Endogenous intoxication of the body. Endogenous intoxication syndrome (EIS)

Currently one of the most difficult problems intensive care is endogenous intoxication syndrome(SEI) accompanying a significant amount pathological conditions(shock, peritonitis, pancreatitis, etc.), which as they develop can lead to death.

Progression of endotoxemia caused by the accumulation in the blood of various origins, chemical structure and the biological effects of substances called endotoxins. Endotoxins contribute to the development of acute renal and hepatic failure, cardiovascular failure, acute respiratory distress syndrome, ultimately leading to the emergence of an extremely serious condition - multi-organ dysfunction syndrome.

Endogenous intoxication- a clinical syndrome that occurs in pathological conditions of various etiologies, caused by the accumulation in the tissues and biological fluids of the body of products of impaired metabolism, metabolites, destructive cellular and tissue structures, destroyed protein molecules, and accompanied by functional and morphological lesions of organs and systems of the body.

There are three main links that determine the severity of the patient’s condition and severity clinical symptoms: toxemia, impaired microcirculation, inhibition of the functions of the body’s own detoxifying and protective systems.

The main link pathogenesis of endogenous intoxication syndrome is toxemia. Unfortunately, clear differentiation of toxic substances of endogenous origin is practically impossible. However, in each specific case, “primary” and “secondary” endotoxins can be distinguished. So, for burns, long-term crush syndrome, obliterative vascular diseases“primary” are the products of protein degradation, “secondary” are the products of natural metabolism, the accumulation of which in the body is a consequence of inhibition of the functions of natural detoxification and excretion.

Endotoxemia, disrupting the tone of peripheral vessels, blood rheology, kinetic and mechanical properties shaped elements blood, leads to tissue hypoxia, which is one of the important links in the pathogenesis of SEI, the course of which is aggravated by a decrease in the function of the organs of natural detoxification and excretion. Toxins block the binding sites of albumin molecules, which leads to a decrease in the effectiveness of the drug treatment, since this protein is a transport agent for many pharmacological drugs.

Clinic of endogenous intoxication syndrome.

Comparison of experimental and clinical trials allowed us to identify the following stages development of endogenous intoxication syndrome.
Stage I of endogenous intoxication syndrome. Reactive toxicity occurs in response to the formation of a primary destructive focus or traumatic injury. Laboratory signs of this stage are an increase in the blood levels of average mass molecules (MSM), lipid peroxidation products (LA and MDA), and an increase in LII.

Stage II of endogenous intoxication syndrome- the stage of severe toxemia develops after a breakthrough of the gastrohematic barrier, when endotoxins formed in the primary focus of intoxication enter the circulating blood, followed by distribution and accumulation in the body. Depending on the state of the body, its resistance and the initial level of detoxifying and immune systems, compensated and decompensated stages of severe toxemia are distinguished.

Stage III of endogenous intoxication syndrome- multi-organ dysfunction (MOD) is observed with further progression of the pathological process as a consequence of severe damage to various organs and systems by endotoxins with the development of their functional decompensation!. Clinically, this stage is manifested by impaired consciousness, hypoxia, severe heart failure, oliguria, and paralytic intestinal obstruction. A high concentration of creatinine, urea, and bilirubin is determined in the blood.

Endogenous intoxication (ICD code 10 X40-49) is a pathological symptom complex that accompanies a large number of diseases (cholecystitis, appendicitis, pancreatitis, peritonitis, septic shock, allergic reactions). It is characterized by the appearance of endotoxins in the bloodstream, with a poisonous effect on internal organs.

In the background inflammatory diseases specific substances accumulate that contaminate the vascular bed. Endotoxins affect the kidneys, heart, liver, causing multiple organ failure, which often ends in death. Substances are produced during metabolic metabolism and are not excreted from the body in sufficient quantities. They cause a number of pathological effects:

1. They act on the nervous system, inhibit the transmission of nerve impulses to cells.
2. Prevents the formation of blood cells and protein molecules.
3. Promote cell death.
4. They inhibit tissue respiration and increase the permeability of cell membranes to foreign agents.
5. Toxins disrupt the processes of sodium-potassium metabolism.
6. Affect microcirculation of blood and lymph.

Pathology leads to the destruction of cells by exogenous and endogenous agents, disruption of intracellular homeostasis. The state of intoxication develops in people with weak immunity, after surgical interventions, against the background of severe poisoning of the body with toxic products.

Types of self-poisoning of the body

Endogenous toxic substances are formed in the external or internal environment. Urea, pyruvate, lactate, creatinine are constantly present in the human body. As a result of inflammatory processes, their level increases, and intoxication occurs with adverse consequences. There are endogenous and autointoxication.

Endogenous intoxication syndrome occurs as a result of the accumulation of endotoxins in the organs and tissues of the body and biological fluids. There is another term - endotoxemia. This process develops with the accumulation of toxic substances in the bloodstream.

Endogenous metabolic intoxication occurs for the following main reasons:

1. Intoxication due to peritonitis.
2. Appendicitis, cholecystitis, pancreatitis are the main provoking factors of the pathology.
3. Infectious-toxic, hemorrhagic, painful, traumatic, hypovolemic, cardiogenic shocks influence microvasculature, The central nervous system, internal organs, contribute to the accumulation of metabolic products in the internal environments of the body.
4. Long-term compression syndrome is observed in patients who have been under rubble for a long time or have been crushed by external objects (wood, car). In such a situation, the muscle is crushed, and myoglobin, creatinine, potassium, and phosphorus exit from it into the bloodstream. Circulatory disorders and acidosis occur. Additionally, breakdown products are released during muscle necrosis.
5. Burns, burn disease and burn shock have similar pathogenesis.
6. Ovarian apoplexy and ectopic pregnancy in women are often complicated by peritonitis, infectious-toxic shock and accompanied by symptoms of metabolic disorders and accumulation of toxic products.
7. Acute and chronic intestinal obstruction often lead to endotoxins entering the blood and internal organs.

In medicine, there are many more conditions that lead to endogenous intoxication.

Symptoms of pathology:

• the patient feels constant fatigue and weakness;
• headaches and muscle pain appear, which are of a pressing, aching nature;
• Over time, dyspeptic syndrome develops: nausea, vomiting, diarrhea;
• pulse is frequent or rare, blood pressure low;
• dry skin and visible mucous membranes;
• bleeding of different locations (gastrointestinal, uterine, rectal, pulmonary);
• mental disorders (hallucinations);
• with late diagnosis and without adequate treatment, a person develops a clinical picture of encephalopathy, coma, and even death.

Endotoxin intoxication occurs in three stages:

1. The first occurs after surgical intervention or mechanical damage. There are no symptoms of metabolic disorders. The development of an inflammatory process can be suspected only after taking blood from the patient. IN general analysis leukocytosis and increase in ESR, which indicates inflammation.
2. The second stage develops when toxins enter the bloodstream. Blood carries harmful substances to all organs and tissues. In people with reduced immunity, a clear clinical picture of intoxication is observed.
3. The third stage is characterized by destruction internal organs(cardiogenic, pancreatogenic shock, acute hepatic and renal failure). Treatment is aimed at maintaining vital functions (respiration, cardiovascular system). Perform mechanical ventilation, tracheal intubation, hemodialysis.

Endointoxication requires an integrated approach to treatment, hospitalization in the intensive care unit. Depending on the severity, degree, and stage of the disease, further treatment tactics are determined. It is imperative to identify the source of inflammation in order to remove it surgically or conservatively. Timely elimination of the root cause helps to fully recover and prevent the development of unwanted complications. Symptomatic therapy + detoxification strengthens the result.

Autointoxication

Autointoxication is a pathological condition that occurs as a result of poisoning of the body with its own metabolic products. There are several types of this pathology:

1. The occurrence of retention autointoxication is associated with disruption of excretory processes (kidneys) and metabolic delay (anuria, uremia).
2. Intestinal autointoxication appears during suppuration, tissue decay, and absorption of rotting products from the intestines and stomach. The intestine contains many substances that, for one reason or another, are not excreted from the body, but enter the bloodstream and cause endogenous intoxication. Such phenomena are observed with intestinal obstruction, prolonged constipation, dysbacteriosis, malabsorption syndromes and maldigestion.
3. People with diabetes mellitus and diffuse toxic goiter suffer from metabolic disorders. Endocrine diseases always accompanied by hormonal dysfunction and accumulation of harmful substances.
4. Autointoxication during pregnancy is distinguished separately. A woman’s body can perceive a child as a foreign object.
5. Intoxication manifestations occur when the body is colonized by bacteria and their metabolic products. In most cases, the process is a combined pathology. In etiology cholelithiasis secrete a microbial factor + mechanical retention of bile + impaired absorption.

Distinctive signs of the disease:

• the patient becomes irritable, aggressive, notes unreasonable weakness, headaches;
• Digestion is disturbed (poor appetite, nausea, vomiting). A person is losing weight before our eyes;
• suffers from intoxication nervous system, paresthesia, neuralgia and other disorders appear.

Active therapeutic measures are aimed at eliminating the primary cause: drainage and washing of cavities with pus, surgery on organs abdominal cavity. Often it is necessary to resort to transfusion of transfusion media (erythrocytes, plasma, platelets) or plasmapheresis.

1. A mild degree of intoxication is characterized by a satisfactory condition of the patient. The clinical picture is not expressed. Pulse, respiratory rate, blood pressure are normal. Hepatic, renal, pancreatic enzymes rise to the upper limit of normal. The general blood test showed slight leukocytosis and increased ESR. Diuresis is not impaired.
2. The average degree is manifested by changes in the skin (become pale), dry, and there may be rashes. The pulse rises to 100 beats per minute (the norm is 60-80), the respiratory rate is 20-30 (the norm is 16-20), blood pressure decreases slightly. IN biochemical analysis blood levels of kidney and liver enzymes increase. Diuresis decreases.
3. Severe - characterized by the serious condition of patients. The clinical picture is manifested by symptoms of shock (low blood pressure, rapid pulse, tachypnea, anuria). Endogenous products poison the blood and internal organs, the patient falls into a coma. Under treatment this state only in intensive care.

Consequences and complications

Acute intoxication with endogenous substances threatens serious complications and an unfavorable prognosis for recovery and work activity. When the disease is detected in the initial stages, with proper treatment the body quickly recovers. Advanced stages require long-term therapy. The problem is that the inflammatory process of an endogenous nature is not easy to identify.

The main complications of endogenous metabolic intoxication include:

• chronic renal failure;
• hepatic encephalopathy;
• cardiovascular disorders (myocarditis, endocarditis, cardiomegaly);
• development of pneumonia, bronchitis;
• relapses of chronic pancreatitis, cholelithiasis.

An endogenous type of intoxication is a pathological condition that occurs as a result of the impact of one’s own metabolic products on organs and tissues.

The development of intensive care and resuscitation, expanding the limits of resuscitation, revealed a number of unresolved problems. One of them should be considered the problem of endogenous intoxication (EI).

The modern concept of EI is associated, first of all, with the concept of multiple organ failure or multiple organ failure, or the 80-year-old syndrome, or MOF syndrome. This implies the simultaneous or sequential onset of failure of the heart, lungs, liver, kidneys, brain, which leads to high mortality - from 60 to 80% or more. Moreover, mortality is directly dependent on the number of organs involved in this syndrome.

It should be noted that among the components of multiple organ dysfunction syndrome (MODS), priority is traditionally given to circulatory and respiratory disorders, which develop in 60% and 65% of cases, respectively. However, it is considered a reliably established fact that the failure of the liver, kidneys, and digestive tract, which accompany MODS in 60%, 56% and 53% of cases, respectively, play a significant role in the outcome of multiorgan damage syndrome. Thus, failure of metabolic homeostasis due to hepatic-renal failure is as common as cardiopulmonary failure. However, the clinical picture of metabolic disorders does not manifest itself as clearly as respiratory and circulatory disorders, especially in the early stages of its development. Therefore, the diagnosis of impaired metabolism, as a rule, lags behind the events of developing processes. This leads to a statement of facts in cases of far-reaching or already irreversible changes that determine the outcome of diseases.

EI can be defined as a syndrome of inconsistency between the formation and elimination of both products of “normal” metabolism and substances of impaired metabolism, which is nonspecific in terms of most clinical, biochemical and immunological manifestations.

The essence of EI is based on the concept of representing it as a reflection of the consequences of disturbances in macrocirculation and microhemolymphocirculation, gas exchange and oxygen budget, immunity and anti-infective “defense” with failure to manage the integration of these processes. In this case, metabolic disorders occur in accordance with the nature of the damaging factor and the response of the macro- and microcirculation system to it in accordance with the disruption of transport and extraction of oxygen by tissues, activation of the sympathetic-adrenal system. This leads to hypermetabolism syndrome, typical for a critical condition - the need of tissues for various substrates to provide compensatory and adaptive mechanisms for energy conservation, prevent the breakdown of proteins, and reduce utilization fatty acids, increasing gluconeogenesis and glucose tolerance, intensifying endothelial permeability.

Depending on the predominance of the mechanism of EI formation, the following forms are conventionally distinguished: retention, exchange, resorption, sepsis, mixed.

The retention mechanism provides mainly a violation of the natural mechanism of removal, as a rule, of the end products of metabolism of low molecular weight compounds (molecule size less than 10 nm, molecular weight [MM] less than 500 daltons). The main route of their elimination is renal filtration and excretion.

The metabolic mechanism is characterized by the accumulation of intermediate metabolic products(molecule size - more than 10 nm, mm - less than 500 daltons), the elimination of which is carried out by the liver and through the alimentary canal.

intoxication endogenous marker

Resorption EI is accompanied by the accumulation of toxins with a molecular weight of more than 500 daltons and a molecular size of more than 200 nm due to the absorption of tissue and cell destruction products.

The infectious component of EI is caused by microbial toxins, including molecules up to 200 nm with MW up to 500 daltons.

Thus, the list of autointoxication substances can be dozens of names, and the level of their “toxic” concentration can be increased hundreds of thousands of times.

Conventionally, 5 classes of endotoxins can be distinguished: 1) substances of normal metabolism in non-physiological concentrations (urea, lactate, glucose, creatinine, bilirubin, etc.); 2) products of impaired metabolism (aldehydes, ketones, acids); 3) immunologically foreign substances (glyco- and lipoproteins, phospholipids); 4) enzymes; 5) inflammatory mediators, including cytokines, biogenic amines, antibodies, circulating immune complexes, adhesion molecules, protein degradation products and others.

In this regard, determining the essence of EI requires taking into account the state of natural detoxification, which includes three interconnected systems: monooxygenase, immune, and excretory.

The activities of the monooxygenase system of microsomal oxidation and immunity are coupled and functionally coordinated to ensure the recognition of toxins with their subsequent sorption and excretion by the liver, kidneys, skin, lungs, spleen, digestive tract. At the same time, the differences between the monooxygenase and immune systems are determined by the recognition of target toxins: the microsomal system metabolizes free xenobiotics and low molecular weight substances, and the prerogative of the immune system (macrophage-lymphocyte complex) is the recognition and neutralization of compounds conjugated with a macromolecular carrier. The essence of these processes is explained by: the theory of non-infectious immunity, including ideas about immunological tolerance (P. Medawar et al., Nobel Prize in Immunology, 1953), immunological surveillance of the genetic constancy of the integrity of the body (F. Bwenet, Nobel Prize in Immunology, 1960); theory of natural immunity to low molecular weight compounds (I.E. Kovalev, 1970), discovery of a cytokine-mediated signaling system in the immune response, hematopoiesis, inflammation. These theories define the role of immune mechanisms in ensuring “chemical” homeostasis, and the immune system is seen as integral component detoxification systems that recognize and neutralize macromolecules of compounds conjugated to a macromolecular carrier.

It becomes clear that disruption of the relationship between monooxygenase and immune systems determines the discrepancy in the rate of formation and elimination of both pathological and physiological metabolic products in fluid sectors and tissues.

Similarities in the reaction to toxins can be traced in the nature of the immune and microsomal systems. In both the first and second systems, the induction of specific proteins occurs that ensure the binding and metabolism of the indicator molecule. Memory for xenobiotics metabolized by the monooxygenase system is similar to immune memory: repeated administrations of a low molecular weight xenobiotic are more powerful than the first time, activating enzymes of the monooxygenase system, just as the height of the immune response increases with repeated administration of an antigen.

Various xenobiotics, when interacting with oxidases, compete for binding sites, and antigens compete in inducing antibody synthesis.

In addition, numerous low-molecular compounds are capable of inducing an immune response, and immunocytes can produce immunoglobulins. Liver cells that metabolize xenobiotics synthesize albumin, the main protein of plasma detoxification, reminiscent of immunoglobulins, but with lower specificity.

These facts are evidence that microsomal oxidation and immunity - equivalent components of the detoxification system - provide the corresponding link in metabolic homeostasis.

In this case, a violation of the relationship in the system between the monooxygenase and immune links is manifested by a discrepancy between the rate of accumulation of both pathological and physiological metabolites through their biotransformation and excretion. This leads to the accumulation of pathological products of cellular decay, endotoxins, pyrogens, and biologically active substances in tissues and fluid sectors various types, neurotransmitters, free radicals and other products.

The result of this is two processes affecting the cells of the monooxygenase system and immunity: uncoupling of redox phosphorylation, which leads either to cell death or to a decrease in its functional activity, as well as, possibly, direct toxic damage to cell structures. The consequence of this is, on the one hand, a violation of the biochemical composition of cells, tissues, including blood cells; on the other hand, a violation of antibody production, lymphocytotoxicity, and a violation of the synthesis of response mediators.

Consequently, EI develops either as a result of an imbalance in the components of the detoxification system, or due to the failure of one of the links, or simultaneously all its components. This determines the essence of EI, its general and distinctive features depending on the underlying cause, i.e. etiology of the disease, as well as the degree of its severity according to the number of organs and components of detoxification involved in the pathological process (Fig. 1).

Along with this, the place of the microbial factor in the structure of endogenous intoxication in a critical condition of any origin should be especially noted. The microbial factor constitutes one of the so-called paradoxes of critical illness:

• * bacteremia sooner or later always accompanies a critical condition;
• * treatment of infection does not increase survival;
• * the trigger for multiple organ failure (MOF) is not necessarily an infection.

The role of the microbial factor is transformed, first of all, due to the release of endotoxins and/or exotoxins, the molecules of which can imitate the structures of enzymes, hormones, neurotransmitters, disrupting physiological metabolic processes.

Thus, exotoxin is the secretion of a living microorganism; it is a thermolabile protein that is highly immunogenic and disrupts intracellular metabolic processes through enzyme-irreversible transformation of A5DF; lytic enzymes damage the cytoplasmic membrane and block synaptic transmission of motor neurons due to inhibition of neurotransmitters (Fig. 2, 3).

Endotoxin is a complex complex of the shell of a microorganism with an active substance - liposaccharide LPS, lipid A. This toxin is thermolabile, it lacks immunogenicity, the main points of its application are endothelial cells and immune response cells. As a result of its effect on monocytes/macrophages, endotoxin ensures the release of biologically active substances: interleukins, leukotrienes, prostaglandins, TNF-, oxygen metabolites, platelet activating factor, serotonin, von Willebrand factor, nitric oxide, Hageman factor, lysosomal enzymes (Fig. 2, 3) .

The liposaccharide substance is integral part membrane toxin of gram-negative microorganisms. Gram-positive microbes are the source of a number of toxins, including toxin-1, pyrogenic endotoxin, L-toxin, O-streptolysin, L-hemolysin, lymphotoxin, shock toxin, teichionic acids (Fig. 4).

When assessing the role of endotoxins of microbial origin in the development of EI syndrome, one should take into account the fact that under physiological conditions, gram-negative microbes inhabit the surface of the skin and mucous membrane, being a source of endotoxin, which in a “physiological” concentration of 0.001 mg/kg stimulates polymorphonuclear leukocytes, macrophages, and other cells immune natural defense, coagulation system, myelopoiesis. However, with an increase in endotoxin concentration due to the failure of antiendotoxin immunity, EI is formed.

Thus, EI, as a component of a critical condition of any origin, develops as a result of the failure of the main components of the detoxification systems: monooxygenase, excretory and immune - to utilize and eliminate both the products of normal and impaired metabolism, and microbial toxins.

Conventionally, indicators reflecting the state of the detoxification system can be divided into:

• * biochemical markers of EI;
• * immunological markers of EI;
• * integral markers of EI.

It is not only toxic substances that enter the body from the external environment that can cause harm to the human body. Intoxication of the endogenous format, not detected in time, is especially dangerous, because may provoke development dangerous pathologies.

Endogenous intoxication (according to ICD-10 code X40 - 49) is a pathology, the development of which leads to the penetration of toxic substances into the body not from environment, but to the formation directly in it. ICD – international classification of diseases, normative document, consisting of 21 sections.

Harmful substances accumulate at the cellular level in the internal organs, and various inflammatory processes, intoxication. Toxins move through the body extremely quickly. Most often, endotoxicosis occurs in people with weak immunity, healthy person successfully avoids trouble.

As a rule, main reason the course of acute or chronic forms of any disease occurs. In order for the negative symptoms to disappear and the body to begin to function correctly and actively, correction of the functioning of the internal organs is required with the help of medicines or surgical intervention.

Distinctive Features

Developing against the background of acute inflammatory processes, endogenous intoxication syndrome leads to multiple irreversible processes if treatment is not carried out in a timely manner. Endogenous toxins contribute to the decomposition of tissues in the immediate vicinity, resulting in poisoning of all organs. The center of the disease most often becomes the abdominal cavity, from where the disease spreads through the structural renal elements, hepatocytes. The cardiac, vascular, and nervous systems are also affected. Malaise is diagnosed mainly during toxic-dystrophic tissue decomposition. The central site of spread of the disease is considered to be the primary infected organ, which includes the greatest accumulation of toxins.

Causes

In surgical patients, the phenomenon occurs much more often than in other medical areas. Self-poisoning can occur due to diseases - sources:

• High degree burns.
• Injuries caused by prolonged compression or bruises.
• Acute stage of pancreatitis.
• Inflamed layers of the peritoneum.
• Benign or malignant tumors.
• Operations for the introduction of donor organs.

Due to the fact that specified disease more often manifested in surgery, do not forget about the sources in the medical department:

• Hospital infection.
• Medical staff in contact with the patient.

• Instruments for operations, suture threads.
• Bedding.
• Exogenous factor, including the state of the environment.

Among the main reasons is oncology in the last stages: the tumor begins to decompose and the whole body is poisoned.

Sources of internal intoxication

The pathological syndrome develops due to the constant release of toxins by damaged cells and tissues.

Toxic substances that systematically destroy human internal organs include:

• Metabolic products in high concentrations (bilirubins, uric acid salts).
• Accumulating due to improper metabolism (free ammonia, aldehydes).
• Compounds, the formation of which occurs due to cell breakdown during disruption of tissue integrity (protein cation, indoles, lipase).
• Substances that provide regulation of the vital system in excessive concentrations (activated enzyme).
• Products of oxidation of fat-soluble compounds.

Stages of occurrence

Doctors divide the pathogenesis of the disease into three main stages of development: acute, subacute and chronic. Each is characterized by features and signs of progression:

Self-medication for endogenous intoxication is strictly contraindicated due to the possibility of complications. To eliminate the disease, hospitalization and medical observation are required.

There is a concept called endotoxicosis. This is the extreme stage of SEI, when the body falls into a critical state, being unable to provide independent compensation for the emerging hemostasis disorders.

Symptoms and signs

Depending on the stage of poisoning, the severity of symptoms also changes.

Acute endogenous intoxication:

• Severe bowel dysfunction is manifested by attacks of nausea, vomiting, bloating, diarrhea or constipation.
• The appearance of chills, cold sweat and increased sweating.
• Hyperthermia, feverish state.

• Severe painful spasms are concentrated in various parts of the body.
• Tremor of the limbs.
• Sudden changes in pressure.

The presence of pathology is additionally determined by the manifestation of convulsions, paralysis, joint and muscle pain. There is a high probability of fainting, coma, pulmonary and cerebral edema.

The most common is chronic endogenous intoxication. The main symptoms appear:

• Disorders of the gastrointestinal tract, duodenum, large and small intestines.
• The appearance of depression, mood swings, feelings of weakness and fatigue, lethargy.
• Chronic headaches.
• Pallor and dry skin.
• A sharp decrease in body weight.
• The appearance of arrhythmia, hypotension or hypertension.

The process also affects appearance the patient experiences rashes, hair loss, and splitting of nails.

Diagnostics

Before prescribing treatment, a thorough diagnosis is carried out. Several examination methods are used:

• Using computed tomography or magnetic resonance imaging.
• Examination of internal organs using ultrasound.

• X-ray with contrast agents.
• Electroencephalogram.
• Laboratory tests of urine, blood, internal tissue taken, etc.

First aid and treatment

The concept of therapy for this pathology involves identifying and eliminating the source of toxins that poison the body. The primary goal is to diagnose and treat the disease, the result of which involves the formation of harmful substances. More often, a method of surgical intervention is used for this, which means washing the inflamed tissues or removing purulent contents from the body. Special ones are also used medicinal solutions, probe, sorbents, antibacterial drugs, along with vitamins and minerals. After which the patient’s blood is cleansed of the toxic substances it contains. In severely advanced conditions, it is permissible to use hemodialysis in intensive care conditions.

Non-drug treatment

To correct the situation and prevent its recurrence in the future, you need surgical intervention and adherence to the rules of a healthy lifestyle. The patient must follow nutritional rules.

The basis of the diet is dietary dishes and foods prepared by steaming. Also does not accommodate abundant amounts of fresh fruits and vegetables.

Consequences and prevention

If you do not see a doctor in time to start a complex of treatment, delay leads to serious consequences. Dangers include: liver and kidney failure, blood poisoning and huge amount diseases. In some cases, even death.

At healthy life, absence bad habits and treatment of diseases, endogenous poisoning cannot occur. In view of this, there are simply no special preventive measures. Therefore, to prevent the development of the disease, the main thing is to consult a doctor on time and not delay treatment.