;
• • increased levels of vasoconstrictors (endothelin-1, thromboxane, etc.);
• • decreased synthesis of prostaglandins and kallikrein by the kidneys, which have a vasodilating effect.

Renal damage occurs as a result of an imbalance between systemic vasodilation and renal vasoconstriction. Despite the systemic vasodilation characteristic of liver cirrhosis, vasoconstriction occurs in the kidneys, as in the liver, which leads to a decrease in the glomerular filtration rate, while the level of renin in the plasma increases. Sodium is compensatoryly reabsorbed in the renal tubules, which causes an increase in urine osmolarity. Fluid accumulates in the body, despite normal urine volume, a low-salt diet and diuretic therapy. In extrarenal vessels, dilatation of the arteries predominates, and as a result, OPS decreases with the development of arterial hypotension. Cardiac output is unchanged or even increased, but effective renal blood flow is reduced as a result of redistribution of blood flow to the spleen, skin and other organs, thus shunting the renal cortex. The earliest sign of activation of the renal mechanism during the development of ascites in patients with liver cirrhosis is sodium retention in the body, which is manifested by a decrease in daily sodium excretion in urine to less than 78 mmol/day [8, 16].

Renal sodium retention is one of the likely causes of ascites, preceding the accumulation of ascitic fluid. In the early stages, it is the result of blockade of venous outflow from the liver and primary vasodilation.

Formation of GHGs. The development of a powerful imbalance of vasoactive substances, causing spasm of the sinusoids, as well as promoting active fibrogenesis in the liver, with the formation of cirrhotic nodes, leads to disruption of the venous bed of the liver and the development of PH.

The reversibility of ascites is determined by the stage of PG. Ascites is potentially reversible if there is a functional PH, and irreversible if changes in the vascular bed of the liver have occurred and organic PH has formed [1, 11].

Functional (sinusoidal) PG is determined [19, 23, 38]:

• vegetative tone;
• contraction of Ito cells and, as a consequence, narrowing of the lumen of the sinusoids and their release of vasoactive substances that stimulate the SAS and RAAS;
• hepatic vascular tone, regulated by vasoactive substances;
• rheological properties of blood in the vessels of the portal system.

Organic PG is formed against the background of a violation of the cytoarchitecture of the liver, it is determined [23]:

• compression and destruction of sinusoids;
• portohepatic shunts;
• proliferation of connective tissue in the centrilobular zones of the lobules.

It is important to note that even at the stage of organic PG, its functional component is preserved, which can be reduced using drug therapy aimed at correcting the condition of the SAS, RAAS, blood rheology and other pathogenetic links.

Blockade of venous and lymphatic drainage from the liver. Increased pressure in the portal system leads to disruption of venous outflow from the liver and unpaired abdominal organs, which is accompanied by overflow of the sinusoids and increased lymph production in the liver.

In patients with liver cirrhosis, the volume of daily lymphatic drainage through the thoracic lymphatic duct can increase to 20 liters. Lymph from the vessels of the liver and unpaired organs sweats into the abdominal cavity, forms ascites, establishing a dynamic equilibrium with the process of its absorption into the intestinal capillaries.

Thus, we can conditionally distinguish several levels of ascites formation, closely interrelated:

• humoral-metabolic, determined by an imbalance of vasoactive substances (vasodilators and vasoconstrictors), hypoalbuminemia, diselectrolyte disorders, hyperestogenemia, an increase in ADH;
• cellular, determined by the specific response of liver cells (hepatocytes, endothelial cells, Kupffer, Ito cells) and peritoneum (mesotheliocytes);
• organ, determined by the initial state, involvement in the process and specific response of target organs (the liver itself, cardiovascular system, kidneys);
• systemic, determined by the nature of the neuroendocrine response of the SAS, RAAS and systemic implementation of PG.

Moreover, the reversibility of these changes depends on the stage of PG (functional or organic).

Classification of ascites

Depending on the amount of ascitic fluid and the effectiveness of therapy, the following are distinguished:

1. initial or transient (up to 400 ml, detected by ultrasound);
2. moderate (when ascites is not intense and responds well to therapy);
3. severe or intense ascites;
4. resistant ascites (a variant of tense ascites resistant to treatment).

The criteria for resistant (refractory) ascites are the absence of a decrease or a decrease in body weight of less than 200 g / day in the patient for 7 days against the background of a low-salt diet (5.2 g of table salt per day) and intensive diuretic therapy (spironolactone 400 mg / day and furosemide 160 mg/day), as well as a decrease in urinary sodium excretion to less than 78 mmol per day [16, 25]. Resistant ascites is also spoken of in cases where it does not decrease or quickly recurs after paracentesis or complications of diuretic therapy do not allow diuretics to be prescribed in effective doses. In practice, criteria for resistant ascites are detected in less than 10% of patients with liver cirrhosis.

The causes of resistant ascites are usually:

• excess sodium and fluid intake;
• inadequate diuretic therapy;
• hypotension;
• alkalosis;
• hypokalemia, hyponatremia, hypoalbuminemia;
• taking non-steroidal anti-inflammatory drugs;
• progression of liver disease;
• Budd–Chiari syndrome;
• peritoneal carcinomatosis;
• spontaneous bacterial peritonitis (SBP).

Many causes of refractory ascites are potentially reversible, so their timely elimination can significantly increase the effectiveness of therapy.

Treatment of ascites in patients with liver cirrhosis

It should be noted that the task of treating ascites in patients with liver cirrhosis is more difficult than treating other forms of fluid accumulation in the body, because the formation of edematous-ascitic syndrome is a manifestation of significant decompensation of the disease. According to the results of controlled studies, the appearance of ascites significantly worsens the quality of life and increases the risk of developing fatal complications of liver cirrhosis [27, 39], so its therapy is one of the most important components of the successful treatment of these patients. However, given that complex neurohormonal mechanisms are involved in the development of ascites, thoughtless dehydration can only cause side effects and “rebound” fluid retention.

Regimen, diet and fluid intake in patients with liver cirrhosis and ascites. In patients with ascites who do not limit dietary salt intake, daily urinary sodium excretion is reduced to 78 mmol or less, while extrarenal sodium losses can reach 10 mmol/day.

Consumption of more than 90 mmol/day of sodium by patients with liver cirrhosis leads to the development of ascites, since each gram of sodium retains up to 200 ml of fluid. Therefore, it is recommended to consume no more than 90 mmol of sodium (5.2 g of table salt) with food during the day, in combination with limiting the amount of liquid to 1 liter per day. It is important to take into account that fluid restriction is not indicated for patients with low serum Na levels (less than 120 mmol/l) [16].

To date, there are no published studies that demonstrate a positive or negative effect of water restriction on the resolution of ascites. Most experts believe that there is no role for water restriction in patients with uncomplicated ascites. Despite this, a water-restricted diet for patients with ascites and hyponatremia has become standard clinical practice in many centers. There is a lot of controversy on this issue, and the best approach has not yet been found. As a rule, hepatologists treat such patients with strict water restriction. From the point of view of the pathogenesis of hyponatremia, such treatment is counterintuitive and may worsen the severity of central hypovolemia, which triggers non-osmotic ADH secretion. An even greater increase in the concentration of circulating ADH leads to a further decrease in renal function. Impaired free water clearance is present in 25–60% of patients with cirrhotic ascites, and they often develop spontaneous hyponatremia.

Errors in diet often cause difficult to treat (resistant, refractory) ascites. If you consume a large amount of salt, the use of modern diuretics, even in high doses, will be ineffective.

The diet should be essentially vegetarian as most high protein foods (meat, eggs and dairy) are high in sodium, so the diet should therefore be supplemented with low sodium protein foods. It is recommended to eat salt-free bread, butter and cook all dishes without adding salt. Products rich in potassium and microelements are also shown. The energy value of the diet should be ~1500–2000 kcal, containing 70 g of protein and 90 mmol of sodium per day.

A patient with ascites is recommended to limit physical activity, which helps reduce the amount of metabolites produced in the liver. Also, in the supine position, portal venous and renal blood flow slightly increases.

General approaches to the treatment of ascites in patients with liver cirrhosis. Strategic directions for the treatment of ascites include limiting salt in food and drug removal of excess fluid from the body. In addition, based on the considered positions of the pathogenesis of ascites in patients with liver cirrhosis, it is important to solve therapeutic problems of correcting PG, PKN, blocking peripheral vasodilators, suppressing the activity of the SAS and RAAS, normalizing the function of the cardiovascular system, kidneys, etc.

For safe drug removal of fluid from the body, three steps must be followed:

1. Excess fluid must be transferred from the extracellular space into the vascular bed.
2. Excess fluid must be delivered to the kidneys, where it can be filtered.
3. When primary urine enters the renal tubules, reabsorption must be blocked, this will ensure the removal of excess fluid from the body [13].

To transfer excess fluid from the extracellular space into the vascular bed, the following are used:

• active diuretics (diuretics), which, by reducing blood volume and hydrostatic pressure, facilitate the transition of fluid from the extracellular space into the vascular bed;
• hemodynamically active neurohormonal modulators: beta blockers, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor antagonists (ARA) [4, 16];
• drugs that increase oncotic pressure in the blood (blood plasma and albumin preparations) and osmotic pressure (aldosterone antagonists, increasing ion exchange and reducing the severity of dilution hyponatremia).

The most optimal beta-blockers in patients with liver diseases, the effectiveness of which is confirmed by the results of a meta-analysis, are non-selective derivatives of the propranolol group - Anaprilin in an individually selected dose - 40-80 mg / day or carvedilol in an individual dose - 25-50 mg / day [3, 14, 28, 31].

Among ACEIs in patients with liver cirrhosis, the drugs of choice are the lisinopril group in an individually selected (2.5–20 mg/day) dose or the dual-excretion drug spirapril 6 mg/day.

Unlike other representatives of this class, they are a ready-made dosage form, and their effectiveness is confirmed by the results of comparative studies [11, 17].

Among the ARAs, eprosartan can be used in this category of patients in an individually selected dose - 300–600 mg/day. Open studies have demonstrated the effectiveness of drugs of this group in patients with liver cirrhosis [32, 40].

Positive inotropic agents are used to deliver excess fluid to the kidneys:

• cardiac glycosides, the criterion for prescribing them in patients with liver cirrhosis is the presence of normal or reduced ejection fraction (EF) (due to the initial hyperkinetic state of central hemodynamics in these patients with increased cardiac output) during ECHO-CG, as well as atrial fibrillation;
• Neoton (for the purpose of metabolic support of the myocardium).

To improve renal filtration, the following are recommended:

• dopamine (better for arterial hypotension; due to its effect on dopaminergic receptors, this drug increases the proportion of renal blood flow);
• Eufillin (with systolic blood pressure (SBP) above 100 mm Hg).

To block the reabsorption of primary urine in the renal tubules, diuretics themselves are used (mainly loop diuretics and aldosterone antagonists).

Diuretic therapy for patients with liver cirrhosis and ascites. Taking into account the complex pathogenesis of the development of edematous-ascitic syndrome, diuretics of various pharmacological groups are used in its treatment: aldosterone receptor antagonists, potassium-sparing, loop, thiazide diuretics and carbonic anhydrase inhibitors. The algorithm for prescribing diuretics to patients with liver cirrhosis is presented in Scheme 1.

The effect of diuretics in liver cirrhosis and ascites is multifaceted and consists of their influence on renal structures and extrarenal mechanisms for regulating water and electrolyte balance [9, 10], including effects at the level of:

• cell membranes - diuretics regulate their permeability, the functions of intracellular transport proteins and the electrochemical processes of ion transport;
• individual nephron - influence on the filtration load of the nephron, the transport function of its various segments;
• kidneys - influence on intrarenal hemodynamics, internephron relationships, activity of tissue components of neurohumoral systems;
• systemic hemodynamics and water-electrolyte balance.

The main principle of unloading therapy for edematous-ascitic syndrome in patients with liver cirrhosis is to obtain a gradually developing and stable diuretic effect, with spironolactone being the drug of choice [15, 23].

In cases of refractoriness to therapy with aldosterone antagonists, before prescribing other diuretics acting on other parts of the nephron, it is advisable to evaluate the indications for the use of additional therapeutic measures, in particular for the administration of albumin and blood-substituting colloid solutions.

With severe edematous-ascitic syndrome, the scope of diuretic therapy can be expanded with loop or thiazide diretics, which suppress the reabsorption of sodium and water.

The combined administration of potassium-sparing and potassium-sparing diuretics is recommended, which helps reduce the risk of electrolyte disturbances [18, 21, 29].

The dosage and frequency of taking the drug are selected individually for each patient. When a patient is admitted to hospital, it is recommended to determine daily sodium excretion, which facilitates the selection of a diuretic and monitoring the effect of treatment [16].

At initial signs of ascites, therapy begins with one of the drugs from the group of potassium-sparing diuretics, usually spironolactone. If ineffective, a loop diuretic is added.

The presence of signs of severe ascites requires the initial use of combination therapy, with spironolactone prescribed as a reliable partner for loop diuretics.

In patients with liver cirrhosis with moderate and severe PH, it is possible to begin treatment with courses of aldosterone antagonists even before the formation of ascites in minimal (25–50 mg/day) dosages that do not change diuresis as a neurohumoral modulator, but this point of view is the author’s and has not been confirmed by wide clinical trials.

In case of decompensation of liver cirrhosis (in the form of development of ascites), the use of spironolactone is absolutely necessary and there is no need to be afraid of its combination with ACE inhibitors or ARAs if, in parallel, active diuretics are correctly used to achieve positive diuresis. The drug is taken in high doses (100–300 mg, given once in the morning or in two doses in the morning and afternoon) for a period of 1–3 weeks until compensation is achieved. After this, the dose of spironolactone should be reduced.

It must be remembered that the concentration of spironolactone in the blood plasma reaches a plateau by the third day of treatment and after discontinuation (or reduction of the dose of the drug), its concentration and effect disappears (decreases) after three days. After compensation is achieved, the use of high doses of spironalactone is stopped and the issue of prescribing small doses of the drug as an additional neurohormonal modulator is considered.

For long-term maintenance therapy of patients with liver cirrhosis, it is recommended to use small (25–50 mg) doses of spironolactone in addition to ACE inhibitors and beta-blockers (BAB), which allows for more complete blocking of the RAAS and SAS.

In cases where it is necessary to replace spironolactone, the drug of choice is amiloride 10–15 mg/day.

The optimal ratio of spironolactone and furosemide is 5:2, for example, 100 mg of spironolactone and 40 mg of furosemide, etc. The maximum daily doses of these drugs are 400 and 160 mg, respectively.

Furosemide, in turn, may be ineffective in severe hyperaldosteronism, when sodium not reabsorbed in the loop of Henle is absorbed in the distal nephron. The second reason is hypokalemia and alkalosis.

Alternative, in cases of ineffectiveness, loop diuretics to furosemide for the treatment of ascites in patients with liver cirrhosis can be considered: Uregit (ethacrynic acid) 25–50 mg/day and bumetanide, which is not weaker than furosemide and is used in doses from 0.5 to 10 mg, which allows you to achieve optimal diuresis.

Ethacrynic acid and thiazides, as long-acting diuretics, are less indicated for patients with liver cirrhosis, since they can aggravate developed electrolyte disturbances, and even after their withdrawal, potassium loss in the urine and an increase in alkalosis may continue.

Therefore, in particular, thiazides are used primarily at the stage of maintenance therapy and/or the inability to use spironolactone. Taking into account possible side effects, thiazide diuretics in patients with liver cirrhosis are prescribed for a course of no more than 7-14 days with a break of 3-4 days.

In addition to the above, in 2006, one of the most effective and safe loop diuretics, torasemide (Diuver), was registered in Russia. Its starting dose is 5–10 mg, and if necessary, it can be increased to 20 mg per day. Torsemide not only has a more pronounced diuretic effect than furosemide, but also has its own activity in relation to aldosterone receptors, which provides it with a potassium-sparing effect. The advantage is the absence of undesirable effects of aldosterone antagonists (hyperkalemia, hirsutism and others), the drug has high bioavailability (80% versus 50% for furosemide), a prolonged effect (half-life 3-5 hours versus 1 hour for furosemide) and a mild hypotensive effect. The pharmacokinetics of torasemide is little dependent on renal function and intestinal condition, which provides a low risk of drug accumulation and lower excretion of potassium, calcium, inorganic phosphates and magnesium compared to furosemide.

In the treatment of edematous-ascitic syndrome in patients with liver cirrhosis, it is possible to use torasemide both as monotherapy and in combination with Veroshpiron. Torsemide therapy is indicated for decompensation of ascites, as well as for the prevention of its occurrence in dosages of 5–20 mg, which do not cause hypokalemia even with long-term use. It is recommended to use a stepwise approach, starting with 5 mg/day, increasing the dose by 5 mg every 2-3 days until the effect is achieved. At the outpatient stage, it is not recommended to exceed the daily dose of 20 mg, since a larger amount of the drug requires frequent monitoring of potassium levels.

To evaluate the effectiveness of diuretic therapy in patients with liver cirrhosis and ascites, a number of comparative studies of torasemide and furosemide were conducted. Thus, in a double-blind crossover study, the results of a single oral dose of furosemide (80 mg) and torasemide (20 mg) were compared in 14 patients. Torsemide was superior to furosemide in diuretic and natriuretic activity. Five patients had a weak response to furosemide, while torasemide caused a significant increase in natriuresis and diuresis [30, 33, 36].

Similarly, in a double-blind, randomized study of 28 patients with ascites treated with spironolactone (200 mg/day), the results of 6 weeks of therapy with torsemide (20 mg/day) and furosemide (50 mg/day) were compared. Both drugs had comparable effects on body weight, diuresis, and excretion of uric acid, sodium, and chloride, but excretion of potassium, calcium, inorganic phosphate, and magnesium was lower in the torsemide group [30, 33, 36].

A group of 46 patients with liver cirrhosis complicated by ascites (randomized trial) were treated with torasemide 20 mg/day or furosemide 40 mg/day in combination with spironolactone 200 mg/day. If it was not possible to achieve a weight loss of 300 g/day, the doses of diuretics were increased every 3 days to 40, 120 and 400 mg/day, respectively. Torsemide caused a more pronounced increase in diuresis than furosemide, although in general the treatment results in the 2 groups were comparable. An increase in diuretic doses was required in 2 patients in the torasemide group and in 9 patients in the furosemide group [33, 36].

That is, according to the results of studies, torasemide can be considered as an alternative to the combination therapy of Furosemide + Veroshpiron in patients with liver cirrhosis and ascites.

Carbonic anhydrase inhibitors have not found widespread use in patients with ascites, since their suppression of sodium and water reabsorption in the proximal tubule is compensated by its increase in the distal segments of the tubules.

Drugs in this group can be used as an adjuvant while taking active diuretics (loop and/or thiazide). Carbonic anhydrase inhibitors block the enzyme in the area of ​​the proximal renal tubules, which is accompanied by slight diuresis (an increase of up to 10–15%), but this increases the “loading” of sodium in the underlying sections of the tubules, which increases the effectiveness of stronger diuretics. When the carbonic anhydrase enzyme is depleted after 3-4 days of continuous use, the activity of acetazolamide decreases, which requires a break in treatment.

Therefore, acetazolamide (Diacarb) is recommended at a dose of 0.25 g three times a day for 3-4 days with a two-week break. This therapeutic tactic helps to acidify the environment, restores the diuretic activity of thiazide and loop diuretics, with long-term use of which alkalosis develops. When combined with Eufillin, the diuretic effect of Diacarb increases.

To avoid the development of refractoriness and side effects of diuretics in patients with ascites, it is important to evaluate the effectiveness of treatment and conduct clinical and laboratory screening to determine indications for subsequent adjustment of the dosage regimen or discontinuation of drugs.

Read the continuation of the article in the next issue.

S. N. Mehdiev , Doctor of Medical Sciences, Professor Yu. A. Kravchuk , Candidate of Medical Sciences I. V. Subbotina O. A. Mehtieva * M. V. Shapovalov VMA named after. S. M. Kirova, *St. Petersburg State Medical Academy named after. I. I. Mechnikova , St. Petersburg

Diagnostics

Hydrocele of the abdomen can be diagnosed by a doctor even without the use of special equipment - it is enough to palpate the patient’s abdominal cavity. If, upon palpation, the doctor detects dullness in the abdomen on the side, while tympanitis is found in the middle, the patient has ascites.

To carry out a more in-depth diagnosis, it is necessary to perform an ultrasound in the peritoneal cavity, examine the liver, and also perform a puncture of the peritoneum (paracentesis). Taking the fluid for analysis allows us to identify the stage of the disease and determine its treatment. Paracentesis is performed to determine the causes of the disease. Paracentesis can also be done if there is difficulty breathing or pain.

In addition to the above diagnostic methods, the patient must undergo urine and blood tests, as well as undergo immunological studies. The possibility of prescribing additional analyzes and tests depends on how much information the obtained tests provide the doctor.

conclusions

The prognosis for the health and life of a patient who has developed ascites in heart failure can be improved by taking active therapeutic measures. However, despite the advances of modern medicine, it remains unfavorable. The presence of concomitant pathology, age, complex cardiac arrhythmias, high arterial hypertension and the presence of effusion in the pleural cavity indicate that death is inevitable. In this case, it is important to ensure a worthy completion of life’s journey and alleviate the suffering of the patient.

Treatment of abdominal ascites

Abdominal ascites, which develops as a complication of cancer, should be treated together with the underlying disease.

1. It is also important to begin eliminating excess fluid in the first two weeks of its formation, since delaying therapy leads to the development of a host of complications. Excess fluid can be removed by puncture and pumping it out - laparocentesis, by taking diuretics.
2. Following a special diet will help reduce intra-abdominal pressure and reduce the likelihood of further production of excessive exudate.

Chemotherapy is effective only if ascites is caused by intestinal cancer. For cancer of the stomach, ovaries and uterus, the use of chemotherapy does not give a significant positive result.

Description of the drug and composition

The drug Veroshpiron is a potassium-sparing diuretic and has a pronounced and long-lasting diuretic effect. The active ingredient of this drug is spironolactone (one of the hormones of the adrenal cortex). This substance has a long-lasting effect and can prevent the retention of water and sodium in the lower parts of the renal tubules. Veroshpiron does not have a significant effect on blood circulation in the kidneys, helps reduce the acidity of urine and reduces the excretion of potassium from the body.

The diuretic effect of this drug helps lower blood pressure. It begins to appear 2-5 days after starting to take Veroshpiron, and persists for 3 days after its discontinuation. After oral administration, spironolactone is completely absorbed from the digestive tract into the blood and enters the kidneys, providing a diuretic effect. The drug is excreted from the body mainly through urine and partly through feces.

Drug treatment

The main drugs that help remove excess fluid from the body are diuretics. Thanks to their intake, it is possible to achieve the transition of excess fluid from the abdominal cavity into the bloodstream, which helps reduce the symptoms of ascites.

• To begin with, patients are prescribed the smallest dose of diuretics to minimize the risk of side effects. An important principle of treatment with diuretics is a slow increase in diuresis, which will not lead to significant losses of potassium and other important metabolites. The most commonly recommended medications are Aldactone, Veroshpiron, Triamterene, and Amiloride. In parallel, potassium supplements are prescribed. At the same time, hepatoprotectors are introduced into the treatment regimen.
• At the same time, doctors monitor the patient’s diuresis on a daily basis and, if treatment is ineffective, increase the dose of drugs or replace them with stronger drugs, for example, Triampur or Dichlorothiazide.

In addition to diuretics, patients are prescribed drugs aimed at strengthening the walls of blood vessels (vitamin C, vitamin P, Diosmin), drugs that prevent fluid from leaving the vascular bed (Reopoliglucin). The introduction of protein preparations improves the metabolism of liver cells. Most often, concentrated plasma or an Albumin solution in a 20% concentration is used for this purpose.

Antibacterial drugs are prescribed if ascites is bacterial in nature. [adsen]

Folk remedies

Complex therapy is often supplemented with medicinal herbs and plants. They help reduce the manifestation of unpleasant symptoms and promote rapid recovery. The following products have proven themselves to be effective:

• Parsley decoction. It is prepared from fresh leaves, which are poured with boiling water and infused for half an hour. You need to take half a glass every hour in the morning. Three days are enough to relieve the condition.
• Bean husk. The main ingredient is boiled for 10 minutes, after which the water is drained and infused. 20 minutes is enough. The resulting remedy must be taken in the morning, the next time - half an hour before breakfast, and the same amount 30 minutes before lunch. The last reception is scheduled for 8 pm.

You cannot cure the disease on your own. Therefore, traditional medicine is used only in conjunction with conventional medicines. To avoid side effects, you should consult your doctor before taking it.

Abdominal laparocentesis

For ascites, abdominal laparocentesis is a surgical procedure in which fluid is removed from the abdominal cavity by puncture. You should not pump out more than 4 liters of exudate at a time, as this threatens the development of collapse.

The more often a puncture is performed for ascites, the higher the risk of developing peritoneal inflammation. In addition, the likelihood of formation of adhesions and complications from the procedure increases. Therefore, for massive ascites, it is preferable to install a catheter.

Indications for laparocentesis are tense and refractory ascites. The liquid can be pumped out using a catheter, or it simply flows freely into a previously prepared container after the trocar is installed in the abdominal cavity.

Drug interactions of Veroshpiron

When prescribing Veroshpiron, you should inform your doctor about taking other medications, since this drug can interact with many of them.

Veroshpiron:

• reduces the effectiveness of anticoagulants (coumarin derivatives, Heparin, Indandione);
• reduces the toxicity of cardiac glycosides (Strophanthin K, Digitoxin, Celanide, Korglikon, etc.);
• reduces vascular sensitivity to Norepinephrine;
• reduces the effectiveness of Mitotane;
• enhances the effectiveness of antihypertensive and diuretic drugs;
• enhances the metabolism of Phenazol;
• increases the toxicity of lithium-containing drugs;
• accelerates the excretion of Carbenoxolone, and their combined use leads to sodium retention;
• enhances the effect of Buserelin, Triptorelin and Gonadorelin;
• when taken simultaneously with salicylates, the diuretic effect of the drug decreases;
• when taken with potassium-sparing diuretics or potassium-containing drugs, Indomethacin, aldosterone blockers, angiotensin II antagonists and cyclosporines, there is a risk of developing hyperkalemia;
• when taken with cholestyramine and ammonium chloride, the risk of developing acidosis increases;
• when taken with nonsteroidal anti-inflammatory drugs, there is a risk of developing hyperkalemia;
• when taken with Fludrocortisone, increased secretion of potassium in the renal tubules develops; combined use with Digoxin can lead to a slower elimination of the latter and cause its toxic effect on the body.

Peritoneovenous shunt (Levine shunt)

Sometimes used to treat refractory ascites, i.e. one that does not respond to drug therapy and quickly returns after puncture. The operation consists of increasing the volume of circulating blood through the constant flow of fluid from the abdominal cavity into the general bloodstream system.

A Levine shunt is a long plastic tube that is inserted into the abdominal cavity, reaching the pelvic floor. Next, the shunt is connected to a valve and a silicone tube, which passes subcutaneously to the neck area for subsequent connection to the internal jugular and superior vena cava. The valve opens with the help of the resulting displacement force of the diaphragm and an increase in intra-abdominal pressure. Thus, there is an unimpeded flow of fluid into the superior vena cava.

Diet

Provides for reducing fluid intake, as well as salt, due to the fact that it retains fluid in the body. Doctors recommend the Avicenna diet. Such a diet for ascites involves almost complete abstinence from fatty foods, eating nuts in large quantities, and abandoning fresh fruits in favor of dry ones.

Also, liquid food (borscht, soup) should be replaced with broth with additives in the form of celery, parsley, fennel. The diet for ascites does not regulate how much meat the patient should eat, but all meat should be lean (chicken, turkey, rabbit).

How long do people with ascites live?

The lifespan of people diagnosed with ascites varies widely, depending on a number of factors. The life expectancy of a patient with ascites is determined by:

1. Time to start treatment. If ascites is detected in the early stages of development, when the functions of vital organs are not impaired (or slightly impaired), elimination of the underlying disease can lead to a complete cure of the patient. At the same time, with long-term progressive ascites, damage to many organs and systems (respiratory, cardiovascular, excretory) can occur, which will lead to the death of the patient.
2. The severity of ascites. Transient (mild) ascites does not pose an immediate threat to the patient's life, while intense ascites, accompanied by the accumulation of tens of liters of fluid in the abdominal cavity, can lead to the development of acute cardiac or respiratory failure and death of the patient within hours or days.
3. The main disease. This is perhaps the main factor determining the survival of patients with ascites. The fact is that even with the most modern treatment, a favorable outcome is unlikely if the patient has failure of several organs at once. For example, with decompensated cirrhosis of the liver (when the function of the organ is almost completely impaired), the patient’s chances of survival for 5 years after diagnosis are less than 20%, and with decompensated heart failure - less than 10%. The prognosis for chronic renal failure is more favorable, since patients on hemodialysis who follow all doctor’s instructions can live for decades or more.

The presence of ascites significantly aggravates the course of the underlying disease and worsens its prognosis. Complications of ascites itself can include spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome, and bleeding.

Characteristics of cirrhosis

The pathological condition of the liver, formed as a result of serious disruptions in the blood circulation of the organ, and which is characterized by persistent tissue damage, is called cirrhosis. It threatens not only the patient’s quality of life, but also often causes death, so it is impossible to treat it at home with folk remedies. The patient is required to comply with the doctor’s instructions, undergo regular examinations, and adjust behavior. And in some cases it is impossible to do without an organ transplant operation.

Hepatitis can provoke the appearance of cirrhosis. It, in turn, causes the development of a number of severe pathologies, such as liver failure, ascites, and portal hypertension. Negative complications are most often the result of an advanced state of the disease and indicate an unfavorable prognosis.