At an early stage, septic shock is observed. Septic shock diagnosis and treatment

Which leads to hypoxia of many organs. Shock can occur as a result of insufficient filling of the vascular system with blood and vasodilation. The disease refers to a group of disorders in which blood flow to all tissues of the body is limited. This leads to hypoxia and dysfunction of vital organs such as the brain, heart, lungs, kidneys, and liver.

Causes of septic shock:

neurogenic shock occurs as a result of damage to the nervous system;
anaphylactic shock develops as a result of a violent reaction of antibodies;
cardiogenic shock occurs as a result of acute heart failure;
neurogenic shock occurs due to dysfunction of the nervous system.

The type of microorganism that provokes the infection is also important, for example, pneumococcal sepsis can occur due to inflammation of the lungs. In hospitalized patients, surgical incisions or bedsores are common sites of infection. Sepsis can accompany bone infections, the so-called inflammation of the bone marrow.

Infection can occur anywhere where bacteria and other infectious viruses can enter the body. The most common cause of sepsis is bacterial infections (75-85% of cases), which, if not treated promptly, can lead to septic shock. Septic shock is characterized by a decrease in blood pressure.

Patients at high risk include:

with a weakened immune system (in particular, with diseases such as cancer or AIDS);
in children under 3 years of age;
advanced age;
using drugs that block the normal functioning of the immune system;
after a long illness;
after surgical operations;
with high sugar levels.

The basis for the occurrence and treatment of sepsis is the immune system, which reacts to infection by causing inflammation. If inflammation engulfs the entire body, in response to infection, the immune system will hit not only the attacking microbes, but also healthy cells. Thus, even parts of the body begin to suffer. In this case, septic shock may occur, accompanied by bleeding and damage to internal organs. For this reason, patients diagnosed or suspected of having sepsis should be treated in intensive care units.

Treatment of sepsis requires bilateral action. Therefore, one should not underestimate any signs and immediately report the symptoms to the doctor. To make the correct diagnosis, the specialist will immediately prescribe studies that will determine the type of pathogen, and develop an effective treatment.

Today, sepsis is being fought using causal treatment. It consists in the use of broad-spectrum antibiotics.

It should be remembered that sepsis is a very dangerous complex of symptoms that can lead to septic shock and even death of the patient. Symptomatic therapy should resume impaired vital functions. Usually in treatment:

carry out dialysis at the slightest sign of renal failure;
put a dropper in order to eliminate circulatory disorders;
use glucocorticoids to capture the inflammatory response;
performs a platelet transfusion;
carry out measures to strengthen the functions of breathing;
in case of carbohydrate imbalance, insulin administration is recommended.

Septic shock - symptoms

It is worth remembering that sepsis is not a disease, but a certain set of symptoms caused by a violent reaction of the body to an infection, which can lead to progressive failure of many organs, septic shock and death.

The main symptoms of sepsis that may indicate septic shock are:

a sharp increase in temperature above 38C;
a sudden decrease in this temperature to 36 degrees;
increased heart rate;
the amount and frequency of breathing increases;
white blood cell count > 12,000/ml (leukocytosis) or< 4.000/мл (лейкопения);
sharp jumps in blood pressure.

If at least three of the factors listed above are confirmed during a medical examination, then most likely sepsis will lead to the development of septic shock.

Before starting treatment, the doctor will certainly prescribe the necessary diagnostic studies, without which it is difficult to accurately determine the nature of the lesion. First of all, this is a microbiological study, a blood test. Of course, before starting treatment, depending on the clinical picture, it may be necessary to analyze urine, cerebrospinal fluid, and mucus from the respiratory tract.

But because of the threat to the life of the patient, the diagnostic period should be as short as possible, the results of the tests should be known as soon as possible. Treatment of a patient with suspected septic shock should begin immediately after diagnosis.

In severe cases, the patient may be subjected to mechanical ventilation and maintenance of peripheral venous pressure in the range of 12-15 mm Hg. Art., to compensate for increased pressure in the chest. Such manipulations may be justified in case of increased pressure in the abdominal cavity.

If within the first 6 hours of treatment, in patients with severe sepsis or septic shock, hemoglobin oxygen saturation does not occur, a blood transfusion may be necessary. In any case, it is important to carry out all activities quickly and professionally.

Why does it arise?

The precursor of the pathology is considered to be a diffuse infectious process, or sepsis.

Infection is caused by ingestion of bacteria, protozoa, viruses, and other agents, as well as an immune response to various foreign substances in the bloodstream.

One of the manifestations of the process is inflammation, which is a key link in pathogenesis.

The immune system of the body responds to the appearance of foreign bodies in two ways:

Activation of lymphocytes that recognize and engulf infectious agents.
Release of cytokines, immune hormones.

Normally, this accelerates the fight against the disease. However, with a long-term and diffuse infection, cytokines lead to a strong vasodilation and a drop in blood pressure.

These factors lead to a violation of the absorption of oxygen and nutrients into the walls of blood vessels, causing hypoxia of the organs and disruption of their function.

Development phases

Septic shock has three successive stages:

Hyperdynamic, warm.
Hypodynamic, cold.
Terminal, irreversible.

The first is characterized by a strong rise in temperature, up to 40-41 degrees Celsius, a drop in blood pressure up to collapse, increased breathing and severe muscle pain. Time runs from 1-2 minutes to 8 hours. It is the body's primary response to the release of cytokines.

Additionally, in the first stage, symptoms of damage to the nervous system may increase - the appearance of hallucinations, depression of consciousness, and incessant vomiting. Prevention of collapse is especially important for obstetrics - newborns are very difficult to tolerate circulatory disorders.

A sign of the second stage is a drop in temperature to 36 degrees and below. Hypotension does not go away, leaving the threat of collapse. Growing symptoms of heart and respiratory failure - rhythm disturbance, tachycardia, which is abruptly replaced by bradycardia, a strong increase in breathing. Necrotic areas appear on the skin of the face and mucous membranes - small dark spots.

Hypodynamic septic shock is reversible - oxygen starvation has not yet led to terminal changes in organs, and most of the resulting adverse pathologies are still amenable to therapy. Usually the duration is from 16 to 48 hours.

The irreversible stage is the last phase of septic shock, which ends with multiple organ failure and death. The process of destruction of the heart muscle progresses, massive necrosis of the lung tissue begins with a violation of the gas exchange process. The patient may develop jaundice, hemorrhages caused by a deterioration in blood clotting. In all organs and tissues, areas of necrosis are formed.

If the patient was able to survive, then the main problem is organ failure and the consequences of hemorrhages due to the concomitant DIC. The prognosis at this stage is also complicated by the slowing down of blood flow, which complicates the already disturbed blood circulation.

And also, septic shock has a classification according to the stages of compensation:

Compensated.
Subcompensated.
Decompensated.
Refractory.

Varieties are important for choosing a treatment method. For a person, they differ in the number of symptoms - the further the disease goes, the stronger the negative effects are felt. The last stage is not treatable.

Also, the disease is classified according to the place of primary infection. Such a division is important in surgical treatment, when the intervention is directed to the removal of a purulent formation.

Main features

The following symptoms indicate the development of septic shock:

Temperature over 38 degrees or below 36.
Tachycardia, heart rate over 90 beats per minute, arrhythmia.
Increased respiratory rate, more than 20 chest contractions per minute.
High, more than 12x10^9/l, or low, less than 4x10^9/l, the number of leukocytes in the blood.

The temperature depends on the stage of the disease and the option with an increase is an indicator that the body is still fighting.

Tachycardia can be replaced by sharp drops in heart rate, which is especially dangerous in the presence of a pathology of the heart muscle. The respiratory rate reflects the total lack of oxygen to the tissues and the body's attempt to reflexively restore balance.

As well as individual symptoms of septic shock can be:

Hallucinations, altered perception, depression of consciousness, coma.
The appearance of necrotic spots on the skin.
Involuntary bowel movements and urination, blood in the stool or urine, little or no urine.

These clinical criteria make it possible to identify specific lesions of the body. The first group displays disorders in the brain, such as a stroke.

Necrotic spots reflect a severe lack of blood to the surface tissues. The last group speaks of the defeat of the digestive and excretory system, with damage to the muscular.

A decrease in the amount of urine indicates the development of renal failure and the need for artificial blood purification - dialysis.

Diagnostic methods

The study for septic shock begins with a blood test - an immunogram.

Important diagnostic indicators are:

General level of leukocytes.
The level of cytokines.
Leukocyte formula.

Pathology is directly related to the immune system, and its altered state is a direct indicator. Leukocytes can be reduced or increased - depending on the stage and strength of the response. More often in patients with this diagnosis, there is an excess of the norm by one and a half to two times.

Since this process is the result of a huge amount of cytokines entering the blood, their level will be significantly exceeded. In some cases, cytokines may not be detected.

The leukocyte formula helps to determine the cause of the pathology. With a microbiological reason, there is an increased number of young forms of leukocytes that are formed to respond to the infection that has arisen.

A general laboratory blood test will also help to conduct a differential study to exclude individual pathologies. In septic shock, ESR will be significantly increased, as a result of a change in the protein composition of the blood - an increase in the concentration of markers of the inflammatory process.

Important is the bacteriological analysis of the discharge to determine the infectious agent. The material can be taken from the mucous membranes of the nasopharynx or purulent focus. A blood culture is required.

Determining the type of pathogen allows you to more accurately select antibiotics.

Another diagnostic method is the study of hemodynamics, in terms of the amount of oxygen carried and carbon dioxide carried. In shock, there is a sharp decrease in the amount of CO2, which means a reduced oxygen consumption.

ECG is used to diagnose myocardial damage. In a state of shock, signs of coronary heart disease are noted - a significant jump in the ST segment ("cat's back").

How is the treatment carried out?

Therapy for septic shock consists of first aid measures, medical and surgical treatment.

Urgent Care

Most patients with a severe infection are referred to a hospital to monitor the development of pathology. However, people often refuse specialized help.

If this condition has developed outside the hospital, then you should urgently call an ambulance, accurately determine the stage of the patient and provide emergency care.

The hyperthermic stage is determined in the presence of:

Temperatures over 39-40 degrees.
Seizures.
Tachycardia, over 90 beats per minute.
Tachypnea, the number of breaths - over 20 per minute.

When the body temperature rises above 41-42 degrees, protein coagulation begins, followed by death, and the work of enzymes stops.

Seizures also indicate the onset of damage to the nervous tissue. Body cooling can be done with ice packs or cold water baths.

You can determine the hypothermic stage by:

The temperature is below 36 degrees.
Blueing of the skin.
Shortened breathing.
Falling heart rate.

With a low pulse rate, there is a risk of cardiac arrest, so you need to be ready to start cardiopulmonary resuscitation.

To alleviate the condition, emergency doctors can introduce drugs that increase vascular tone and support the work of the heart. If necessary, artificial ventilation of the lungs and oxygen supply are carried out to improve oxygenation of the brain and other tissues.

In the hospital, the patient is connected to a ventilator, the temperature is lowered or raised.

The location in the intensive care unit allows the team to quickly respond to organ damage, cardiac arrest and take measures to restore the activity of the cardiovascular system.

Medical therapy

In septic shock, the drug treatment algorithm consists of:

elimination of the risk of toxic damage;
reduction of hypoglycemia;
preventing blood clotting;
facilitating the penetration of oxygen through the vascular wall and accelerating its uptake in cells;
elimination of the main cause of the disease - sepsis.

The first step is to detoxify the body and restore the electrolyte balance necessary for the easy transport of oxygen and nutrients. For this, infusion therapy with the help of glucose-salt solutions, the introduction of sorbents can be used.

Hypoglycemia is eliminated by the introduction of glucose and glucocorticoids, which accelerate metabolic processes in cells. They also allow you to eliminate blood clotting, so they are usually administered together with Heparin.

Steroid anti-inflammatory drugs increase cell permeability. And also the achievement of this goal is facilitated by vasopressor substances - Adrenaline, Norepinephrine, Dopamine. In addition, inotropic drugs like Dopamine are prescribed.

In the presence of acute renal failure, the administration of solutions is contraindicated - too much fluid in the body will cause swelling and intoxication, therefore, for such patients, blood is purified using hemodialysis.

Surgical intervention

Septic shock itself is not treated surgically, but side effects such as suppuration, necrosis, and abscesses can significantly interfere with recovery. A complication for the operation may be respiratory and heart failure, and therefore, the indications for the operation are determined by a council of doctors.

Radical surgery is performed in the presence of purulent lesions on the limbs - for example, gas gangrene. In this case, the limb is amputated, preventing further development of septicopyemia (or septicemia).

With accumulations of pus in certain parts of the body, they are opened and sanitized to remove it, preventing further spread throughout the body. In order to facilitate the impact on the heart, sanitation is carried out under local anesthesia.

Interventions in pregnant women are of particular difficulty. Gynecological sepsis has a very complex specificity due to the risk of pregnancy disorders. The spread of bacterial infection often leads to the fact that the child dies in the womb.

How is prevention carried out?

It is possible to prevent the development of septic shock by timely treatment of its cause.

To do this, you should contact the clinic in time with the development of symptoms characteristic of bacterial lesions of the body.

In case of a severe infection, for this, antibiotic treatment should be started on time, which intensively affect the existing pathogenic microflora. Surgical correction is the timely removal of purulent foci.

Consequences of septic shock

The main possible complication is multiple organ failure. The gradual failure of organs leads to the death of the patient.

Due to the large toxic load, the first to develop is renal and hepatic insufficiency with a deterioration in the course of the picture, and after - pulmonary and cardiac failure.

Another possible consequence is DIC. Two stages are clinically important: hypercoagulation and.

The first is characterized by massive thrombosis, and the second - by bleeding.

Massive internal bleeding complicates the situation created by hypotension, and the patient dies in a few days. The syndrome can be prevented either in the first stage, by introducing heparin, or in the second, by transfusing plasma with clotting elements that prevent bleeding.

Very often, the clinic of the syndrome develops as a consequence of a difficult birth, which, with septic shock, is dangerous for both the mother and the child, whose immune system is not ready to respond to a bacterial agent. The baby often dies.

In general, even in patients with milder diagnoses, DIC is often fatal, and under conditions of severe sepsis, it becomes the primary cause of death. Medical statistics show that the chance of survival is much higher when starting treatment in the first phase.

And also often with the development of severe sepsis or septic shock, the patient begins to develop superinfection - re-infection with another bacterial or viral agent.

life forecast

As already mentioned, pathology has a lethality of up to 50%. Recovery depends on how quickly treatment was started, how adequately antibiotics were selected, and how severe the complications were.

The infectious agent that caused the septic lesion also plays a role. Hospital strains are considered the most dangerous, for example, Staphylococcus aureus. Usually it is resistant to most antibiotics, so the process is most difficult for the patient's body.

Symptoms often begin with chills and include fever and hypotension, oliguria, and confusion. There may be acute failure of several organs, such as the lungs, kidneys, and liver. Treatment is intensive fluid therapy, antibiotics, surgical removal of infected or necrotic tissue and pus, supportive care, and sometimes blood glucose control and administration of corticosteroids.

Sepsis is an infection. Acute pancreatitis and serious trauma, including burns, may present with symptoms of sepsis. The inflammatory response is usually manifested by two or more symptoms:

Temperature >38 °C or<36 °С.
Heart rate >90 bpm.
Respiratory rate >20 per minute or PaCO 2<32 мм рт.ст.
White blood cell count >12x109/l or<4х109/л или >10% immature forms.

However, at present, the presence of these criteria is only a suggestive factor and is not sufficient for making a diagnosis.

Severe sepsis is sepsis accompanied by signs of failure of at least one organ. Cardiovascular insufficiency, as a rule, is manifested by hypotension, respiratory failure - by hypoxemia.

Septic shock is severe sepsis with hypoperfusion and hypotension that is not relieved by adequate fluid resuscitation.

Causes of septic shock

Septic shock is more common in neonates, patients older than 35, and pregnant women. Predisposing factors include diabetes mellitus; cirrhosis of the liver; leukopenia.

Pathophysiology of septic shock

The pathogenesis of septic shock is not fully understood. Inflammatory agents (eg, bacterial toxin) lead to the production of mediators, including tumor necrosis factor and IL-1. These cytokines cause neutrophil-endothepial-cell adhesion, activate blood coagulation mechanisms and lead to the formation of microthrombi. They also promote the release of other mediators, including leukotrienes, lipoxygenase, histamine, bradykinin, serotonin, and IL-2. They are opposed by anti-inflammatory mediators such as IL-4 and IL-10 as a result of a negative feedback mechanism.

First, the arteries and arterioles dilate, and cardiac output increases. Later, cardiac output may decrease, blood pressure falls, and the typical signs of shock appear.

Even at the stage of increased cardiac output, vasoactive mediators cause blood flow to bypass the capillaries (distributive defect). Capillaries fall out of this shunt along with capillary obstruction by microthrombi, which reduces O2 delivery and reduces the excretion of CO2 and other waste products. Hypoperfusion leads to dysfunction.

Coagulopathy may develop due to intravascular coagulation involving major coagulation factors, increased fibrinolysis, and more often a combination of both.

Symptoms and signs of septic shock

In patients with sepsis, as a rule, there are: fever, tachycardia and tachypnea; BP remains normal. Other signs of infection are also usually present. Confusion may be the first sign of both severe sepsis and septic shock. BP usually drops, but paradoxically, the skin remains warm. There may be oliguria (<0,5 мл/кг/ч). Органная недостаточность приводит к появлению определенных дополнительных симптомов.

Diagnosis of septic shock

Sepsis is suspected when a patient with a known infection develops systemic symptoms of inflammation or organ dysfunction. If there are signs of systemic inflammation, the patient should be examined for infection. This requires a thorough history, physical examination and laboratory tests, including general urinalysis and urine culture (especially in patients with indwelling catheters), the study of blood cultures of suspicious body fluids. In severe sepsis, blood levels of procalcitonin and C-reactive protein are elevated and may facilitate diagnosis, but these values are not specific. Ultimately, the diagnosis is based on the clinic.

Other causes of shock (eg, hypovolemia, myocardial infarction) should be identified by history, physical examination, ECG, and serum cardiac markers. Even without MI, hypoperfusion can lead to ECG evidence of ischemia, including nonspecific ST-T wave abnormalities, T-wave inversions, and supraventricular and ventricular premature beats.

Hyperventilation with respiratory alkalosis (low PaCO 2 and elevated blood pH) appears early as compensation for metabolic acidosis. Serum HSO; usually low, and serum lactate levels are elevated. Shock progresses, metabolic acidosis worsens, and blood pH decreases. Early respiratory failure leads to hypoxemia with Pa02<70 мм рт.ст. Уровень мочевины и креатинина обычно прогрессивно возрастают.

Nearly 50% of patients with severe sepsis develop relative adrenal insufficiency (i.e. normal or slightly elevated basal cortisol levels. Adrenal function can be checked by measuring serum cortisol at 8 am.

Hemodynamic measurements may be used when the type of shock is unclear or when large volumes of fluid are needed. Echocardiography (including transesophageal echocardiography) is the main method for assessing the functional state of the heart and the presence of vegetations.

Treatment of septic shock

Infusion therapy with 0.9% saline.
02-therapy.
Broad spectrum antibiotics.
Drainage of abscesses and removal of necrotic tissue.
Normalization of blood glucose levels.
Replacement therapy with corticosteroids.

Patients with septic shock should be treated in an intensive care unit. Continuous monitoring of the following parameters is shown: system pressure; CVP, PAOR or both; pulse oximetry; ABGs; blood glucose, lactate and electrolyte levels; kidney function, and possibly sublingual PCO 2 . diuresis control.

If hypotension persists, dopamine may be given to increase mean blood pressure to at least 60 mmHg. If the dose of dopamine exceeds 20 mg/kg/min, another vasoconstrictor, usually norepinephrine, may be added. However, vasoconstriction caused by an increased dose of dopamine and norepinephrine poses a threat of both organ hypoperfusion and acidosis.

02 is given with a mask. Tracheal intubation and mechanical ventilation may be needed later if breathing is impaired.

Parenteral administration of antibiotics should be prescribed after taking blood, various media (fluids, body tissues) for sensitivity to antibiotics and culture. Early empiric therapy initiated immediately after sepsis is suspected is important and may be decisive. The choice of antibiotic should be justified, based on the suspected source, based on the clinical setting.

Treatment regimen for septic shock of unknown etiology: gentamicin or tobramycin, in combination with cephalosporins. Additionally, ceftazidime may be used in combination with fluoroquinolones (eg, ciprofloxacin).

Vancomycin should be added if resistant staphylococci or enterococci are suspected. If the source is localized in the abdominal cavity, a drug effective against anaerobes (for example, metronidazole) should be included in the therapy.

In corticosteroid therapy, replacement doses are used, not pharmacological ones. The regimen consists of hydrocortisone in combination with fludrocortisone for hemodynamic instability and for 3 consecutive days.

Description:

Septic shock is a complex pathophysiological process resulting from the action of an extreme factor associated with the breakthrough of pathogens and their toxins into the bloodstream, which, along with tissue and organ damage, causes excessive, inadequate tension of nonspecific adaptation mechanisms and is accompanied by hypoxia, tissue hypoperfusion, and profound metabolic disorders. processes.

Symptoms:

Symptoms of septic shock depend on the stage of shock, the microorganism that caused it, and the age of the patient.

Initial stage: decrease in urination, a sudden increase in temperature above 38.3 °, diarrhea and loss of strength.

Late stage: restlessness, feeling irritable, thirst due to reduced blood flow to the brain tissues, rapid heart rate and rapid breathing. In infants and old people, the only signs of shock may be low blood pressure, clouding of consciousness, and rapid breathing.

Low body temperature and decreased urination are common late signs of shock. Complications of septic shock are disseminated intravascular coagulation, renal and peptic ulcers, and liver dysfunction.

Causes of occurrence:

Septic shock (infectious-toxic, bacteriotoxic or endotoxic) develops only with generalized infections that occur with massive bacteremia, intense decay of bacterial cells and the release of endotoxins that disrupt the regulation of the volume of the vascular bed. Septic shock can develop not only with bacterial, but also with viral infections, protozoan invasions, fungal sepsis, severe injuries, and so on.

Treatment:

For treatment appoint:

The first step is to stop the progression of shock. Fluids are usually administered intravenously and pressure in the pulmonary artery is monitored. Infusion of whole blood or plasma can raise the pressure in the pulmonary artery to a satisfactory level. To overcome hypoxia may be required. The introduction of a catheter into the urinary tract allows you to accurately assess the amount of urine separated per hour.

Antibiotics are given immediately (intravenously) to fight the infection. Depending on which microorganism is the causative agent of the infection, complex antibiotic treatment is carried out (usually an aminoglycoside is used in combination with penicillin). If a staphylococcal infection is suspected, a cephalosporin is used. If the infection is caused by non-spore-forming anaerobic organisms, chloromycetin or cleocin is prescribed. However, these drugs can cause unpredictable reactions. All products should only be used as directed by a physician. In the presence of abscesses, they are excised and drained to clear the purulent focus.

If fluids do not relieve shock, dopastat increases blood pressure to maintain blood perfusion in the brain, liver, gastrointestinal tract, kidneys, and skin. Bicarbonate is used as a remedy for acidosis (intravenously). Intravenous corticosteroids may improve blood perfusion and cardiac output.

In 2016, new definitions of sepsis and septic shock. Because current data on epidemiology, prognosis, and treatment refer to conditions diagnosed according to previously used definitions, and because the new nomenclature equivalent of the previously used term “severe sepsis” is “sepsis,” this edition of the guideline these concepts are used in parallel ( , ). The new definitions do not include the term "infection" - below are presented in the traditional sense of the word.

Table 18.8-1. Definition and diagnostic criteria for sepsis and septic shock

Definitions and Criteria	Previous (1991, 2001)	Proposed New (2016)
	SIRS resulting from infection	life-threatening organ dysfunction caused by dysregulation of the body's response to infection; this response leads to damage to organs and tissues (corresponding to the previous concept of "severe sepsis")
severe sepsis	sepsis causing failure or dysfunction of organs (or organ systems → see below); equivalent of the concept of "sepsis" in the new nomenclature	the equivalent is "sepsis" see above
diagnostic criteria for organ dysfunction	used to diagnose severe sepsis ()	used to diagnose sepsis - a sudden increase in the score on the SOFA scale by ≥2 points ()a, with the presence or suspicion of infection
septic shock	a form of severe sepsis with acute circulatory failure characterized by persistent hypotension (systolic blood pressure<90 мм рт. ст., средние <65 мм рт. ст. или снижение систолического давления на >40 mmHg Art.) despite appropriate infusion therapy (with the need for the use of vasopressors in the future)	sepsis, in which circulatory, cellular and metabolic disorders are so severe as to significantly increase mortality is diagnosed if, despite correct fluid therapy, persists: 1) hypotension requiring the use of vasopressors to maintain mean arterial pressure ≥65 mm Hg. Art., and 2) plasma lactate concentration> 2 mmol / l (18 mg / dl)
scale proposed for early detection of patients at increased risk of death	not defined, both criteria for SSOC and organ dysfunction were used, as well as extended criteria for the diagnosis of sepsis that included them ()	score on the Quick SOFA (qSOFA) scale - ≥2 with the following symptoms: 1) impaired consciousness b 2) systolic blood pressure ≤100 mm Hg. Art. 3) respiratory rate ≥22/min
determination of the severity of the inflammatory response	used in the definition of sepsis - SIRS, i.e. ≥2 with the following symptoms: 1) body temperature>38 °C or<36 °C 2) heart rate>90/minv 3) respiratory rate >20/min or PaCO2<32 мм рт. ст. 4) WBC count >12,000/mcL or<4000/мкл, или >	not given (inflammatory response has been established to be only one and not the most important component of the body's response to infection; emphasis is placed on organ dysfunction, suggesting that it significantly increases the risk of death)
a Patients without acute organ dysfunction usually have a SOFA score of 0. b Glasgow Coma Scale score (→)<15 баллов a May be absent in patients taking β-blockers. PaCO2 - partial pressure of carbon dioxide in arterial blood, SIRS - systemic inflammatory response syndrome based: Intensive Care Med. 2003; 29:530–538, also JAMA. 2016; 315:801–810. doi:10.1001/jama.2016.0287

Table 18.8-2. Traditional diagnostic criteria for sepsis-associated organ dysfunctiona

1) sepsis-associated tissue hypoperfusion, or

2) dysfunction of organs or organ systems caused by infection, i.e. ≥1 s of the following dysfunctions:

a) hypotension caused by sepsis

b) lactate concentration>ULN

c) diuresis<0,5 мл/кг/ч в течение >2 h despite appropriate fluid therapy

d) PaO2 /FiO2<250 мм рт. ст., если легкие не являются очагом инфицирования, либо <200 мм рт. ст., если легкие являются очагом инфицирования

e) creatininemia >176.8 µmol/l (2 mg/dl)

f) bilirubinemia >34.2 µmol/l (2 mg/dl)

g) the number of platelets<100 000/мкл

g) coagulopathy (INR>1.5)

a Previously proposed criteria for the diagnosis of severe sepsis.

FiO2 - oxygen concentration in the inhaled air, expressed as a decimal fraction, ULN - upper limit of normal, PaO2 - partial pressure of oxygen in arterial blood

Table 18.8-3. Sepsis-associated organ dysfunction score (SOFA)a

Organ or system	Result
Organ or system
respiratory system
PaO2 /FiO2 , mmHg Art. (kPa)				<200 (26,7)б	<100 (13,3)б
blood clotting
platelet count, × 103 / µl
liver
bilirubinemia, µmol/l (mg/dl)		20–32 (1,2–1,9)	33–101 (2,0–5,9)	102–204 (6,0–11,9)
circulatory system	SBP ≥70 mmHg	GARDEN<70 мм рт.ст.	dobutamine (any dose) or dopamine<5в	norepinephrine ≤0.1 or epinephrine ≤0.1 or dopamine 5.1–15c	norepinephrine >0.1 or epinephrine >0.1 or dopamine >15v
nervous system
glasgog coma scale
kidneys
creatininemia, µmol/l (mg/dl) or diuresis, ml/day		110–170 (1,2–1,9)	171–299 (2,0–3,4)	300–440 (3,5–4,9)
and the calculator in Polish - http://www.mp.pl/oit/wpraktyce/show.html?id=57427 b during mechanical ventilation c doses of catecholamines given in mcg / kg / min and used for ≥1 h FiO2 - concentration of oxygen in the inhaled air, expressed as a decimal fraction, MAP - mean arterial pressure, PaO2 - partial pressure of oxygen in arterial blood based: Intensive Care Med. 1996; 22:707–710

Infection is an inflammatory response to microorganisms in tissues, fluids, or body cavities that are normally sterile.

Microbiologically confirmed infection- isolation of pathogenic microorganisms (or determination of their antigens or genetic material) from body fluids or tissues that are normally sterile.

Clinical suspicion of infection- the presence of clinical symptoms strongly suggestive of infection, e.g. leukocytes in the systemic fluid of the body, which is normally sterile (except for blood), perforation of internal organs, on radiography, a picture of pneumonia in combination with purulent discharge from the respiratory tract, an infected wound.

Multiple Organ Dysfunction Syndrome (MOS)- severe organ dysfunction during an acute illness, indicating the impossibility of maintaining homeostasis without therapeutic intervention.

Bacteremia - live bacteria in the blood. Viremia - viruses are able to replicate in the blood. Fungemia - live fungi in the blood (candidemia - live Candida fungi in the blood).

The type of microorganism is not determinative during sepsis, since the microbes must not be present in the blood. In most cases, there are no previous immune disorders, although they are risk factors for sepsis.

Infections and inflammations that cause sepsis initially affect various organs, including the abdominal cavity (eg, peritonitis, cholangitis, acute pancreatitis), urinary system (pyelonephritis), respiratory tract (pneumonia), CNS (neuroinfections), pericardium, bones and joints, skin and subcutaneous tissue (wounds resulting from trauma, decubitus and postoperative), reproductive system (including blastocyst infections). The source of infection is often hidden (eg, teeth and periodontal tissues, paranasal sinuses, tonsils, gallbladder, reproductive system, abscesses of internal organs).

Iatrogenic risk factors: vascular cannulas and catheters, catheter in the bladder, drains, implanted prostheses and devices, mechanical ventilation of the lungs, parenteral nutrition, transfusion of contaminated fluid and blood products, wounds and bedsores, impaired immunity as a result of pharmacological treatment and radiation therapy, etc.

Pathogenesis

Sepsis is an abnormal response of the body to an infection involving components of the microorganism and endotoxins, as well as mediators of the inflammatory response produced by the host body (cytokines, chemokines, eicosanoids, etc., responsible for SIRS) and substances that damage cells (for example, oxygen free radicals ).

Septic shock (hypotension and hypoperfusion of tissues) is a consequence of an inflammatory reaction caused by inflammatory mediators: insufficient vascular filling - relative (expansion of blood vessels and a decrease in peripheral vascular resistance) and absolute (increased vascular permeability) hypovolemia, less often - a decrease in myocardial contractility (usually in septic in shock, cardiac output is increased, provided that the vessels are adequately filled with fluid). Hypotension and hypoperfusion lead to a decrease in oxygen delivery to tissues and their hypoxia. Finally, a decrease in oxygen delivery and consumption increases anaerobic metabolism in cells and leads to lactic acidosis. Other elements of septic shock: acute respiratory distress syndrome (ARDS), acute renal failure, impaired consciousness caused by CNS ischemia and exposure to inflammatory mediators, digestive tract disorders - paralytic ileus due to intestinal ischemia and damage to the mucous membrane, which leads to the movement of bacteria from the lumen gastrointestinal tract into the blood (bacterial translocation) and bleeding (hemorrhagic gastropathy and stress ulcers →, ischemic colitis →), acute liver failure →, decreased adrenal reserve (relative adrenal insufficiency).

CLINICAL PICTURE AND NATURAL COURSE

Symptoms of sepsis →Definition and. Other symptoms depend on the initially affected organs. If the progression of the infection is not stopped in the early stages of sepsis, then symptoms of dysfunction of other organs begin to appear: the respiratory system (acute respiratory failure - ARDS; →) the cardiovascular system (hypotension, shock) and the kidneys (acute kidney injury, initially prerenal →), as well as disorders of hemostasis (DIC → ; initially, as a rule, thrombocytopenia) and metabolic disorders (lactacidosis). If effective treatment is not started, shock worsens, multiple organ failure develops, and death occurs.

Table 18.8-4. Advanced diagnostic criteria and consequences of sepsis

infection (confirmed or suspected) and some of the following criteria

general indicators

– body temperature >38 °C or<36 °C

– tachycardia >90/min

– tachypnea >30/min (or mechanical ventilation)

- mental status disorders

– significant edema or positive water balance (>20 ml/kg/day)

- hyperglycemia (> 7.7 mmol / l), in the absence of diabetes

inflammatory indicators

– leukocytosis >12,000/µl or leukopenia (white blood cell count<4000/мкл)

– Presence >10% of immature forms of neutrophils

– C-reactive protein >2 standard deviations from the mean

– procalcitonin >2 deviations from the mean

hemodynamic and tissue perfusion parameters

- low blood pressure (systolic<90 мм рт. ст., среднее <70 мм рт. ст., падение систолического на >40 mmHg Art. in people with hypertension)

– lactate concentration in blood serum > upper limit of normal

– slowing down of capillary filling

emerging and growing symptoms of organ dysfunction

– hypoxemia (PaO2 /FiO2<300 мм рт. ст., а если имеются первичные заболевания дыхательной системы <200)

- acute oliguria (diuresis<0,5 мл/кг/ч в течение >2 h despite adequate fluid resuscitation)

– increase in creatinineemia by >44.2 µmol/l (0.5 mg/dl) within 48 hours

- violations of hemostasis (number of platelets<100 000/мкл, МНО >1.5, APTT >60 s)

– concentration of total bilirubin in blood plasma > 70 µmol/l (4 mg/dl)

- paralytic ileus (peristalsis is not auscultated)

DIAGNOSTICS

Additional research methods

1. Laboratory research: to assess the degree of organ dysfunction (arterial and venous blood gasometry, plasma lactate concentration [determine within a few hours after the onset of severe sepsis], hemostasis study, indicators of kidney and liver function), as well as the intensity of the inflammatory process (complete blood count, CRP or procalcitonin [PCT, PCT] is now much less common than ESR; a decrease in PCT may suggest a reduction in the duration of antibiotic therapy in patients with a diagnosed infection, and a negative PCT result may justify the decision to stop empirical antibiotic therapy in patients who are suspected of having sepsis, but later infection was not confirmed).

2. Microbiological studies

1) blood - ≥2 samples, including ≥1 from a separately punctured vein and one from each vascular catheter inserted >48 hours; all samples should be cultured to identify aerobic and anaerobic pathogens;

2) others depending on the suspected etiology - material from the respiratory tract, urine, other body fluids (eg, cerebrospinal fluid, pleural fluid), swabs or discharge from wounds.

3. Imaging studies: radiography (especially of the lungs), ultrasound and CT (especially of the abdominal cavity).

Diagnostic criteria

It is shown in parallel to carry out etiotropic and symptomatic therapy. Primarily, the prognosis depends on the rapid initiation of antibiotics and fluids. The initial algorithm of actions (the so-called sets of tasks) → .

Table 18.8-5. T. n. "quest packages" according to the Surviving Sepsis Campaign

Within 3 hours:

1) determine the concentration of lactate in the blood

2) take a blood sample for culture (before using antibiotics)

3) Use broad-spectrum antibiotics

4) Transfuse 30 ml/kg of crystalloid solutions if hypotension occurs or if blood lactate concentration is ≥4 mmol/L (36 mg/dL).

Within 6 hours:

5) Use vasoconstrictors (for hypotension unresponsive to initial fluid resuscitation) to keep mean arterial pressure (MAP) ≥65 mmHg. Art.

6) with sustained arterial hypotension despite fluid resuscitation (MAP<65 мм рт. ст.), или если начальная концентрация лактата составляет ≥4 ммоль/л (36 мг/дл), занесите в документацию обновлённую оценку волемии и тканевой перфузии, выполненную по одной из следующих методик:

a) assessment of vital functions and an objective examination of the circulatory and respiratory systems, with an assessment of capillary filling, pulse and the condition of the skin

b) performing 2 of the following studies: CVP, Scv O2 , bedside circulatory echocardiography, dynamic assessment of response to fluid loading by elevating the lower extremities in the supine position, or using trial infusion therapy

7) re-determine the lactate concentration if it was initially elevated a.

CVP - central venous pressure, Scv O2 - oxygen saturation of blood hemoglobin from the superior vena cava

Etiotropic therapy

1. Antimicrobial therapy: initial (empirical), as soon as possible, i.e. within 1 hour (every hour of delay increases mortality), but before that (if it is possible and does not delay the treatment by more than 45 minutes), it is necessary to take the appropriate material for microbiological examination (→ Diagnosis). Use ≥1 broad-spectrum IV antibiotic; take into account activity against the most likely etiological factors (bacteria, fungi, viruses), penetration into the site of infection, as well as local sensitivity of microorganisms. In septic shock, at the initial stage, the use of ≥2 antibiotics from different groups that are active against the most likely bacterial pathogens is recommended. The routine use of ≥2 antibiotics from different groups targeting the same suspected or confirmed pathogen is not recommended for sepsis or bacteremia associated with neutropenia, or for severe infections with bacteremia or sepsis without shock. Although in these situations the use of combined antibiotic therapy is not excluded in order to expand the spectrum of antibacterial action (that is, the use of ≥2 antibiotics from different groups that are active against ≥2 confirmed or suspected bacteria). Combination antibiotic therapy (in the meaning given above, i.e. directed to a single pathogen) is usually used for suspected or confirmed infection with Pseudomonas or Acinetobacter (this tactic is recommended especially for antibiotic-resistant strains), as well as for shock with S. pneumoniae bacteremia (in another situation a β-lactam antibiotic with a macrolide is used). Every day, the patient's condition should be assessed for the possibility of switching to antibiotic therapy with a narrower spectrum or monotherapy. In septic shock, this modification is recommended within a few days as clinical improvement is achieved and signs of infection disappear; this applies to concomitant (directed to the same pathogen) therapy, both empiric and specific, depending on the susceptibility of pathogens. Specific therapy (in most cases monotherapy) based on antibiotic susceptibility should be applied as early as possible. Dosing should take into account the pharmacokinetic and pharmacodynamic characteristics of the medicinal product, e.g.:

1) the use of large saturating doses - for example. vancomycin;

2) dosing of certain drugs based on body weight or serum concentration results - aminoglycosides and vancomycin;

3) consideration of the issue of permanent or long-term intravenous administration of drugs, the effect of which is dependent on the time at which their concentration is above the MIC - mainly β-lactam antibiotics;

4) the introduction of 1r / d drugs, the effect of which depends on their maximum concentration, and having a distinct post-antibiotic effect - aminoglycosides;

5) the properties of drugs in patients with sepsis or in a state of septic shock - for example. an increase in the volume of distribution of hydrophilic antibiotics and glomerular filtration (renal clearance) occurring especially in patients undergoing resuscitation with solutions suggests the use of higher doses. Duration of treatment: usually 7–10 days (longer if response to treatment is slow, source of infection cannot be completely removed, neutropenia → or other immune disorders, certain organisms, S. aureus bacteremia; a shorter course of treatment may be warranted in some patients , especially with rapid clinical improvement after sanitation of the focus of infection located in the abdominal cavity or associated with urosepsis, as well as uncomplicated [i.e., without anatomical abnormalities] pyelonephritis). The role of determining the level of procalcitonin in reducing the duration of antibiotic therapy → see. higher.

2. Elimination of the source of infection- infected tissues or organs (eg gallbladder, necrotized segment of the intestine), catheters (intravenous catheter, which may be the source of infection, should be removed immediately after a new vascular access is provided), implanted prostheses and devices; drainage of abscesses, empyema and other foci of infection. Least invasive but effective intervention is preferred (eg, percutaneous rather than surgical drainage of abscesses if possible). In the case of infected pancreatic necrosis, a delay in surgical intervention is suggested.

Symptomatic treatment

Mandatory for sepsis (according to the past terminology - severe sepsis) and septic shock.

1. Initial anti-shock measures: rapid onset, especially intravenous fluids → see below, and evaluation of efficacy are at least as important as the management of individual algorithms and achievement of target parameters. The most important, in addition to improving the general clinical condition (and such simple parameters as heart rate, blood pressure, arterial hemoglobin oxygen saturation, respiratory rate, body temperature, diuresis), is the reduction (normalization) of elevated lactate concentration in patients with hypoperfusion, and also achieving mean arterial pressure ≥65 mm. rt. Art. in septic shock (if vasoconstrictors are used → see below). It was previously recommended to achieve “normal” central venous pressure (CVP; 8–12 mmHg, mean arterial pressure ≥65 mmHg, spontaneous diuresis ≥0.5 ml/kg/h) within the first 6 hours from the start of treatment. and central venous hemoglobin oxygen saturation (from superior vena cava, SvO2) ≥70% or mixed venous blood ≥65%.The current SSC guidelines do not directly list all of these targets, although measurements of these parameters can serve to assess the clinical situation.It is recommended that however, further hemodynamic assessment (as a cardiac assessment, eg echocardiography) when the type of shock is in doubt (eg cardiogenic shock may coexist with septic shock), and the use of dynamic (rather than static) hemodynamic parameters to predict response is preferred to fluid transfusion → If, after reaching the target mean arterial pressure (after fluid transfusion and vasopressors), no reduction in lactate concentration (or target venous hemoglobin oxygen saturation) is achieved within the first few hours, consideration should be given, depending on the circumstances (frequency heart rate, left ventricular function, fluid response, hemoglobin levels), ≥1 of the following: further fluid transfusion, packed packed red blood cells transfusion to obtain hematocrit ≥30%, use of dobutamine (max. dose 20 mcg/kg/min).

2. Treatment of disorders of the cardiovascular system

1) proper filling of the vascular bed with solutions - in patients with tissue hypoperfusion and suspected hypovolemia it is necessary to start the infusion with the introduction of crystalloids in an amount of ≥30 ml/kg in during the first 3 hours, with simultaneous monitoring of signs of the appearance of hypervolemia. Some patients may need a rapid (or later) transfusion of large amounts of fluid. Large volumes of fluid (eg >30 ml/kg) should be given in small doses (eg 200–500 ml) and response to treatment should be assessed each time after transfusion (see also ). The SSC (2016) guidelines lack evidence of a benefit of balanced crystalloids over 0.9% NaCl (but balanced solutions are generally preferred, especially when large IV volumes are required →), but crystalloids are favored over solutions gelatin. The latter, however, do not have such contraindications as solutions of hydroxyethyl starch (HES). Transfusion of albumin solutions (usually at 4% or 5% concentrations) is recommended in addition to crystalloid transfusion during the initial period and during further solution therapy in patients requiring transfusion of large volumes of crystalloids.

2) vasopressors - norepinephrine (preferred), if ineffective, vasopressin or adrenaline should be added; vasopressin can also be used to reduce the dose of norepinephrine. Indications: persistent hypotension that persists despite the transfusion of an appropriate volume of fluid. It should be administered (as soon as possible) through a catheter inserted into the vena cava and monitor blood pressure invasively (insert the catheter into the artery). The use of dopamine is proposed to be limited to a small group of patients, especially those with bradycardia and reduced cardiac output, as well as those with a low risk of cardiac arrhythmia.

3) treatment that increases myocardial contractility - dobutamine: consideration should be given to administration in patients with persistent hypoperfusion despite appropriate hydration and the use of vasopressors. When dosing (→131), it should be taken into account that the goal is to eliminate hypoperfusion. The introduction should be stopped with an increase in hypotension and / or the appearance of arrhythmia.

3. Treatment of respiratory failure→ . Artificial ventilation is usually required. Treatment of pneumonia → .

4. Treatment of kidney failure: of primary importance is the stabilization of the activity of the cardiovascular system (normalization of blood pressure); if necessary, renal replacement therapy (it has not been established whether early initiation is more effective, but probably not recommended if oliguria and hypercreatininemia are the only indications for renal replacement therapy).

5. Treatment acidosis : aimed at removing the cause. Coming out of pathophysiological aspects, NaHCO3 can be administered intravenously at blood pH<7,15; но клинические эффекты не определены.

6. Corticotherapy : if hypotension persists despite adequate hydration and use of vasopressors, IV hydrocortisone 200 mg/day may be considered (at least until the shock resolves). If hydrocortisone is not available and another glucocorticoid without significant mineralocorticoid activity is being used, additional fludrocortisone 50 µg 1× daily (which can also be used in combination with hydrocortisone) should be given.

7. Glycemic control: in the event of hyperglycemia caused by severe sepsis (>10 mmol / l in 2 consecutive measurements), insulin should be prescribed (usually by intravenous infusion); target is glycemia<10 ммоль/л (180 мг/дл), чем <6,1 ммоль/л (110 мг/дл). В начальной фазе лечения инсулином требуется контроль гликемию каждые 1–2 ч, a после стабилизации - каждые 4–6 ч. Следует избегать гипогликемии. Лабораторные исследования капиллярной крови на гликемию могут быть у таких пациентов ошибочны. У пациентов с артериальным катетером для прикроватного определения гликемии рекомендуется набирать кровь из катетера (не капиллярную).

8. Additional treatment

1) transfusion of blood products

a) erythrocyte mass, if hemoglobin<7 г/дл, для достижения концентрации 7,0–9,0 г/дл; исключения: переливание эритроцитарной массы при гемоглобине >7 g/dl if there is tissue hypoperfusion, active bleeding, or significant coronary artery disease;

b) platelet concentrate - regardless of other factors, if the platelet count is ≤10,000/µl; transfusion may be useful if platelet count is 10,000–20,000/mcL and there is a state of increased risk of bleeding (including sepsis or septic shock); invasive procedures may require platelet counts ≥50,000/mcL;

c) fresh frozen plasma and cryoprecipitate - mainly when there is active bleeding or invasive procedures are planned;

2) nutrition - as far as possible by the enteral route, in the amount tolerated by the patient (it is not necessary to satisfy the full need for calories);

3) stress ulcer prevention- proton pump inhibitor or H2-blocker in patients with risk factors for bleeding (in seriously ill patients, the most significant is coagulopathy and mechanical ventilation lasting > 48 hours);

4) prevention of venous thromboembolic disease(VTE) → . Pharmacological prophylaxis should be used if there are no contraindications due to bleeding or a high risk of its occurrence; it is recommended to use LMWH rather than fractionated heparin, and, if possible, the initiation of mechanical prophylaxis (only if there are contraindications to pharmacological prophylaxis).

5) algorithm of actions during mechanical ventilation l easy- including the use of sedatives at the lowest possible doses to achieve an established (as best tolerated) level of sedation, avoid muscle relaxants except for ARDS (for ARDS with PaO2/FiO2<150 мм рт. ст. рекомендуется рассмотреть целесообразность их введения до 48 ч), показано приподнятое положение изголовья кровати на 30–45° с целью предотвращения ИВЛ-ассоциированной пневмонии.

6) treatment of DIC → - etiotropic treatment of sepsis is of primary importance.