inflammatory syndrome. Laboratory diagnosis of sepsis

SIRS

Systemic inflammatory response syndrome
(SIRS) is a systemic inflammatory response in
response to various severe damaging
exposure to infectious and non-infectious
nature.

SIRS

SIRS - systemic inflammatory response syndrome
– SIRS (Systemic Inflammatory Response Syndrome) –
systemic response not only to infection, but also to
various extreme effects.

Systemic inflammatory response syndrome (SIRS)

Criteria:
Tachycardia > 90 beats per minute
Tachypnea > 20/min or PaCO2< 32 мм рт. ст. на
background IV L
Temperature > 38.0 °C or< 36,0 °С
The number of leukocytes in peripheral blood
>12 x 109 /l or< 4 х 109 /л
or the number of immature forms > 10%
Presence of at least 2 of these symptoms
confirm the possible presence of sepsis

Sepsis classification criteria (Vincent J.-L. et al., 2001)

Sepsis - SIRS and the focus of infection
Severe sepsis - sepsis + signs
organ failure
Septic shock - severe sepsis +
signs of arterial hypotension
(BPmean less than 90, despite sufficient
infusion supply)
Multiple organ syndrome
insufficiency - insufficiency 2 and
more bodies

Criteria for organ failure

cardiovascular
system
Systolic blood pressure less than 90 mm Hg, within 1 hour, not
despite adequate fluid supply
kidneys
Urine output less than 0.5 ml/kg body weight/hour or creatinine level
more than 0.21 µmol/l
Breath
Respiratory index less than 300, bilateral infiltration
according to X-ray of OGK
Liver
Hyperbilirubinemia more than 30 µmol/l, increase in Ast/AlT in
twice the normal
Metabolism
Decompensated acidosis, lactate more than 2.5 mmol/l
Coagulogram
Platelet count less than 100, 50% decrease from baseline
in two days
CNS
GCS less than 15 points

Theories of sepsis

Bacteriological theory (I.V. Davydovsky, 1928). All
changes occurring in the body are the result of
development of a purulent focus.
Toxic theory (V.S. Saveliev et al., 1976).
Proponents of this theory give great importance not by myself
microorganism, and the products of its vital activity - exo- and
endotoxins.
Allergic Theory (I.G. Royx, 1983). Based on
evidence that bacterial toxins cause
an allergic reaction in the patient's body.
neurotrophic theory. Built on the work
I.P. Pavlova on the role of the nervous system in regulation
neurovascular responses in the body.
Cytokine theory (W. Ertel, 1991)
time dominance. She was nominated for
based on experimental and clinical studies.
The infectious agent itself or through
endotoxin induces the entry into the blood of a significant
the amount of cytokines.

The nature of the infectious agent

Gram (-) - 25-30%
E. coli - 9-27%
Pseudomonas aeruginosa - 8-15
Klebsiella pneumonia - 2-7%
Other enterobacteria - 6-16%
Haemophilus infl. – 2-10%
Gram (+) - 30-50%
Staphylococcus aureus - 19-36%
Other staphylococci - 1-3%
Streptococcus pneumoniae - 9-12%
Other streptococci - 6-11%
Mixed bacterial flora - 25%
Mushrooms (Candida and others) - 1-5%

Sepsis classification

Primary (cryptogenic) occurs relatively
rarely. Its origin is not clear. Supposed to be associated with
autoinfection (chronic tonsillitis, carious teeth).
Secondary sepsis develops against the background of existence in
the body of the purulent focus:
-otogenic
-oral
- sinusogenic
-tonsilogenic
- bronchopulmonary
- enterogenic
-cholangitic
- wound
- burn
-urological
-gynecological
-surgical

2% Lightning (1-3 days)
40% Acute (5-7 days)
50% Subacute (7-14 days)
10-15 Chronic (months)
Origin:
Wound (after a purulent wound).
Postoperative (violation of asepsis).
Inflammatory (after acute surgical infection).
By activator:
Staphylococcal.
streptococcal, etc.
By time of occurrence:
Early (up to 14 days from the onset of the primary focus).
Late (after 14 days from the moment of the appearance of the primary focus).
According to clinical and anatomical features:
Septicopyemia - sepsis with "metastases", i.e. with the formation in
organs and tissues of purulent foci.
Septicemia - sepsis without "metastases", without the formation of purulent
foci (clinically more severe).

PIRO concept (Predisposition, Infection, Response, Organ dysfunction)

PIRO Concept
(Predisposition, Infection, Response,
Organ dysfunction)
Predisposition:
genetic factors
immune imbalance, comorbidity,
age, gender,
socio-economic factors
Infection
Inflammatory response
Organ dysfunction

The pathogenesis of sepsis

Central link - part of the shell of gram (-) bacteria
(endotoxin or lipopolysaccharide). The source of which
is a saprophytic gram-negative flora of the gastrointestinal tract. During the life of the microorganism
some intestinal endotoxin constantly
penetrates into lymphatic system and blood from the portal
veins, despite the fact that the mucosa of the gastrointestinal
path is a powerful barrier. Absence
toxic reactions to the presence of systemic circulation(SK)
LPS is explained by the presence in the body of natural
humoral and cellular anti-endotoxic systems,
able to effectively bind and
detoxify LPS.
With the development of various infectious processes, stress,
as well as diseases of non-infectious origin increases
penetration of intestinal LPS into the SC, which leads to
depletion of antiendotoxin immunity factors,
decrease in the titer of antiendotoxin antibodies.

Endotoxemia

Increasing the concentration of catecholamines.
Spasm of arterioles.
Decreased blood flow.
Sludge syndrome.
Increasing the concentration of acidic
metabolites.
Violation of microcirculation.

LPS circulating in the SC interacts with
plasma lipopolysaccharide-binding
protein (LBP), forming the LBP-LPS complex. Receptor for
complex of LBP-LPS and LPS is a cluster of differentiation
(CD). CD is expressed to varying degrees on the membrane
all cells of the macroorganism, especially abundant on the membrane
monocytes, macrophages, neutrophils. The task of CD is
presentation of LPS and LBP-LPS to the next receptor
complement (CR), which provides transmembrane
signal transmission into the cell.
Since CD is able to form complexes with LPS and with
HSP, it is rightly considered the central launch molecule
inflammatory response.
Cytokines indirectly affect the functional
cell activity and survival, as well as stimulation or
inhibition of their growth. They provide consistency
actions of the immune, endocrine and nervous systems in
under normal conditions and in response to pathological influences, and their
accumulation in the blood is considered by many scientists as SIRS.

The cytokine system includes 5 extensive
classes grouped by their dominant
action in cells
1. Interleukins (IL).
2. Interferons.
3. Tumor necrosis factors (TNF).
4. Chemokines.
5. Colony stimulating factor.
Cytokines cause migration
immunocompetent cells in the focus of inflammation. At
This cytokines activates the vascular endothelium.
Generalized activation of the endothelium
is a key pathogenetic
factor in the development of SIRS.

Substances secreted by the endothelium
controlling vascular tone
(endothelial modulators of vascular tone),
are divided into 2 groups:
1) vasodilators (nitric oxide (NO)),
prostacyclin, undifferentiated
hyperpolarizing factor);
2) vasoconstrictors (endothelin-1, endothelin2, endothelin-3).

Nitric oxide and the pathogenesis of sepsis

Picks
inflammation
iNOS
free radicals
Activity change
enzymes
(HC, COX, etc.)
Nitrogen oxide
Cellular
signals
Other effects
Cytotoxic
effects
decline
adhesion
leukocytes
Oppression
functions
mitochondria
Systemic
vasodilation and
myocardial depression
inhibition of adhesion and
platelet aggregation
multi-organ dysfunction and
septic shock
Feihl F et al.
Pharmacol Ther 2001;91:179-213

Development of DIC

Aggregates of erythrocytes + fibrin;
Activation of the fibrinolytic system;
Release of vasoactive substances from blood clots
damaging the wall of blood vessels;
Depletion of coagulation proteins.

Cellular
link
Endotox
emia
System
coagulation
System
compliment
Cytokines
(TNF, IL-1,
NO)
Damage
cells
Violation
perfusion

The diagnosis of sepsis is beyond doubt in the presence of 3 criteria:
infectious focus, which determines the nature of the pathological
process; SIRS (criterion for penetration of inflammatory mediators into
systemic circulation). signs of organ system dysfunction
(criterion for the spread of an infectious-inflammatory reaction
beyond the primary site).

Laboratory diagnosis of sepsis

UAC
Blood test for sterility (2 days for 3
fence per day)
Seeding of pus and other discharge
Thrombocytopenia, decreased factors
coagulation
Increase in CRP
Determination of the concentration of procalcitonin

Differential diagnosis between
infectious and non-infectious etiology
pathological process accompanied by
development of SIRS, allows you to conduct a test with the definition
procalcitonin (PCT) levels. Procalcitonin
characterized by a short latent period (3 hours
after infection), for a long period
elimination half-life (25 - 30 hours) and is stable
protein in vitro even at room temperature.
Healthy faces 0.5
Chronic inflammatory processes and autoimmune
diseases 0.5
Viral infections 0.5
Small and moderate local infections 0.5
SSVR, polytrauma, burns 0.5-2.0
Sepsis, multiple organ failure 2 (usually 10-100)

Dynamics of plasma concentrations of various markers of sepsis

0
1
2
6
12
24
48
72
PCT, C-reactive protein, TNF, IL-6 and IL-8

Treatment

Therapeutic measures consist of
treatment (antibacterial, immunotherapy,
maintenance of the homeostasis system) and
surgical impact on the foci
infections.
Treatment of patients with sepsis and septic shock
should be carried out under conditions
specialized chambers or block
intensive care using
modern monitoring.

Early and effective treatment of the focus of infection.

Every patient with severe sepsis should be evaluated for
the subject of the presence of a focus of infection, with an assessment of a possible connection
sepsis with a potentially infected object (vascular
catheter, urethral catheter, endotracheal tube,
intrauterine device).
When choosing methods for the rehabilitation of the focus, it is necessary to assess the risk
complications, such as bleeding, fistula formation, etc.
Simultaneously with the search for the focus, a complex is carried out
initial therapy aimed at stabilization
hemodynamics. After identifying the source of severe sepsis or
septic shock, measures are needed to sanitize the focus
must be completed as quickly as possible.
After sanitation of the primary focus, the doctor must constantly remember and
conduct diagnostic search regarding secondary
foci, primarily pneumonia, angiogenic infection,
urinary infection.

Antibacterial therapy

As a rule, on initial stage treatment of a patient with sepsis,
in the absence of bacteriological diagnosis, is prescribed
empirical antibiotic therapy, which
depends on:
spectrum of suspected pathogens depending on
localization of the primary focus;
pharmacokinetic characteristics
antibacterial drugs that provide
penetration and activity in the focus of infection;
previous antibiotic therapy;
the level of resistance of nosocomial pathogens according to
hospital microbiological monitoring data;
conditions for the onset of sepsis - community-acquired or
nosocomial;
the severity of the condition, assessed according to the APACHE II scale, by the presence
multiple organ failure - SOFA scale.

Antibacterial therapy (ABT) should be
started within the first hour, if
diagnosis of severe sepsis.
Antibacterial drugs are prescribed
intravenously.
All patients should receive an adequate dose
antibiotic, taking into account the possible organ
dysfunction. Presence of renal or hepatic
insufficiency usually requires modification
doses and dosing regimen.
Antibacterial therapy should always
be reassessed after 48-72 hours, based on
received microbiological and clinical
data for the purpose of prescribing a narrow-spectrum antibiotic
action spectrum.

Antibacterial therapy for sepsis
carried out until reaching the
positive dynamics
the patient's condition.
Sufficiency criteria
antibiotic therapy may be
presented like this:
stable normalization of body temperature;
positive dynamics of the main symptoms of infection;
no signs of systemic inflammation
reactions;
normalization of the function of the gastrointestinal tract;
normalization of the number of leukocytes in the blood and
leukocyte formula;
negative blood culture.

Infusion therapy

During the first 6 hours of therapy for severe sepsis and septic shock,
the following indicators have been achieved:
Central venous pressure (CVP) 8-12 mm Hg. (108.8 -163.2 mm w.c.)
(in patients on mechanical ventilation, CVP up to 15 mm Hg (204 mm water column) is acceptable)
Average arterial pressure greater than or equal to 65 mmHg
Diuresis greater than or equal to 0.5 ml/kg/hour
Saturation of hemoglobin with oxygen (saturation, SatO2) in the superior vena cava
or mixed venous blood > 70%
Infusion therapy may consist of natural or artificial colloids
or crystalloids. Indicative recommendations for quality composition
infusion program in patients with severe sepsis - colloids / crystalloids
- 1:3, with septic shock - 1:2 and may vary depending on the clinical
situations. The colloid preparations of choice are solutions of the modified
gelatin (Gelofusin) and preparations of hydroxyethyl starch (HES).
The rate of fluid therapy in patients with suspected hypovolemia is
500-1000 ml of crystalloids or 300-500 ml of colloids in 30 minutes and can be
repeated after evaluating response (increased BP, urine output) and tolerability
(no evidence of intravascular fluid volume overload).
In the absence of deficiency coronary circulation, acute blood loss,
correction of anemia is recommended only when the hemoglobin level drops below 70
g/l.
Use of fresh frozen plasma to correct laboratory abnormalities
in the hemostasis system in the absence of bleeding or planned procedures with
risk of bleeding is not recommended. It is not recommended to transfuse
fresh frozen plasma to fill the volume of circulating fluid.
In patients with severe sepsis, platelets should be transfused when
their level is less than 5 * 109 / l, regardless of the presence of a bleeding clinic. If a
platelet count 5-30*109/l, platelet mass is transfused if present
bleeding risk.

Vasopressors

Vasopressor therapy should be
started if against the background of adequate
infusion therapy is maintained
hypotension and hypoperfusion.
It is important to achieve adequate perfusion
by prescribing vasopressors and
achievement of systolic blood pressure of 70 mm Hg.
Dopamine is used in the absence
contraindications (primarily
violations heart rate) at a dose up to
10 mcg/kg/min, hypotension persists or
heart rhythm disturbances,
The drug of choice is adrenaline.
The use of vasopressin can
considered in patients with
refractory shock.

Corticosteroids

intravenous
corticosteroids -
hydrocortisone - 200-300
milligram/day divided by
3-4 injections or as
continuous infusion, during
7 days recommended in patients
with septic shock, in which,
despite adequate
infusion therapy,
there remains a need for
the introduction of vasopressors for
content of adequate
blood pressure.

Recombinant human activated protein C.

Activated protein C, drotrecogin-alpha.
Indication: severe sepsis with PON (APACHE-II
>25).
Pharmachologic effect:
1. indirect anticoagulant
2. profibrinolytic action
3. anti-inflammatory action
The drug is Zigris.
Administration of Zigris 24 mcg/kg/h.

Respiratory support

Target:
SpO2 > 90%, PaO2 > 60 Hg, FiO2< 0,6
Elevated head end 45° (prevention
pneumonia)
IVL:
with respiratory rate > 40 per minute, encephalopathy, SpO2< 90% на фоне
O2
Lung protection:
Vt (VT - Tidal Volume) 6-7 ml / kg, Ppeak (peak pressure
breath)<30 cм H2O, РЕЕР (положительное давление
end of exhalation) - 10-15 cm. water. Art.
with a need for FiO2 > 0.6 - position on the stomach,

Nutritional Support

Nutritional support can be provided
enteral, parenteral or combined
way, depending on the clinical situation.
The calculation of the volume of nutritional support is carried out
taking into account the indicators of the ideal (calculated) mass
bodies:
Protein 1.5-2.5 g/kg/day
Fats 0.5-1.5 g/kg/day
Glucose 2-6 g/kg/day
Energy 30-35 kcal/kg/day (b:g:y=20%:30%:50%)
To monitor nutritional status, it is necessary to assess
dynamics level total protein, blood urea, and
daily urinary excretion of urea (in patients without
signs kidney failure).

Sepsis: prevention of infection

Usage
high quality
disposable consumables
materials in the ICU
(breathing filters,
contours, endotracheal and
tracheostomy tubes).
Maximum
transmission warning
nosocomial infection
patient
Sanitation of the trachea without
ventilator interruptions

Prevention
deep vein thrombosis:
patients with severe
sepsis should be carried out
thrombosis prevention
deep veins
low molecular weight
heparins or low
doses
unfractionated
heparin; shown
use of mechanical
means of prevention
(special
graduated
compression stockings,
intermittent devices
compression),
is a contraindication
the presence of diseases
peripheral vessels.
Prevention of stress
ulcers:
stress ulcer prevention
should be done for everyone
patients with severe
sepsis. Most
effective H2hisaminoblockers.

There are ailments that concern one, specific organ. Of course, a failure in its work in one way or another affects the activity of the whole organism. But a systemic disease is fundamentally different from all the others. What it is, we will now consider. This definition can often be found in the literature, but its meaning is not always disclosed. But this is very important for understanding the essence.

Definition

Systemic disease - what is it? Defeat of one system? No, this definition means a disease that affects the entire body. Here we need to reveal one more term that we need today. All of these diseases are autoimmune in nature. More precisely, some autoimmune diseases are systemic. The rest are organ-specific and mixed.

Today we will talk specifically about systemic autoimmune diseases, or rather, those that appear due to impaired functioning of the immune system.

Development mechanism

We haven't fully explored the term yet. What is it - systemic diseases? It turns out that immunity fails. The human body produces antibodies to its own tissues. That is, in fact, destroys its own healthy cells. As a result of such a violation, the whole organism as a whole is under attack. For example, a person is diagnosed with rheumatoid arthritis", and the skin, lungs and kidneys are also affected.

View of modern medicine

What are the reasons? This is the first question that comes to mind. When it becomes clear what this systemic disease is, you want to know what leads to the development of a serious illness. At least in order to determine the measures of prevention and treatment. But just with the last moment there are a large number of problems.

The fact is that doctors do not diagnose systemic diseases and do not prescribe complex treatment. Moreover, usually people with such ailments get to different specialists.

With diabetes - to the endocrinologist.
For rheumatoid arthritis, see a rheumatologist.
For psoriasis, see a dermatologist.
In autoimmune lung diseases - to a pulmonologist.

Drawing conclusions

Treatment of systemic diseases should be based on the understanding that this is primarily an ailment of the immune system. Moreover, regardless of which organ is under attack, it is not the immune system itself that is to blame. But instead of actively supporting it, the patient, as prescribed by the doctor, begins to take various drugs, antibiotics, which for the most part depress the immune system even more. As a result, we try to act on the symptoms without treating the disease itself. Needless to say, the situation will only get worse.

Five root causes

Let's look at what underlies the development of systemic diseases. Let's make a reservation right away: these reasons are considered as the most probable, since so far it has not been possible to establish exactly what underlies the ailments.

A healthy gut means a strong immune system. It really is. This is not just an organ for removing food residues, but also a gate through which pathogenic microorganisms begin to capture our body. For intestinal health, lactobacilli and bifidobacteria alone are clearly not enough. We need a complete set. With a shortage of certain bacteria, some substances are not completely digested. As a result, the immune system perceives them as foreign. A failure occurs, an inflammatory process is provoked, and autoimmune diseases intestines.
Gluten, or gluten. It often causes an allergic reaction. But it's even deeper than that. Gluten has a similar structure with thyroid tissue, which causes malfunctions.
toxins. This is another common reason. AT modern world There are many ways for them to enter the body.
infections- bacterial or viral, they greatly weaken the immune system.
stress- live in modern city abounds in them. It is not only emotions, but also biochemical processes that take place inside the body. And often they are destructive.

Main groups

The classification of systemic diseases allows you to better understand what violations are in question, which means that you can quickly find a solution to the problem. Therefore, doctors have long identified the following types:

Symptoms of systemic diseases

They can be very different. Moreover, it is extremely difficult to determine at the initial stage that this is an autoimmune disease. Sometimes it is impossible to distinguish symptoms from SARS. In this case, a person is recommended to rest more and drink tea with raspberries. And everything would be fine, but then the following symptoms begin to develop:

Migraine.
Pain in the muscles, which indicates the slow destruction of their tissues.
Development of the lesion cardiovascular systems s.
Next, along the chain, the whole organism begins to collapse. The kidneys and liver, lungs and joints, connective tissue, nervous system and intestines suffer.

Of course, this seriously complicates the diagnosis. In addition, the above processes are often accompanied by other symptoms, so only the most experienced doctors do not get confused.

Diagnosis of systemic diseases

This is not an easy task, it will require maximum commitment from doctors. Only by collecting all the symptoms into a single whole and analyzing the situation well, you can come to the right conclusion. The main mechanism for diagnosis is a blood test. It allows:

Identify autoantibodies, since their appearance is directly related to the activity of the disease. At this stage, possible clinical manifestations. Another important point: at this stage, the course of the disease is predicted.
The doctor should assess the state of the immune system. This will depend on the prescribed treatment.

Laboratory diagnostics - key moment in determining the nature of the disease and drawing up a scheme for its treatment. It involves the evaluation of the following antibodies: C-reactive protein, antistreptolysin-O, antibodies to native DNA, and a number of others.

Diseases of the cardiovascular system

As mentioned above, autoimmune diseases can affect all organs. Systemic blood diseases are by no means rare, although they are often disguised as other diagnoses. Let's look at them in more detail.

Infectious mononucleosis, or monocytic angina. The causative agent of this disease has not yet been found. It is characterized by sore throat, as with angina, leukocytosis. An early sign disease is an increase lymph nodes. First on the neck, then in inguinal region. They are firm and painless. In some patients, the liver and spleen are enlarged at the same time. A large number of altered monocytes are found in the blood, and the ESR is usually increased. Often there is bleeding from the mucous membranes. Systemic blood diseases lead to serious consequences, so it is important to start adequate treatment as soon as possible.
Angina agranulocytic. Another serious disease that is very easy to mistake for a complication after a cold. Moreover, the defeat of the tonsils is evident. The disease begins with high temperature and fever. At the same time, ulcers open in the region of the tonsils, gums and larynx. A similar situation can be observed in the intestine. Necrotic processes can also spread deep into the soft tissues, as well as to the bones.

Damage to the skin

Often they are extensive in nature, and treatment is very difficult. Systemic skin diseases can be described for a very long time, but today we will focus on a classic example, which is also the most difficult in clinical practice. It is not contagious and is quite rare. This is a systemic disease called lupus.

In this case, the human immune system begins to actively attack the body's own cells. This disease primarily affects the skin, joints, kidney and blood cells. Other organs may also be affected. Often lupus is accompanied by arthritis, cutaneous vasculitis, jade, pankartid, pleurisy and other disorders. As a result, the patient's condition can quickly go from stable to very severe.

Symptom this disease is an unmotivated weakness. A person loses weight for no reason, his temperature rises, his joints ache. After that, a rash appears on the nose and cheeks, in the décolleté area and on back side hands
But this is all just the beginning. Systemic skin disease affects the entire body. A person develops ulcers in the mouth, soreness in the joints, the lining of the lungs and heart is affected. The kidneys are also affected, the functions of the central nervous system suffer, regular convulsions are observed. Treatment is often symptomatic. Eliminate completely this disease does not seem possible.

Connective tissue diseases

But the list doesn't end with lupus. Rheumatic diseases are a group of ailments characterized by damage to connective tissue and impaired immune homeostasis. This group includes a large number of diseases. These are rheumatism and rheumatoid arthritis, ankylosing spondylitis, systemic scleroderma, Schegner's disease and a number of other ailments.

All these diseases are characterized by:

The presence of a chronic focus of infections. These can be viruses, mycoplases and bacteria.
Violation of homeostasis.
vascular disorders.
The undulating course of the disease, that is, remission and exacerbation replace each other.

Rheumatism

A very common ailment that some inhabitants associate with joint pain. This is not excluded, but first of all it is an infectious-allergic disease, which is characterized by damage to the heart and blood vessels. Usually the disease develops after a sore throat or scarlet fever. This disease threatens with a large number of complications. Among them cardiovascular failure, thromboembolic syndrome.

Treatment must be under the supervision of the attending cardiologist, because it must include supportive therapy for the heart. The choice of drugs is up to the doctor.

Rheumatoid arthritis

This is a systemic joint disease that develops most often over the age of 40 years. The basis is the progressive disorganization of the connective tissue synovial membranes and cartilage of the joints. In some cases, this leads to their complete deformation. The disease goes through several stages, each of which is somewhat more complicated than the previous one.

synovitis. Occurs in small joints brushes and feet, knee joints. It is characterized by multiple polyarthritis and symmetrical joint damage.
Hypertrophy and hyperplasia of synovial cells. As a result, damage to the articular surfaces occurs.
The appearance of fibro-osseous ankylosis.

Treatment is required complex. These are drugs for restoring immunity, for supporting and restoring bone and cartilage tissue, as well as aids that help improve the functioning of all organs and systems.

Which doctor will treat

We figured out a little about what systemic diseases exist. Of course, medical practitioners also face other autoimmune ailments. Moreover, each of the above has several various forms, each of which will be radically different from the others.

Which doctor will contact for diagnosis and treatment? If it comes to systemic forms of the disease, then several specialists will have to be treated. Each of them will make their own recommendations, and the task of the therapist is to draw up a treatment plan from them. To do this, you will have to visit a neurologist and a hematologist, a rheumatologist and a gastroenterologist, a cardiologist and a nephrologist, a pulmonologist and a dermatologist, as well as an endocrinologist.

Instead of a conclusion

Systemic, autoimmune diseases are among the most difficult to diagnose and treat. To determine what is the cause of the ailment, you will have to conduct a series of examinations. But the most revealing is the blood test. Therefore, if you feel bad, everything hurts, and there is no improvement, then consult a doctor for a referral for tests. If a specialist suspects that you have one of the listed diseases, he will send you to additional examination to narrow specialists. As the examination progresses, the treatment plan may gradually change.

Among surgical diseases, a significant place is occupied by acute inflammatory diseases abdominal organs and thoracic cavities, soft tissues of the body. Achievements in molecular biology have provided a basis for revising previous ideas about the essence of inflammation and the regulation of the immune response to it. It has been established that intercellular relationships are a universal mechanism that determines the physiological and pathological processes in the body.

The main role in the regulation of intercellular relationships is played by a group of protein molecules called the cytokine system. In this regard, we considered it appropriate, before presenting particular issues of inflammatory diseases, to give brief information about modern ideas about the essence of inflammation and the regulation of the immune response to it.

The body's response to inflammation, regardless of location inflammatory process, develops in accordance with the general laws inherent in any acute inflammation. The inflammatory process and the response to it develop with the participation of numerous inflammatory mediators, including the cytokine system, according to the same patterns, both during the introduction of an infection and under the influence of trauma, foci of tissue necrosis, burns and some other factors.

Clinical manifestations of acute inflammatory diseases, along with symptoms common to inflammation, have specific symptoms due to damage to one or another organ, its localization: for example, with acute appendicitis and acute cholecystitis, the common inflammation symptoms are pain, fever, leukocytosis, increased pulse rate. During the physical examination, symptoms specific to each disease are revealed, allowing to differentiate one disease from another. The body's response to inflammation the functions of the vital systems of the body are not disturbed, called local.

With phlegmon or gangrene of the affected organ, the symptoms characteristic of inflammation become more pronounced, usually begin to appear signs of impaired function of vital body systems in the form of significant tachycardia, tachypnea, hyperthermia, high leukocytosis. The response to severe inflammation becomes systemic and flows like a heavy common disease inflammatory nature, involving in the response almost all body systems. This type of reaction, at the suggestion of the conciliation commission of American surgeons (1992), is called syndrome of the body's systemic response to inflammation (Sys temic Inflammatory Response Syndrome - SIRS).

Inflammation is an adaptive reaction of the body aimed at destroying the agent that caused the inflammatory process and restoring damaged tissue.

The inflammatory process, developing with the obligatory participation of inflammatory mediators, may be accompanied by a predominantly local reaction with typical local manifestations of the disease and moderate, inconspicuous general reaction organs and systems of the body. The local reaction protects the body, frees it from pathogenic factors, delimits "foreign" from "own", which contributes to recovery.

mediators of inflammation. AT this group includes many active chemical compounds: 1) cytokines (pro-inflammatory and anti-inflammatory); 2) interferons; 3) eicosanoids; 4) active oxygen radicals; 5) blood plasma complement; 6) biologically active substances and stress hormones (histamine, serotonin, catecholamine, cortisol, vasopressin, prostaglandins, growth hormone); 7) platelet activating factor; 8) nitrogen monoxide (N0), etc.

Inflammation and immunity function in close interaction, they cleanse the internal environment of the body both from foreign elements and from damaged, altered tissues with their subsequent rejection. and elimination of the consequences of damage. Normally functioning control mechanisms of the immune system prevent the uncontrolled release of cytokines and other mediators of inflammation, provide an adequate local response to the process (see diagram).

Local reaction of the body to inflammation. The penetration of infection and the impact of other damaging factors cause complement activation, which in turn promotes the synthesis of C-reactive proteins (C-3, C-5), stimulates the production of platelet activating factor, the formation of opsonins involved in the process of phagocytosis and chemotaxis. The main task of the inflammatory phagocytic reaction is to remove microorganisms and limit inflammation. During this period, transient bacteremia may appear. Microorganisms that have penetrated into the blood are destroyed by neutrophilic leukocytes, macrophages, freely circulating in the blood, and Kupffer cells, which act as macrophages. The most important role in the removal of microorganisms and other foreign substances, as well as in the production of cytokines and various inflammatory mediators, belongs to activated macrophages, both freely circulating in the blood and resident, fixed in the liver, spleen, lungs, and other organs. It should be emphasized that Kupffer cells, which are resident macrophages, make up more than 70% of all macrophages in the body. They play the main role in the removal of microorganisms in the event of the appearance of transient or persistent bacteremia, degradation products of proteins, xenogeneic substances, neutralization of endotoxins.

Simultaneously with the activation of complement, activation of neutrophils and macrophages occurs. Neutrophils are the first phagocytic cells that appear in the focus of inflammation, they release active oxygen radicals, which lead to damage and at the same time to the activation of endothelial cells. Neutrophils begin to secrete pro-inflammatory and anti-inflammatory interleukins (IL) related to the cytokine system. At the same time, anti-inflammatory drugs are able to weaken the action of pro-inflammatory interleukins. Thanks to this, their balance and a decrease in the severity of inflammation are achieved.

macrophage activation. Macrophages appear in the lesion within 24 hours from the onset of the inflammatory response. Activated macrophages carry out the transcription of antigens (bacteria, endotoxins, etc.). Through this mechanism, they present antigens to lymphocytes, promote their activation and proliferation. Activated T-lymphocytes acquire significantly greater cytotoxic and cytolytic properties, sharply increase the production of cytokines. B-lymphocytes begin to produce specific antibodies. In connection with the activation of lymphocytes, the production of cytokines and other mediators of inflammation increases sharply, hypercytokinemia occurs. Inclusion of activated macrophages in developing inflammation is the line between local and systemic response to inflammation.

The interaction of macrophages with T-lymphocytes and "natural killer" cells, mediated by cytokines, provides the necessary conditions for the destruction of bacteria and the neutralization of endotoxins, the localization of inflammation, and the prevention of infection generalization. An important role in protecting the body from infection is played by natural (natural) killer cells (Natural Killer - NK cells). They come from bone marrow and represent a subpopulation of large granular lymphocytes, which, unlike killer T-cells, are capable of lysing bacteria and target cells without prior sensitization. These cells, like macrophages, remove particles and microorganisms alien to the body from the blood, provide adequate production of inflammatory mediators and local protection against infection, maintain a balance between pro-inflammatory and anti-inflammatory inflammatory mediators. Thus, they prevent the disruption of microcirculation and damage parenchymal organs an excessive amount of cytokines produced, localize inflammation, prevent the development of a severe general (systemic) reaction of vital organs in response to inflammation, and prevent the development of dysfunction of parenchymal organs.

Great importance for regulation acute inflammation through the tumor necrosis factor, they have a protein molecule known as nuclear factor kappa B (Nuclear factor k-kappa B), which plays an important role in the development of systemic inflammation reaction syndrome and multiple organ dysfunction syndrome. For therapeutic purposes, it is possible to limit the activation of this factor, which will lead to a decrease in the production of inflammatory mediators and may have a beneficial effect in reducing tissue damage by inflammatory mediators and reducing the risk of developing organ dysfunction.

The role of endothelial cells in the development of inflammation. Endothelial cells are a link between the cells of parenchymal organs and platelets, macrophages, neutrophils, cytokines and their soluble receptors circulating in the bloodstream, therefore the endothelium of the microvasculature reacts subtly both to changes in the concentration of inflammatory mediators in the blood and to their content outside the vascular bed.

In response to injury, endothelial cells produce nitric monoxide (NO), endothelium, platelet activating factor, cytokines, and other mediators. Endothelial cells are at the center of all reactions that develop during inflammation. It is these cells, after being stimulated by their cytokines, that acquire the ability to "direct" leukocytes to the site of injury.

Activated leukocytes located in the vascular bed make rotational movements along the surface of the endothelium of the microvasculature; there is a marginal standing of leukocytes. Adhesive molecules are formed on the surface of leukocytes, platelets and endothelial cells. Blood cells begin to adhere to the walls of the venules, their movement stops. In the capillaries, microthrombi are formed, consisting of platelets, neutrophils and fibrin. As a result, first, in the area of the focus of inflammation, blood circulation in the microcirculatory bed is disturbed, capillary permeability increases sharply, edema appears, leukocyte migration outside the capillaries is facilitated, and typical signs of local inflammation appear.

In severe aggression, hyperactivation of cells producing cytokines and other inflammatory mediators occurs. The amount of cytokines and nitric monoxide increases not only in the focus of inflammation, but also outside it in the circulating blood. Due to the excess of cytokines and other mediators in the blood, the microcirculatory system of organs and tissues outside the primary focus of inflammation is damaged to some extent. Vital function is impaired important systems and organs, the syndrome begins to develop systemic response to inflammation (SIRS).

At the same time, against the background of pronounced local signs of inflammation, there is a violation of the function of the respiratory and cardiovascular systems, kidneys, liver, and inflammation proceeds as a severe general disease involving all functional systems organism.

Cytokines are relatively large protein molecules with a molecular weight of 10,000 to 45,000 daltons. In terms of chemical structure, they are close to each other, but they have different functional properties. They provide interaction between cells that are actively involved in the development of local and systemic responses to inflammation by enhancing or inhibiting the ability of cells to produce cytokines and other inflammatory mediators.

Cytokines can affect target cells - endocrine, paracrine, autocrine and intercrine action. The endocrine factor is secreted by the cell and affects the target cell located at a considerable distance from it. It is delivered to the target cell by the blood stream. The paracrine factor is secreted by the cell and affects only nearby cells. An autocrine factor is secreted by a cell and affects the same cell. The intercrine factor acts inside the cell without leaving it. Many authors consider these relationships as "microendocrine system".

Cytokines are produced by neutrophils, lymphocytes, endothelial cells, fibroblasts, and other cells.

Cytokine system includes 5 broad classes of compounds, grouped according to their dominant effect on other cells.

1. Cytokines produced by leukocytes and lymphocytes are called interleukins (IL, IL), because, on the one hand, they are produced by leukocytes, on the other hand, leukocytes are target cells for IL and other cytokines.

Interleukins are subdivided into inflammatory(IL-1,6,8,12); anti-inflammatory (IL-4,10,11,13, etc.).

Tumor necrosis factor [TNF].

Factors of growth and differentiation of lymphocytes.

Factors stimulating the growth of macrophage and granulocyte populations.

5. Factors causing the growth of mesenchymal cells. Most cytokines belong to IL (see table).

Table

	Place of synthesis	target cells
GM-CSF (identical in effect to IL-3) Interferons-al-fa, beta, gamma	fibroblasts, monocytes Endothelium, fibroblasts, Bone marrow, T-lymphocytes Epithelial cells, fibroblasts, lymphocytes, macrophages, neutrophils Endothelial cells, keratin cells, lymphocytes, macrophages	Predecessor of CFU-G Cell precursors of granulocytes, erythrocytes, monocytes CFU-GEMM, MEG, GM Lymphocytes, macrophages, infected and cancerous cells Monocytes, macrophages, T and B cells	Supports neutrophil production Supports the proliferation of macrophages, neutrophils, eosinophils and colonies containing monocytes, supports long-term bone marrow stimulation Inhibits the proliferation of viruses. Activates defective phagocytes, inhibits reproduction cancer cells, activates T-killers, inhibits collagenase synthesis Stimulates T-, B-, NK- and LAK-cells. Induces the activity and production of cytokines that can destroy the tumor, stimulates the production of endogenous pyrogen (through the release of prostaglandin PGE 2). Stimulates the release of steroids, early proteins phases of inflammation, hypotension, neutrophil chemotaxis. Stimulates respiratory burst
	Monocytes	Blocks IL-1 receptors on T cells fibroblasts, chondrocytes, endothelial cells	Blocks IL-1 type receptors on T-cells, fibroblasts, chondrocytes, endothelial cells. Improves experimental model of septic shock, arthritis and intestinal inflammation
	Lymphocytes	T, NK, B-activated monocytes	Stimulates the growth of T-, B- and NK-cells
	T-, N K-cells	All hematopoietic cells and many others, express receptors	Stimulates the growth of T- and B-cells, the production of HLA-class 11 molecules
	Cells endo- telium, fibro- blasts, lim- phocytes, some tumors	T-, B- and plasma cells, keratinocytes, hepatocytes, stem cells	Differentiation of B cells, stimulation of growth of T cells and hematopoietic stem cells. Stimulates the production of proteins of the early phase of inflammation, the growth of keratinocytes
	Cells endo- telium, fibro- blasts, lim- phocytes, mono-	basophils, neutrophils,	Causes the expression of LECAM-1 receptors by endothelial cells, beta-2-integrins and transmigration of neutrophils. Stimulates respiratory burst
	Cells endo- telium, fibro- blasts, mono-	Monocyte precursor CFU-M Monocytes	Supports the proliferation of monocytoforming colonies. Activates macrophages
	Monocytes. Some tumors secrete similar peptides Macrophages	Non-activated monocytes	Only specific monocyte chemoattractants are known
	NK-, T-cell- ki, B cells	Endothelial cells, monocytes, neutrophils	Stimulates the growth of T-lymphocytes. Directs cytokine to certain tumor cells. A pronounced pro-inflammatory effect by stimulating IL-1 and prostaglandin E-2. When administered to experimental animals, it causes numerous symptoms of sepsis. Stimulates respiratory burst and phagocytosis

List of term abbreviations in the table

English		English
	colony forming unit		Monocyte chemotaxis and activating factor
	Granulocyte colony stimulating factor		macrophage colony stimulating factor
	Granulocyte-macrophage colony-stimulating factor		monocytic chemotaxis peptide- 1
	Interferon		natural killer
	Interleukin
	receptor antagonist Torah IL-1		Transform- growth factor beta
	Lipopolysaccharides		Transform- growth factor alpha
	lymphotoxin

Normally, cytokine production is negligible and is designed to maintain interaction between cells producing cytokines and cells releasing other inflammatory mediators. But it increases dramatically during inflammation due to the activation of the cells that produce them.

In the initial stage of the development of inflammation, pro-inflammatory and anti-inflammatory interleukins are simultaneously released. The damaging effect of pro-inflammatory interleukins is largely neutralized by anti-inflammatory ones, and balance is maintained in their production. Anti-inflammatory cytokines have a beneficial effect, they help limit inflammation, reduce the overall response to inflammation, and heal the wound.

Most reactions during the development of inflammation are mediated by cytokines. For example, IL-1 activates T- and B-lymphocytes, stimulates the formation of C-reactive proteins early phase inflammation, production of pro-inflammatory mediators (IL-6, IL-8, TNF) and platelet activating factor. It increases the procoagulant activity of the endothelium and the activity of adhesive molecules on the surface of endothelial cells, leukocytes and platelets, causes the formation of microthrombi in the vessels of the microvasculature, and causes an increase in body temperature.

IL-2 stimulates T- and B-lymphocytes, growth of NK-cells, production of TNF and interferon, increases the proliferation and cytotoxic properties of T-lymphocytes.

TNF has the strongest pro-inflammatory effect: it stimulates the secretion of pro-inflammatory interleukins (IL-1, IL-6), the release of prostaglandins, enhances the activation of neutrophils, eosinophils, monocytes; activates complement and coagulation, increases the molecular adhesion of the endothelium of leukocytes and platelets, resulting in the formation of microthrombi in the vessels of the microvasculature. This increases the permeability vascular wall, the blood supply to the vital important organs in which foci of ischemia occur, which is manifested by various signs of dysfunction internal organs.

Excessive production of cytokines and other mediators of inflammation causes a violation of the regulatory function of the immune system, leads to their uncontrolled release, imbalance between pro-inflammatory and anti-inflammatory cytokines in favor of pro-inflammatory ones. In this regard, mediators of inflammation from the factors that protect the body become damaging.

Nitrogen monoxide (N0) - potentially toxic gas. It is synthesized from a-arginine and predominantly acts as an inhibitory neurotransmitter. Nitric oxide is synthesized not only by leukocytes, but also by the vascular endothelium.

The small size of this particle, the absence of an electric charge and lipophilicity allow it to easily penetrate cell membranes, take part in many reactions, and change the properties of some protein molecules. NO is the most active of the inflammatory mediators.

The optimal level of NO in the blood is necessary to maintain normal venous tone and permeability of the vascular wall. in the microcirculation. NO protects the vascular endothelium (including the liver) from the damaging effects of endotoxins and tumor necrosis factor.

Nitric oxide inhibits excessive activation of macrophages, thereby helping to limit the synthesis of excess cytokines. This weakens the degree of violation of the regulatory role of the immune system in the production of cytokines, helps to maintain a balance between pro-inflammatory and anti-inflammatory cytokines, limits the ability of inflammatory mediators to cause dysfunction of parenchymal organs and the development of a systemic response to inflammation syndrome.

Nitrogen monoxide relaxes muscle cells in the walls of blood vessels, is involved in the regulation of vascular tone, relaxation of sphincters and permeability of the vascular wall.

Excessive production of NO under the influence of cytokines contributes to a decrease in venous tone, impaired tissue perfusion, and the occurrence of ischemic foci in various bodies, which favors the further activation of cells that produce cytokines and other inflammatory mediators. This increases the severity of the dysfunction of the immune system, impairs its ability to regulate the production of inflammatory mediators, leads to an increase in their content in the blood, progression of the systemic reaction to inflammation syndrome, a decrease in venous tone, a decrease in peripheral vascular resistance, the development of hypotension, blood deposition, and the development of edema. , the occurrence of multiple organ dysfunction, often ending in irreversible multiple organ failure.

Thus, the action of NO can be both damaging and protective in relation to tissues and organs.

Clinical manifestationssystemic reaction syndrome for inflammation include signs characteristic of it: 1) an increase in body temperature above 38 ° C or a decrease below 36 ° C with anergy; 2) tachycardia - an increase in the number of heartbeats over 90 in 1 min; 3) tachypnea - an increase in respiratory rate over 20 in 1 min or a decrease in PaCO 2 less than 32 mm Hg; 4) leukocytosis over 12 10 3 in 1 mm 3, or a decrease in the number of leukocytes below 4 10 3 in 1 mm 3, or a stab shift of more than 10%

The severity of the syndrome is determined by the number of signs of organ dysfunction in a given patient. In the presence of two of the four signs described above, the syndrome is assessed as moderate (mild) severity, with three signs - as moderate, with four - as severe. When three and four signs of the systemic response syndrome to inflammation are identified, the risk of disease progression, the development of multiple organ failure, which requires special measures for correction, increases dramatically.

Microorganisms, endotoxins and local mediators of aseptic inflammation usually come from the primary site of infection or foci of aseptic inflammation.

In the absence of a primary focus of infection, microorganisms and endotoxins can enter the bloodstream from the intestine due to tran slocation and through the intestinal wall into the blood or from primary sterile foci of necrosis when acute pancreatitis. This is usually observed with severe dynamic or mechanical intestinal obstruction due to acute inflammatory diseases of the abdominal organs.

Mild systemic inflammatory response syndrome is primarily a signal of excessive production of cytokines by overly activated macrophages and other cytokine-producing cells.

If preventive measures and treatment of the underlying disease are not taken in time, the syndrome of the systemic response to inflammation will continuously progress, and the incipient multiple organ dysfunction can turn into multiple organ failure, which, as a rule, is a manifestation of a generalized infection - sepsis.

Thus, the syndrome of a systemic response to inflammation is the beginning of a continuously developing pathological process, which is a reflection of excessive secretion of cytokines and other inflammatory mediators, insufficiently controlled by the immune system, due to a violation of intercellular relationships in response to severe antigenic stimuli of both bacterial and non-bacterial nature.

The syndrome of a systemic reaction to inflammation resulting from a severe infection is indistinguishable from the reaction that occurs in response to aseptic inflammation in massive trauma, acute pancreatitis, traumatic surgery, organ transplantation, and extensive burns. This is due to the fact that the same pathophysiological mechanisms and mediators of inflammation are involved in the development of this syndrome.

Diagnosis and treatment. The definition and assessment of the severity of the systemic inflammation response syndrome is available to any medical institution. This term is accepted by the international community of doctors of various specialties in most countries of the world.

Knowledge of the pathogenesis of the syndrome of systemic reaction to inflammation allows the development of anticytokine therapy, prevention and treatment of complications. For these purposes, monoclonal antibodies against cytokines, antibodies against the most active pro-inflammatory cytokines (IL-1, IL-6, tumor necrosis factor) are used. There are reports on the good efficiency of plasma filtration through special columns that allow the removal of excess cytokines from the blood. To inhibit the cytokine-producing function of leukocytes and reduce the concentration of cytokines in the blood, they are used (although not always successfully) large doses steroid hormones. The most important role in the treatment of patients belongs to the timely and adequate treatment of the underlying disease, comprehensive prevention and treatment of dysfunction of vital organs.

The frequency of systemic response syndrome to inflammation in patients in intensive care units in surgical clinics reaches 50%. At the same time, in patients with high body temperature (this is one of the signs of the syndrome) who are in the intensive care unit, the syndrome of a systemic response to inflammation is observed in 95% of patients. A collaborative study covering several medical centers in the United States showed that of the total number of patients with systemic inflammation reaction syndrome, only 26% developed sepsis and 4% - septic shock. Mortality increased depending on the severity of the syndrome. In severe systemic response syndrome to inflammation, it was 7%, in sepsis - 16%, in septic shock - 46%.

The systemic inflammatory response syndrome may last only a few days, but it can exist for a longer period of time, until the level of cytokines and nitric monoxide (NO) in the blood decreases, until the balance between pro-inflammatory and anti-inflammatory cytokines is restored, the function of the immune system is restored to control production cytokines.

With a decrease in hypercytokinemia, the symptoms may gradually subside, in these cases the risk of complications is sharply reduced, and recovery can be expected in the coming days.

In severe form of the syndrome, there is a direct correlation between the content of cytokines in the blood and the severity of the patient's condition. Pro- and anti-inflammatory mediators may eventually mutually reinforce their pathophysiological effects, creating a growing immunological dissonance. It is under these conditions that inflammatory mediators begin to have a damaging effect on the cells and tissues of the body.

A complex complex interaction of cytokines and cytokine-neutralizing molecules probably determines the clinical manifestations and course of sepsis. Even a severe systemic response syndrome to inflammation cannot be considered as sepsis if the patient does not have a primary focus of infection (gate of entry), bacteremia, confirmed by the isolation of bacteria from the blood during multiple cultures.

Sepsis as a clinical syndrome is difficult to define. The Conciliation Commission of American Physicians defines sepsis as a very severe form syndrome of a systemic response to inflammation in patients with the presence of a primary focus of infection, confirmed by blood culture, in the presence of signs of CNS depression and multiple organ failure.

We should not forget about the possibility of developing sepsis in the absence of a primary focus of infection. In such cases, microorganisms and endotoxins may appear in the blood due to the translocation of intestinal bacteria and endotoxins into the blood.

Then the intestine becomes a source of infection, which was not taken into account when searching for the causes of bacteremia. Translocation of bacteria and endotoxins from the intestine into the bloodstream becomes possible when the barrier function of the intestinal mucosa is impaired due to ischemia of its walls in peritonitis, acute intestinal obstruction, shock, and other factors. Under these conditions, the intestine becomes like an "undrained purulent cavity."

Also known as SIRS, systemic inflammatory response syndrome (SIRS) is a pathological condition associated with heightened dangers severe consequences for the patient's body. SIRS is possible against the background of surgical interventions, which are currently extremely widespread, in particular when it comes to malignant pathologies. Otherwise, except for the operation, the patient cannot be cured, but the intervention can provoke SIRS.

Question Features

Since the systemic inflammatory response syndrome in surgery occurs more often in patients who were prescribed treatment against the background of general weakness, diseases, probability severe course conditioned side effects other therapeutic methods applied in a particular case. Regardless of where exactly the injury caused by the operation is located, early rehabilitation period associated with increased risks secondary damage.

As known from pathological anatomy, systemic inflammatory response syndrome is also due to the fact that any operation provokes inflammation in acute form. The severity of such a reaction is determined by the severity of the event, a number of auxiliary phenomena. The more unfavorable the background of the operation, the more difficult the VSSO will be.

What and how?

Systemic inflammatory response syndrome is a pathological condition that indicates itself tachypnea, fever, heart rhythm disturbance. Analyzes show leukocytosis. In many ways, this response of the body is due to the peculiarity of the activity of cytokines. Pro-inflammatory cell structures that explain SIRS and sepsis form the so-called secondary wave of mediators, due to which systemic inflammation does not subside. This is associated with the danger of hypercytokinemia, a pathological condition in which damage is done to the tissues and organs of one's own body.

The problem of determining and predicting the likelihood of a systemic inflammatory response syndrome, in the ICD-10 encrypted with the R65 code, in the absence of suitable method evaluation of the initial state of the patient. There are several options and gradations that allow you to determine how bad the patient's state of health, but none of them is linked to the risks of SIRS. It is taken into account that in the first 24 hours after the intervention, SIRS appears in without fail, but the intensity of the state varies - this is determined by a complex of factors. If the phenomenon is severe, prolonged, the likelihood of complications, pneumonia, increases.

About terms and theory

Systemic inflammatory response syndrome, coded as R65 in the ICD-10, was considered in 1991 at a conference that brought together leading experts in intensive care and pulmonology. It was decided to recognize SIRS as a key aspect reflecting any inflammatory process. infectious nature. Such a systemic reaction is associated with the active distribution of cytokines, and it is not possible to take this process under control by the forces of the body. Inflammatory mediators are generated in the primary focus infection, from where they move to the tissues around, thus getting into circulatory system. The processes proceed with the involvement of macrophages, activators. Other tissues of the body, remote from the primary focus, become the area of generation of similar substances.

According to the pathophysiology of the systemic inflammatory response syndrome, histamine is most often used. Similar effects have factors that activate platelets, as well as those associated with necrotic tumor processes. Possible involvement of adhesive molecular structures cells, complement parts, nitric oxides. SIRS can be explained by the activity of toxic products of oxygen transformation and lipid peroxidation.

Pathogenesis

The systemic inflammatory response syndrome, fixed by the R65 code in the ICD-10, is observed when a person’s immunity cannot take control and extinguish the active systemic spread of factors that initiate inflammatory processes. There is an increase in the content of mediators in the circulatory system, which leads to a failure of fluid microcirculation. The endothelium of capillaries becomes more permeable, toxic components from the bed penetrate through the cracks of this tissue into the cells surrounding the vessels. Over time, inflamed foci appear remote from the primary area, there is a gradually progressive insufficiency of the work of various internal structures. As a result of such a process - DIC syndrome, paralysis of immunity, insufficiency of functioning in a multiple organ form.

As shown by numerous studies on the occurrence of systemic inflammatory response syndrome in obstetrics, surgery, oncology, such a response appears both when an infectious agent enters the body, and as a response to a certain stress factor. SIRS can be triggered or by a person's injury. In some cases, the root cause allergic reaction for medication, ischemia individual sections body. To some extent, SIRS is such a universal response human body on the unhealthy processes taking place in it.

Subtleties of the question

Studying the systemic inflammatory response syndrome in obstetrics, surgery, and other branches of medicine, scientists special attention paid attention to the rules for defining such a state, as well as the subtleties of using different terminology. In particular, it makes sense to talk about sepsis if the cause of inflammation in a systemic form is infectious focus. In addition, sepsis is observed if the functioning of some parts of the body is disrupted. Sepsis can only be diagnosed with mandatory allocation both signs: SSVR, infection of the body.

If manifestations are observed that allow one to suspect dysfunction of internal organs and systems, that is, the reaction has spread wider than the primary focus, a severe variant of the course of sepsis is detected. When choosing a treatment, it is important to remember the possibility of transient bacteremia, which does not lead to generalization. infectious process. If this has become the cause of SIRS, organ dysfunction, it is necessary to choose a therapeutic course indicated for sepsis.

Categories and severity

Focusing on diagnostic criteria systemic inflammatory response syndrome, it is customary to distinguish four forms of the condition. Key signs that allow you to talk about SIRS:

fever above 38 degrees or temperature less than 36 degrees;
the heart is reduced with a frequency of more than 90 acts per minute;
breathing in frequency exceeds 20 acts per minute;
with IVL RCO2 less than 32 units;
leukocytes in the analysis are defined as 12 * 10 ^ 9 units;
leukopenia 4*10^9 units;
new leukocyte forms more than 10% of the total.

For the diagnosis of SIRS, the patient must have two of the following signs or large quantity.

About Options

If a patient has two or more signs of the above manifestations of the systemic inflammatory response syndrome, and studies show a focus of infection, analysis of blood samples gives an idea of the pathogen that caused the condition, sepsis is diagnosed.

In case of insufficiency that develops according to a multi-organ scenario, with acute failures in the patient's mental status, lactic acidosis, oliguria, pathologically severely reduced blood pressure in the arteries, a severe form of sepsis is diagnosed. The condition can be maintained through intensive therapeutic approaches.

Septic shock is detected if sepsis develops in a severe form, low blood pressure is observed in a stable variant, perfusion failures are stable and cannot be controlled by classical methods. In SIRS, hypotension is considered to be a condition in which the pressure is less than 90 units or less than 40 units relative to the initial state of the patient, when there are no other factors that can provoke a decrease in the parameter. It is taken into account that the intake of certain medications may be accompanied by manifestations indicating organ dysfunction, a problem of perfusion, while the pressure is maintained adequately.

Could it be worse?

The most severe variant of the course of the systemic inflammatory response syndrome is observed if the patient has impaired functionality of the couple or more organs needed to maintain viability. This condition is called multiple organ failure syndrome. This is possible if SIRS is very difficult, while drug and instrumental methods do not allow to control and stabilize homeostasis, with the exception of methods and methods of intensive treatment.

Development concept

Currently, a two-phase concept is known in medicine that describes the development of SIRS. The cytokine cascade becomes the basis of the pathological process. At the same time, cytokines that initiate inflammatory processes are activated, and with them mediators that inhibit the activity of the inflammatory process. In many ways, how the systemic inflammatory response syndrome will proceed and develop is determined precisely by the balance of these two components of the process.

SIRS progresses in stages. The first in science is called induction. This is the period during which the focus of inflammation is local, due to a normal organic reaction to the impact of some aggressive factor. The second stage is a cascade, in which too many inflammatory mediators are generated in the body that can penetrate the circulatory system. At the third stage, secondary aggression takes place, directed at one's own cells. This explains the typical course of the systemic inflammatory response syndrome, early manifestations insufficient functionality of organs.

The fourth stage is immunological paralysis. At this stage of development, a deeply depressed state of immunity is observed, the work of the organs is very much disturbed. Fifth, The final stage- terminal.

Can something help?

If necessary, alleviate the course of the systemic inflammatory response syndrome clinical recommendation- monitor the patient's condition, regularly taking indicators of the work of vital organs, as well as apply medications. If necessary, the patient is connected to special equipment. Recently, medications designed specifically for the relief of SIRS in its various manifestations look especially promising.

Effective in SIRS medications based on diphosphopyridine nucleotide, also include inosine. Some versions of the release contain digoxin, lisinopril. Combination medications, chosen at the discretion of the attending physician, inhibit SIRS, regardless of what caused the pathological process. Manufacturers assure that a pronounced effect can be achieved in as soon as possible.

Is an operation necessary?

In SIRS, additional surgery may be prescribed. Its necessity is determined by the severity of the condition, its course and development forecasts. As a rule, it is possible to carry out an organ-preserving intervention, during which the area of suppuration is drained.

More about medicines

Revealing medicinal features diphosphopyridine nucleotide, combined with inosine, gave doctors new opportunities. Such a drug, as practice has shown, is applicable in the work of cardiologists and nephrologists, surgeons and pulmonologists. Preparations with this composition are used by anesthesiologists, gynecologists, endocrinologists. Currently, drugs are used in surgical operations on the heart and blood vessels, if necessary, to assist the patient in the intensive care unit.

Such a wide area of use is associated with the general symptoms of sepsis, the consequences of burns, manifestations of diabetes occurring in a decompensated handicap, shock on the background of trauma, DFS, necrotic processes in the pancreas and many other severe pathological uprisings. The symptom complex inherent in SIRS, and effectively stopped by diphosphopyridine nucleotide in combination with inosine, includes weakness, pain, and sleep disturbances. Medicine relieves the condition of a patient who has a headache and dizziness, symptoms of encephalopathy appear, the skin turns pale or yellow, the rhythm and frequency of heart contractions are disturbed, and blood flow fails.

Relevance of the issue

As shown statistical studies, SIRS is currently one of the most common options for the development of severe hypoxia, a strong destructive activity of cells in individual tissues. In addition, such a syndrome with a high degree of probability develops against the background of chronic intoxication. The pathogenesis and etiology of conditions leading to SIRS differ greatly.

With any shock, SIRS is always observed. The reaction becomes one of the aspects of sepsis, a pathological condition caused by trauma or burns. It cannot be avoided if the person has had a TBI or surgery. As observations have shown, SIRS is diagnosed in patients with diseases of the bronchi, lungs, uremia, oncology, and surgical pathological conditions. It is impossible to exclude SIRS if an inflammatory or necrotic process develops in the pancreas, abdominal cavity.

As shown specific studies, SIRS is also observed in a number of more favorably developing diseases. As a rule, with them, this condition does not threaten the patient's life, but lowers its quality. We are talking about a heart attack, ischemia, hypertension, preeclampsia, burns, osteoarthritis.