Systemic Inflammatory Response Syndrome (CERD), or simply sepsis, is a terrible and life-threatening disease (or condition) known as blood poisoning. CVD begins as mild sepsis, but the immune response caused by an infection - most often bacteria, but sometimes viruses, parasites or fungi - can build up very quickly. [
Definition: in case of sepsis, the immune system begins to intensively fight the infection, resulting in an extensive inflammatory process throughout the body that stimulates the formation of microscopic blood clots. Microscopic blood clots begin to block small blood vessels called capillaries, weakening the flow of blood and oxygen and causing malfunctioning of vital organs (resulting in tissue death), for example: brain, heart and kidney tissues, as well as tissues of the hands, feet, fingers arms and legs. Sepsis occurs when the body's own chemicals enter the bloodstream to fight infection and initiate inflammation in the immune system throughout the body. Mild sepsis can sometimes quickly lead to another condition called “shock” or “septic shock”, causing blood pressure to drop so low that it can lead to death.
Inflammation can kill a person, not just dangerous microbes. Inflammation is the body’s natural defense against disease, necessary to fight germs, however, if the reaction is excessive, it can also lead to [your] death!
Mild sepsis begins as a “complication” of seemingly less serious infections - it develops while the body is struggling with the initial infection.
What are these simple words?
Sepsis is a general infection of the body in which the infection spreads with the blood stream. With sepsis, not a single organ is inflamed, but the whole organism.
In 70% of patients, sepsis is a complication of local inflammation: abscess, phlegmon, boils, meningitis, pneumonia, pleurisy, lymphadenitis, etc., as well as the wound process: trauma, surgery, etc. It is important to emphasize that sepsis develops when the body's defenses are depleted (immunity) as a result of a protracted primary inflammatory process. As a rule, this is due to delayed or improper treatment of the primary inflammatory process.
The causative agents of sepsis are various bacteria (staphylococci, streptococci, meningococci, pneumococci, enterococci, Escherichia coli, Salmonella, etc.) and fungi (Candida, Aspergillus, etc.).
Forms of sepsis are classified depending on the location of the primary infectious focus. Based on this feature, primary (cryptogenic, essential, idiopathic) and secondary sepsis are distinguished. In primary sepsis, the entrance gates cannot be detected. The secondary septic process is divided into:
- pleuro-pulmonary - develops against a background of purulent lung diseases (abscessed pneumonia, pleural empyema, etc.)
- odontogenic - due to diseases of the dentofacial system (caries, root granulomas, apical periodontitis, periostitis, periandibular phlegmon, jaw osteomyelitis)
- tonsillogenic - occurs against the background of severe tonsillitis caused by streptococci or staphylococci
- surgical - develops when the infection enters the bloodstream from a postoperative wound
- obstetric and gynecological - occurs after complicated abortions and childbirth
- urosepsis - characterized by the presence of an entrance gate in the genitourinary system (pyelonephritis, cystitis, prostatitis)
- cutaneous - a source of infection are purulent skin diseases and damaged skin (boils, abscesses, burns, infected wounds, etc.)
- peritoneal (including biliary, intestinal) - with localization of primary foci in the abdominal cavity
- rhinogenic - develops due to the spread of infection from the nasal cavity and paranasal sinuses, usually with sinusitis
- otogenic - associated with inflammatory diseases of the ear, often purulent otitis media.
- umbilical - occurs with omphalitis in newborns
By the time of occurrence, sepsis is divided into early (occurs within 2 weeks from the appearance of the primary septic focus) and late (occurs later than a two-week period). In terms of the rate of development, sepsis can be lightning fast (with the rapid development of septic shock and the onset of death within 1-2 days), acute (lasting 4 weeks), subacute (3-4 months), recurring (lasting up to 6 months with alternating decay and exacerbations) and chronic (lasting more than a year).
Sepsis in its development passes through three phases: toxemia, septicemia and septicopyemia. The toxemia phase is characterized by the development of a systemic inflammatory response due to the onset of the spread of microbial exotoxins from the primary focus of infection, in this phase bacteremia is absent. Septicemia is marked by the dissemination of pathogens, the development of multiple secondary septic foci in the form of microthrombi in the microvasculature, and persistent bacteremia is observed. The septicopyemia phase is characterized by the formation of secondary metastatic purulent foci in the organs and bone system.
Causes of sepsis
For the development of sepsis, it is necessary that pathogenic bacteria - pathogens of infection (bacteria, viruses, fungi) enter the body. As a result of mass infection with putrefactive products of the destruction of pathogenic microorganisms and toxins, an inflammatory process occurs.
The inflammatory reaction of the body that occurs in response to the introduction of infectious agents is associated not so much with the pathogens themselves as with the state of the human immune forces. The decrease in protective forces leads to the fact that the body cannot timely localize pathogenic organisms and prevent their spread into various organs.
The following can contribute to the development of sepsis:
- Violation of the rules of antiseptics and asepsis in the treatment of purulent wounds, as well as during surgical interventions.
- Wrong selection of antibacterial agents in the treatment of internal inflammatory processes.
- Immune System Disorders.
The highest likelihood of developing sepsis in people with long-term chronic diseases, in which immunity is observed against this background.
What diseases can be complicated by sepsis:
- Burns, extensive injuries,
- Infectious and inflammatory diseases
- Wounds and ulcers on the skin,
- Pneumonia, purulent formations in the lungs,
- Severe tonsillitis,
- Infectious and inflammatory complications after surgery,
- Purulent otitis media
- Carbuncle, boil,
- Congenital pathologies of the immune system,
- Infection after childbirth, miscarriage, abortion,
- HIV infection
- Oncological diseases.
This list is rather conditional, because sepsis can complicate any infectious and inflammatory process in the body.
For the development of sepsis, certain conditions must be met:
- The presence of a primary focus (source of infection) from which pathogens enter the bloodstream.
- The spread of pathogens with the bloodstream throughout the body.
- The formation of secondary foci, of which in the future pathogens will also spread throughout the body.
- The response of a protective system that responds to the penetration of pathogens by the inflammatory process.
- The inability of the body to build the necessary immune defense and respond in a timely manner to the introduction of pathogens.
To successfully treat a patient, it is first necessary to determine the “gateway” through which sepsis has entered the body, and only then activate the body’s defenses to neutralize harmful pathogens.
Patients' complaints are very diverse, but the main symptoms should be given to the following symptoms of sepsis:
- severe chills
- a change in the patient’s mental state (euphoria or, on the contrary, apathy),
- tired, blank stare
- pallor of the skin,
- hollow cheeks
- hyperemia of the face,
- profuse sweating,
- petechial hemorrhages in the form of stripes and spots on the surface of the forearms and legs.
In addition, sepsis can occur with herpes on the lips, bleeding of the mucous membranes of the oral cavity, shortness of breath, the appearance of seals and pustules on the skin.
Symptoms of sepsis in adults
The clinical course of sepsis can be lightning fast (rapid development of manifestations within 1-2 days), acute (up to 5-7 days), subacute and chronic.
Often there are atypicality or "attrition" of its symptoms (for example, and at the height of the disease there may not be a high temperature), which is associated with a significant change in the pathogenic properties of pathogens as a result of the massive use of antibiotics. Sepsis can occur with the formation of local abscesses in various organs and tissues (infection from the primary focus) - the so-called. septicopyemia, in which the course of sepsis depends on the location of ulcers (for example, an abscess in the brain with corresponding neurological disorders), and without metastatic ulcers - the so-called. septicemia, often with a more rapid course, pronounced general symptoms.
When diagnosing, they distinguish:
- Syndrome of a systemic inflammatory reaction. It is characterized by a change in body temperature (both upward, more than 38 ° C, and downward, below 36 ° C), heart palpitations (more than 90 beats per minute) and breathing (more than 20 breaths per minute), a change in the number of leukocytes in blood (less than 4 × 109 or more than 12 × 109 cells per liter of blood).
- Sepsis. With the same symptoms as in the case of a systemic inflammatory syndrome, one of the known pathogens is found in one of the normally sterile tissues (blood, cerebrospinal fluid, urine ...), signs of peritonitis, pneumonia, purpura and other local inflammatory processes are detected.
- Severe sepsis. It is characterized in the same way as usual sepsis, but with hypotension, hypoperfusion or dysfunction of individual organs.
- Septic shock. The most serious condition, after which every second patient due to a violation of the blood supply to organs and tissues, death occurs. It is determined by the same symptoms as sepsis, when intensive resuscitation measures do not lead to normalization of blood flow and blood pressure. Other signs of septic shock include slower urine production and confusion.
In February 2016, the concepts and diagnostic criteria for sepsis were revised. The concept of a systemic inflammatory response syndrome and severe sepsis is considered irrelevant, the concepts of sepsis and septic shock are given new definitions.
For the detection and diagnosis of sepsis, the use of SOFA and qSOFA scales is recommended.
With the development of sepsis in newborns (the source is a purulent process in the tissues and vessels of the umbilical cord - umbilical sepsis), vomiting, diarrhea, complete abandonment of the baby from the chest, rapid weight loss, dehydration, skin lose their elasticity, become dry, sometimes earthy in color, often local suppuration in the navel, deep phlegmon and abscesses of various localization.
The sepsis factors in newborns include:
- Infectious and inflammatory diseases in a pregnant woman (pyelonephritis, adnexitis, colpitis),
- Signs of amnion infection (dirty water, placenta overlay),
- Community-assisted birth
- Infections in the puerperas (endometritis, mastitis),
- Anhydrous period in childbirth> 6 hours.
The most severe complication of sepsis. The work of all organs, metabolism, blood flow is disrupted.
The highest risk of developing septic shock in elderly people with immunocompromised patients. Up to half of all patients with this complication die.
Symptoms of septic shock:
- an increase in body temperature over 39 ° C,
- or a decrease in body temperature below 36 ° C,
- heart rate more than 90 beats per minute,
- frequent breathing, shortness of breath,
- nausea, vomiting, diarrhea,
- urine reduction
- significant deterioration of the patient’s condition,
- impaired consciousness: at first the patient becomes agitated, claims that everything is in order with him, and then lethargy, lethargy,
- drop in blood pressure
- dryness and pallor of the skin,
- then a cold, sticky sweat occurs
- skin hemorrhages,
- cyanosis of the tips of the fingers, nose, lips, earlobes.
If a patient in a state of septic shock does not immediately receive medical attention, he will die.
Most often it is a complication of thrombophlebitis. With thromboembolism, a piece of a thrombus comes off, enters with a blood stream into the heart, and then into the pulmonary vessels. Reaching a sufficiently small vessel, a blood clot blocks it.
- the skin becomes pale, acquires an ash gray hue,
- cyanosis of the tips of the fingers, nose, lips, earlobes,
- shortness of breath, wheezing
- a cough during which blood can flow out with sputum,
- pain in the half of the chest,
- drop in blood pressure
- an increase in heart rate to 100 beats per minute,
- severe pain behind the sternum,
- heart rhythm disturbance,
- dizziness, tinnitus,
- loss of consciousness, fainting,
- pain under the right rib
- belching, nausea, vomiting.
The course of pulmonary embolism may be different. Sometimes it is not accompanied by practically no symptoms, and sometimes quickly leads to the death of the patient.
It is usually a complication of thrombophlebitis. Often occurs at night.
- impaired consciousness, a state of stupor,
- increased drowsiness
- disorientation in time and space,
- headaches, symptoms resembling meningitis,
- disturbances in movements and sensitivity, reflexes, depending on which vessel the blood clot is stuck in, and which part of the brain was therefore deprived of oxygen.
Diagnosis of sepsis is carried out using laboratory and clinical methods:
- a general blood test allows you to identify the inflammatory picture as a whole,
- blood culture For an accurate diagnosis, it is recommended to do multiple seeding, which allows you to take into account the life cycle of the pathogen at different stages of therapy. Blood is taken from the patient’s vein and subjected to laboratory analysis,
- Bakseeding contained in the purulent focus,
- biochemical blood test (taken from a vein, the analysis is performed on an empty stomach),
- PCR method allows you to isolate the DNA of the pathogen,
- X-ray, ultrasound, computed tomography, MRI are used to search for primary foci.
All these methods allow you to diagnose blood poisoning, including cryptogenic sepsis, and determine how to treat it.
Sepsis is treated only in an infectious or therapeutic hospital, in the intensive care unit and intensive care. The principles of treatment are similar to the treatment of other foci of infection, but the general serious condition and risk of death are taken into account.
For the treatment of sepsis in adults, apply:
- antibiotics at maximum doses given sensitivity, intravenously.
- conduct an active fight against toxicosis,
- activate their own immune system, correct disturbed vital processes.
It is necessary to create peace and isolation, a special diet is prescribed, in case of a serious condition - artificial intravenous nutrition.
It is important to remove the infection from the primary focus, the use of two or more antibiotics, sometimes in combination with hormones.
If necessary, patients receive an infusion of blood plasma, gamma globulin and glucose.
When forming secondary purulent foci, their surgical treatment is necessary - opening abscesses, removing pus and washing the wounds, excising the affected areas.
Prevention of sepsis is based on the correct and timely treatment of local purulent processes and compliance with aseptic conditions during operations and other medical procedures.
The prevention of sepsis can also include the competent use of antibacterial agents. It should be understood that any bacteria and fungi can develop resistance to drugs. The stronger antibiotics we use, the stronger and “smarter” our opponents become. The use of antibiotics of the latest generations without appropriate indications deprives us of the means of struggle in really serious situations when these drugs could save lives. Any antibiotics should be used strictly as prescribed by your doctor.
The main content of modern concepts of inflammation
Inflammation has an adaptive character, due to the reaction of the body's defense mechanisms to local damage. The classic signs of local inflammation - hyperemia, local temperature increase, edema, pain - are associated with:
- morphological and functional rearrangement of endotheliocytes of postcapillary venules,
- coagulation of blood in postcapillary venules,
- adhesion and transendothelial migration of leukocytes,
- complement activation,
- expansion of arterioles,
- degranulation of mast cells.
Особое место среди медиаторов воспаления занимает цитокиновая сеть, контролирующая процессы реализации иммунной и воспалительной реактивности Главные продуценты цитокинов - Т-клетки и активированные макрофаги, а также, в той или иной степени, другие виды лейкоцитов, эндотелиоциты посткапиллярных венул, тромбоциты и различные типы стромальных клеток. Cytokines act primarily in the focus of inflammation and in the reacting lymphoid organs, eventually performing a number of protective functions.
Mediators in small quantities are able to activate macrophages and platelets, stimulate the release of adhesion molecules from the endothelium and the production of growth hormone. The developing acute phase reaction is controlled by the pro-inflammatory mediators IL-1, IL-6, IL-8, TNF, as well as their endogenous antagonists, such as IL-4, IL-10, IL-13, soluble TNF receptors, called anti-inflammatory mediators . Under normal conditions, by maintaining a balance of relationships between pro- and anti-inflammatory mediators, prerequisites are created for healing wounds, destroying pathogenic microorganisms, and maintaining homeostasis. Systemic adaptive changes in acute inflammation include:
- stress reactivity of the neuroendocrine system,
- the release of neutrophils into the circulatory bed from the vascular and bone marrow depot,
- increased leukocytopoiesis in the bone marrow,
- hyperproduction of acute phase proteins in the liver,
- development of generalized forms of the immune response.
The normal concentration of key pro-inflammatory cytokines in the blood usually does not exceed 5-10 pkg / ml. With pronounced local inflammation or the failure of the mechanisms that limit its course, some of the cytokines — TNF-a, IL-1, IL-6, IL-10, TCP-beta, γ-INF — can enter the systemic circulation, exerting long-distance effects for the limits of the primary focus. In these cases, their blood content can be tens or even hundreds of times higher than normal values. With the inability of regulatory systems to maintain homeostasis, the destructive effects of cytokines and other mediators begin to dominate, which leads to impaired permeability and capillary endothelial function, triggering of DIC, the formation of distant foci of systemic inflammation, and the development of organ dysfunction. Secondary humoral factors of systemic inflammation include almost all known endogenous biologically active substances, enzymes, hormones, products and metabolic regulators (more than 200 biologically active substances in total).
The total effects provided by mediators form a systemic inflammatory response syndrome (SVR).
In its development began to distinguish three main stages
Stage 1. Local production of cytokines in response to infection
A special place among inflammatory mediators is occupied by the cytokine network, which controls the processes of realization of immune and inflammatory reactivity. The main producers of cytokines are T-cells and activated macrophages, as well as to some extent other types of leukocytes, postcapillary venule endotheliocytes (PCV), platelets and various types of stromal cells. Cytokines act priority in the focus of inflammation and on the territory of the reacting lymphoid organs, ultimately performing a number of protective functions, participating in the healing processes of wounds and protecting body cells from pathogenic microorganisms.
Stage 2. The release of a small amount of cytokines into the systemic circulation
Small numbers of mediators are able to activate macrophages, platelets, the release of adhesion molecules from the endothelium, and the production of growth hormone. The developing acute phase reaction is controlled by pro-inflammatory mediators (IL-1, IL-6, IL-8, tumor necrosis factor (TNF), etc.) and their endogenous antagonists, such as IL-4, IL-10, IL-13, soluble receptors to TNF and others, called anti-inflammatory mediators. By maintaining balance and a controlled relationship between pro- and anti-inflammatory mediators under normal conditions, prerequisites are created for healing wounds, destroying pathogenic microorganisms, and maintaining homeostasis. Systemic adaptive changes in acute inflammation include stress reactivity of the neuroendocrine system, fever, release of neutrophils into the circulation from the vascular and bone marrow depot, increased leukocytopoiesis in the bone marrow, overproduction of acute phase proteins in the liver, development of generalized forms of the immune response.
Stage 3. Generalization of the inflammatory reaction
With severe inflammation or its systemic failure, some types of cytokines TNF-a, IL-1, IL-6, IL-10, transforming growth factor ß, IFN-y (for viral infections) can penetrate into the systemic circulation, accumulate there in quantities sufficient to realize their long-distance effects. In the case of the inability of the regulatory systems to maintain homeostasis, the destructive effects of cytokines and other mediators begin to dominate, which leads to impaired permeability and function of the capillary endothelium, triggering of DIC, the formation of distant foci of systemic inflammation, and the development of mono- and multi-organ dysfunction. Apparently, any disturbances in homeostasis that can be perceived by the immune system as damaging or potentially damaging can also act as factors of systemic damage.
At this stage of SVR syndrome, from the perspective of the interaction of pro- and anti-inflammatory mediators, it is possible to conditionally separate two periods.
The first, initial - period of hyperinflammation, characterized by the release of ultra-high concentrations of pro-inflammatory cytokines, nitric oxide, which is accompanied by the development of shock and early formation of multiple organ failure syndrome (PON). However, already at the moment there is a compensatory release of anti-inflammatory cytokines, the rate of their secretion, concentration in the blood and tissues is gradually increasing with a parallel decrease in the content of inflammatory mediators. A compensatory anti-inflammatory response develops, combined with a decrease in the functional activity of immunocompetent cells — the period of “immune paralysis”. In some patients, the formation of a stable anti-inflammatory reaction is immediately recorded due to genetic determination or reactivity altered by environmental factors.
The fundamental differences between systemic inflammation and “classic” are expressed in the development of a systemic reaction to primary alteration. In this case, the pro-inflammatory mechanisms lose their protective function of localizing damage factors and themselves become the main driving force of the pathological process.
The accumulation of pro-inflammatory mediators in the blood and the resulting clinical changes are considered as SSVR. The formalization of the nature of inflammation in the form of SSVR was somewhat random, the concept of sepsis syndrome was introduced when trying to more accurately determine the group of patients with sepsis during clinical trials. The next step was decisive - working on the task of determining sepsis, the 1991 conciliation conference of the American College of Chest Physicians / Society Critical Care Medicine, starting from basic research in the field of inflammation, formulated the concept of SSVR, emphasizing its non-specificity.
Pathogenesis of sepsis
A figurative definition of the pathogenesis of sepsis was formulated by I. V. Davydovsky in the 30s of the XX century “Infectious disease is a kind of reflection of bilateral activity, it has nothing to do with either banal intoxication or the attack of an“ aggressor ”that uses poisonous substances.
The causes of infection must be sought in the physiology of the body, and not in the physiology of the microbe. ”
In the XXI century (2001), this definition was reflected in the concept of PIRO (PIRO), which involves 4 pathogenesis of sepsis. Predisposition, including various genetic factors (genetic polymorphism of Tall-like receptors, polymorphism of gene coding IL-1, TNF, CD14, etc.), the presence of concomitant diseases, immunosuppression, age factor, Infection, pathogenicity factors, localization focus, the Response of the body to the infection - CBP syndrome and Organ dysfunction.
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|Pathological process||Clinical and laboratory characteristics|