In the early stages of 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 dilation of blood vessels. The disease belongs 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 antibody reaction;
cardiogenic shock occurs as a result of acute heart failure;
neurogenic shock occurs due to dysfunction of the nervous system.

The type of microorganism causing the infection is also important; for example, pneumococcal sepsis can occur due to pneumonia. In hospitalized patients, surgical incisions or pressure ulcers are common sites of infection. Sepsis can accompany bone infections, called bone marrow inflammation.

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 increased risk include:

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

The basis for the occurrence and treatment of sepsis is the immune system, which responds to infection by causing inflammation. If inflammation spreads throughout the body, the immune system will respond to infection by attacking not only the attacking microbes, but also healthy cells. In this way, 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 in whom sepsis is diagnosed or suspected should be treated in intensive care units.

Treatment of sepsis requires a two-pronged approach. Therefore, you should not underestimate any signs and report symptoms to your doctor immediately. To make a correct diagnosis, a specialist will immediately prescribe tests that will determine the type of pathogen and develop effective treatment.

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

It should be remembered that sepsis is a very dangerous set of symptoms that can lead to septic shock and even death of the patient. Symptomatic therapy should restore impaired vital functions. Typically during treatment:

carry out dialysis when the slightest signs of renal failure appear;
a drip is placed to eliminate blood supply disturbances;
use glucocorticoids to capture the inflammatory response;
gives platelet transfusions;
carry out measures to strengthen respiratory functions;
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 the body’s violent reaction 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);
sudden jumps in blood pressure.

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

Before starting treatment, the doctor will certainly prescribe the necessary diagnostic tests, 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, you may need to analyze urine, cerebrospinal fluid, and mucus from the respiratory tract.

But due to the threat to the patient’s life, the diagnostic period must be shortened as much as possible; test results must 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, during 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 occur?

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

The infection is caused by bacteria, protozoa, viruses and other agents entering the body, 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 body's immunity responds to the appearance of foreign bodies in two ways:

Activation of lymphocytes, which recognize and absorb infectious agents.
Release of cytokines and immune hormones.

Normally, this speeds up the fight against the disease. However, with a long-term and widespread infection, cytokines lead to severe vasodilation and a drop in blood pressure.

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

Phases of development

Septic shock has three sequential 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. The duration varies 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. Preventing collapse is especially important for obstetrics - newborns have a very difficult time with circulatory disorders.

A sign of the second stage is a drop in temperature to 36 degrees and below. Hypotension does not go away, leaving a threat of collapse. Symptoms of cardiac and respiratory failure increase - rhythm disturbances, tachycardia, which abruptly gives way to bradycardia, severe increased 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 the organs, and most of the resulting side pathologies are still treatable. Typically the duration is from 16 to 48 hours.

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

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

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

Compensated.
Subcompensated.
Decompensated.
Refractory.

Varieties are important for the choice of treatment method. For a person, they differ in the amount of symptoms - the further the disease progresses, the stronger the negative effects are felt. The last stage cannot be treated.

The disease is also classified according to the site of primary infection. This division is important in surgical treatment, when the intervention is aimed at removing purulent formation.

Main features

The following symptoms indicate the development of septic shock:

Temperature above 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 an increase in temperature is an indicator that the body is still struggling.

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

Some symptoms of septic shock may also include:

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

These clinical criteria allow us to identify specific lesions in the body. The first group reflects disorders in the brain, such as stroke.

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

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

Diagnostic methods

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

Important diagnostic indicators are:

Total leukocyte level.
Cytokine levels.
Leukocyte formula.

The pathology is directly related to the immune system, and its altered state is a direct indicator. White blood cells may be decreased or increased, depending on the stage and strength of the response. More often, patients with this diagnosis experience an excess of one and a half to two times the norm.

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

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

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

Bacteriological analysis of the discharge to determine the infectious agent is important. The material can be taken from the mucous membranes of the nasopharynx or purulent focus. Blood cultures are 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 transferred and carbon dioxide removed. In shock, there is a sharp decrease in the amount of CO2, which means reduced oxygen consumption.

An ECG is used to diagnose myocardial lesions. 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, medication and surgical treatment.

Urgent Care

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

If this condition develops outside the hospital, then you should urgently call an ambulance, accurately determine the patient’s stage and provide emergency assistance.

The hyperthermic stage is determined by the presence of:

Temperatures above 39-40 degrees.
Cramps.
Tachycardia, over 90 beats per minute.
Tachypnea, number of respirations - 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 beginning of damage to nerve tissue. Cooling of the body can be done using ice heating pads or a cold water bath.

The hypothermic stage can be determined by:

Temperature below 36 degrees.
Blue discoloration of the skin.
Reduced breathing.
Heart rate drop.

If your heart rate is low, there is a risk of cardiac arrest, so you need to be prepared to start cardiopulmonary resuscitation.

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

In the hospital, the patient is connected to a ventilator and 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.

Drug therapy

For septic shock, the drug treatment algorithm consists of:

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

The first step is to detoxify the body and restore the electrolyte balance needed to easily transport oxygen and nutrients. For this, infusion therapy with glucose-saline solutions and the introduction of sorbents can be used.

Hypoglycemia is eliminated by administering glucose and glucocorticoids, which accelerate metabolic processes in cells. They also help prevent blood clotting, so they are usually administered along with Heparin.

Steroidal anti-inflammatory drugs increase cell permeability. Vasopressor substances - Adrenaline, Norepinephrine, Dopamine - also contribute to the achievement of this goal. Additionally, inotropic agents such as 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 purification is carried out using hemodialysis.

Surgical intervention

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

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

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

Interventions in pregnant women are particularly difficult. Gynecological sepsis has very complex specifics due to the danger of pregnancy disruption. The spread of bacterial infection often leads to the child dying 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 if symptoms characteristic of bacterial lesions of the body develop.

In case of severe infection, this requires prompt treatment with antibiotics, which have an intensive effect on the existing pathogenic microflora. Surgical correction involves timely removal of purulent foci.

Consequences of septic shock

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

Due to the large toxic load, renal and liver failure develops first, with a worsening of the picture, and then pulmonary and cardiac failure.

Another possible consequence is disseminated intravascular coagulation syndrome. Clinically, two stages are 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 within a few days. The syndrome can be prevented either in the first stage, by administering heparin, or in the second, by transfusing plasma with clotting elements that prevent bleeding.

Very often, the clinical picture of the syndrome develops as a consequence of a difficult birth, which in 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 in conditions of severe sepsis it becomes the primary cause of death. Medical statistics show that the chance of survival is significantly higher when treatment is started in the first phase.

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

Life forecast

As already mentioned, the pathology has a mortality rate of up to 50%. Recovery depends on how quickly treatment was started, how adequate the antibiotics were, 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. It is usually resistant to most antibiotics, which is why the process is most difficult for the patient’s body.

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

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

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

However, at present, the presence of these criteria is only a presumptive factor and is not sufficient to make a diagnosis.

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

Septic shock is severe sepsis with hypoperfusion and hypotension that does not resolve with adequate intensive fluid therapy.

Causes of septic shock

Septic shock occurs more often in newborns, patients over 35 years of age, and pregnant women. Predisposing factors include diabetes mellitus; cirrhosis; 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 induce neutrophil-endothepial cell adhesion, activate blood coagulation mechanisms and lead to the formation of microthrombi. They also promote the release of other neurotransmitters, including leukotrienes, lipoxygenase, histamine, bradykinin, serotonin and IL-2. They are counteracted 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 drops, and typical signs of shock appear.

Even at the stage of increased cardiac output, vasoactive mediators cause blood flow to bypass the capillaries (distribution defect). Capillaries fall out of this shunt along with capillary obstruction by microthrombi, which reduce the delivery of O2 and reduce 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

Patients with sepsis typically present with: fever, tachycardia and tachypnea; Blood pressure remains normal. Other signs of infection are also usually present. The first sign of both severe sepsis and septic shock may be confusion. Blood pressure usually drops, but paradoxically, the skin remains warm. Oliguria may occur (<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 the presence of infection. This requires a thorough history, physical examination and laboratory tests, including a general urinalysis and urine culture (especially in patients with indwelling catheters), and blood cultures of suspicious body fluids. In severe sepsis, blood levels of procalcitonin and C-reactive protein are elevated and may aid 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, cardiogram, and serum cardiac markers. Even without myocardial infarction, hypoperfusion can lead to cardiac signs of ischemia, including nonspecific ST-T 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 HCO; usually low and serum lactate levels 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.

Almost 50% of patients with severe sepsis develop relative adrenal insufficiency (i.e., normal or slightly elevated basal cortisol levels. Adrenal function can be tested by measuring serum cortisol at 8 a.m.

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 solution.
02-therapy.
Broad-spectrum antibiotics.
Drainage of abscesses and removal of necrotic tissue.
Normalization of blood glucose levels.
Corticosteroid replacement therapy.

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

If hypotension persists, dopamine can be given to increase mean blood pressure to at least 60 mmHg. If the dopamine dose 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 to both organ hypoperfusion and acidosis.

02 is given using a mask. Tracheal intubation and mechanical ventilation may subsequently be necessary if breathing becomes compromised.

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

Treatment regimen for septic shock of unknown etiology: gentamicin or tobramycin, in combination with cephalosporins. In addition, ceftazidime may be used in combination with a fluoroquinolone (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.

Corticosteroid therapy uses replacement doses rather than pharmacological doses. The regimen consists of hydrocortisone in combination with fludrocortisone for hemodynamic instability and for 3 subsequent days.

Description:

Septic shock is a complex pathophysiological process that occurs as a result of the action of an extreme factor associated with the breakthrough of pathogens and their toxins into the bloodstream, which, along with damage to tissues and organs, 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: decreased urination, sudden increase in temperature above 38.3°, diarrhea and loss of strength.

Late stage: restlessness, feeling, irritability, thirst due to decreased blood flow to brain tissue, increased heart rate and rapid breathing. In infants and older adults, the only signs of shock may be low blood pressure, confusion, and rapid breathing.

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

Causes:

Septic shock (infectious-toxic, bacteriotoxic or endotoxic) develops only in generalized infections that occur with massive bacteremia, intense breakdown 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 infestations, fungal sepsis, severe injuries, and so on.

Treatment:

For treatment the following is prescribed:

The first step is to stop the progression of shock. Typically, intravenous fluids are given and pulmonary artery pressure is monitored. Infusion of whole blood or plasma can raise pulmonary artery pressure to a satisfactory level. To overcome hypoxia may be required. Inserting a catheter into the urinary tract allows you to accurately estimate the amount of urine released per hour.

Antibiotics (intravenously) are immediately prescribed to fight the infection. Depending on which microorganism is the causative agent of the infection, complex treatment with antibiotics 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 microorganisms, chloromycetin or cleocin is prescribed. However, these drugs can cause unpredictable reactions. All products should be used only as directed by your doctor. If abscesses are present, they are excised and drained to cleanse the purulent focus.

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

In 2016, new definitions of sepsis and septic shock. Because existing data on epidemiology, prognosis, and treatment relate to conditions diagnosed according to previously used definitions, and because the equivalent of the previously used term “severe sepsis” under the new nomenclature is “sepsis,” in 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 results in organ and tissue damage (corresponding to the previous concept of "severe sepsis")
severe sepsis	sepsis causing failure or dysfunction of organs (or organ systems →see below); equivalent to 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 SOFA score by ≥2 points ()a, in 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 to use vasopressors in the future)	sepsis, in which circulatory, cellular and metabolic abnormalities are so severe that they significantly increase mortality diagnosed if, despite proper fluid therapy, the following 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 CVS and organ dysfunction were used, as well as expanded criteria for diagnosing sepsis that included them ()	Quick SOFA (qSOFA) score - ≥2 with the following symptoms: 1) impaired consciousness b 2) systolic blood pressure ≤100 mm Hg. Art. 3) respiratory rate ≥22/min
determining the severity of the inflammatory response	used in the definition of sepsis - SIRS, i.e. ≥2 of 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) leukocyte count >12,000/µl or<4000/мкл, или >	not shown (it has been established that the inflammatory response is 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 In patients without acute organ dysfunction, the SOFA score is usually 0. b result of assessment on the Glasgow Coma Scale (→)<15 баллов c May be absent in patients taking β-blockers. PaCO2 - partial pressure of carbon dioxide in arterial blood, SIRS - systemic inflammatory response syndrome based on: 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) tissue hypoperfusion associated with sepsis 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 hours 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)

e) platelet count<100 000/мкл

g) coagulopathy (INR >1.5)

a Previously proposed criteria for the diagnosis of severe sepsis.

FiO2 is the concentration of oxygen in the inspired air, expressed as a decimal fraction, ULN is the upper limit of normal, PaO2 is the 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 adrenaline ≤0.1, or dopamine 5.1–15v	norepinephrine >0.1 or adrenaline >0.1, or dopamine >15v
nervous system
Glasgow 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 is in Polish - http://www.mp.pl/oit/wpraktyce/show.html?id=57427 b during artificial ventilation of the lungs in doses of catecholamines given in mcg/kg/min and used for ≥1 hour FiO2 - concentration of oxygen in inspired air, expressed as a decimal fraction, MAP - mean arterial pressure, PaO2 - partial pressure of oxygen in arterial blood based on: 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- presence of clinical symptoms strongly indicating infection, e.g. leukocytes in the systemic fluid of the body, which is normally sterile (except for blood), perforation of internal organs, radiography shows a picture of pneumonia in combination with purulent discharge from the respiratory tract, an infected wound.

Multiple organ dysfunction syndrome (MODS)- severe organ dysfunction during an acute illness, indicating the impossibility of maintaining homeostasis without therapeutic intervention.

Bacteremia is live bacteria in the blood. Viremia - viruses are capable of replication in the blood. Fungemia - live fungi in the blood (candidemia - live Candida fungi in the blood).

The type of microorganisms does not determine the course of sepsis, since microbes should not be present in the blood. In most cases there are no pre-existing immune disorders, although these 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), central nervous system (neuroinfections), pericardium, bones and joints, skin and subcutaneous tissue (wounds resulting from trauma, bedsores and post-operative wounds), 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, bladder catheter, drainages, implanted prostheses and devices, mechanical ventilation, parenteral nutrition, transfusion of contaminated fluids and blood products, wounds and bedsores, immune disorders 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 tissue hypoperfusion) is a consequence of an inflammatory reaction caused by inflammatory mediators: insufficient vascular filling - relative (dilation of blood vessels and decreased peripheral vascular resistance) and absolute (increased vascular permeability) hypovolemia, less often - decreased myocardial contractility (usually in septic shock, cardiac output is increased, provided that the vessels are adequately filled with fluid). Hypotension and hypoperfusion lead to decreased 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, disturbances of consciousness caused by ischemia of the central nervous system and the effects of inflammatory mediators, disorders of the digestive tract - paralytic intestinal obstruction due to 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 organs initially affected. 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 hemostasis disorders (DIC →; initially, as a rule, thrombocytopenia) and metabolic disorders (lactic acidosis). If effective treatment is not started, shock worsens, multiple organ failure develops, and death occurs.

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

presence of 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 artificial ventilation)

– mental status disorders

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

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

inflammatory indicators

– leukocytosis >12,000/μl or leukopenia (number of white blood cells<4000/мкл)

– presence of >10% immature forms of neutrophils

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

– procalcitonin >2 deviations from the mean value

hemodynamic parameters and tissue perfusion parameters

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

– serum lactate concentration > upper limit of normal

– slowing down capillary refill

emerging and increasing 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 hours, despite adequate fluid resuscitation)

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

– hemostasis disorders (platelet count<100 000/мкл, МНО >1.5, aPTT >60 s)

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

– paralytic intestinal obstruction (peristalsis cannot be heard)

DIAGNOSTICS

Additional research methods

1. Laboratory research: to assess the degree of organ dysfunction (arterial and venous blood gasometry, plasma lactate concentration [determine within several hours after the onset of severe sepsis], hemostasis study, kidney and liver function tests), as well as the intensity of the inflammatory process (complete blood count, CRP or procalcitonin [PCT], now much less common than ESR; a decrease in PCT may suggest a reduction in the duration of antibiotic therapy in patients with diagnosed infection, and a negative PCT result may justify the decision to discontinue empirical antibiotic therapy in patients in whom infection is suspected. 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 must 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), smears or discharge from wounds.

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

Diagnostic criteria

It is indicated to carry out etiotropic and symptomatic therapy in parallel. The prognosis primarily depends on prompt initiation of antibiotics and fluids. Initial algorithm of actions (so-called task sets) → .

Table 18.8-5. T. n. "challenge packs" 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) Infuse 30 mL/kg 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 maintain mean arterial pressure (MAP) ≥65 mmHg. Art.

6) with persistent 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 objective examination of the circulatory and respiratory systems, with assessment of capillary refill, pulse and skin condition

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

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

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

Etiotropic therapy

1. Antimicrobial therapy: initial (empirical), as soon as possible, that is within 1 hour (each hour of delay increases mortality), but before this (unless this is possible and does not slow down the treatment by more than 45 minutes), it is necessary to collect the appropriate material for microbiological testing (→ Diagnosis). Use ≥1 broad-spectrum IV antibiotic; take into account activity against the most likely etiological factors (bacteria, fungi, viruses), penetration into the source of infection, as well as the local sensitivity of microorganisms. In case of septic shock, at the initial stage it is recommended to use ≥2 antibiotics from different groups that are active against the most likely bacterial pathogens. 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 active against ≥2 confirmed or suspected bacteria). Combination antibiotic therapy (in the sense given above, that is, aimed at a single pathogen) is usually used when infection with Pseudomonas or Acinetobacter is suspected or confirmed (this tactic is recommended especially for antibiotic-resistant strains), as well as in shock with S. pneumoniae bacteremia (in another situation a β-lactam antibiotic with a macrolide is used). The patient's condition should be assessed daily for the possibility of switching to antibiotic therapy with a narrower spectrum or monotherapy. For septic shock, this modification is recommended over several days as clinical improvement is achieved and signs of infection resolution; this applies to combination (targeting the same pathogen) therapy, both empirical and specific, depending on the sensitivity of the pathogens. Specific therapy (in most cases monotherapy) based on antibiotic sensitivity should be used as early as possible. When dosing, the pharmacokinetic and pharmacodynamic characteristics of the drugs should be taken into account, for example:

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

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

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

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

5) 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), which occurs 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, the source of infection cannot be completely removed, neutropenia → or other immune disorders, some microorganisms, S. aureus bacteremia; a shorter course of treatment may be warranted in some patients , especially with rapid clinical improvement after sanitation of the source of infection located in the abdominal cavity or associated with urosepsis, as well as with uncomplicated [that is, without anatomical disorders] pyelonephritis). The role of determining procalcitonin levels in reducing the duration of antibiotic therapy →see. higher.

2. Elimination of the source of infection- infected tissues or organs (eg gallbladder, necrotic segment of the intestine), catheters (intravenous catheter, which can be a source of infection, should be removed immediately after new vascular access has been secured), implanted prostheses and devices; drainage of abscesses, empyema and other foci of infection. The least invasive but effective intervention is preferred (eg, if possible, performing percutaneous rather than surgical drainage of abscesses). In the case of infected pancreatic necrosis, surgical intervention is expected to be delayed.

Symptomatic treatment

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

1. Initial anti-shock measures: rapid initiation, especially IV administration of solutions → see below, as well as evaluation of effectiveness are at least as important as tactics according to individual algorithms and achievement of target parameters. The most important thing, in addition to improving the general clinical condition (and such simple parameters as heart rate, blood pressure, oxygen saturation of arterial hemoglobin, respiratory rate, body temperature, diuresis), is considered to be a decrease (normalization) of elevated lactate concentrations in patients with hypoperfusion, and also achieving mean arterial pressure ≥65 mm. rt. Art. for septic shock (if vasoconstrictors are used →see below). Previously, it was recommended to achieve “normal” central venous pressure (CVP; 8–12 mm Hg, mean arterial pressure ≥65 mm Hg, spontaneous diuresis ≥0.5 ml/kg/h) within the first 6 hours from the start of treatment and central venous hemoglobin oxygen saturation (superior vena cava, SvO2) ≥70% or mixed venous blood ≥65% The current SSC guidelines do not directly list all of these goals, although measurements of these parameters can serve to assess the clinical situation. however, further hemodynamic assessment (such as cardiac assessment, e.g. echocardiography) if there is doubt about the type of shock (e.g. cardiogenic shock may co-occur with septic shock), and preference is given to the use of dynamic (rather than static) hemodynamic parameters to predict response to transfuse solutions → If, after achieving the target mean arterial pressure (after transfusion of solutions and the use of vasopressors), a decrease in the lactate concentration (or the target level of oxygen saturation of venous hemoglobin) is not achieved within the first few hours, the appropriateness should be considered, depending on the circumstances (frequency heart rate, left ventricular function, response to fluids, hemoglobin level), ≥1 of the following: further fluid transfusion, red blood cell transfusion to achieve hematocrit ≥30%, use of dobutamine (max. dose 20 mcg/kg/min).

2. Treatment of cardiovascular system disorders

1) proper filling of the vascular bed with solutions - in patients with tissue hypoperfusion and suspected hypovolemia Infusion should be started with ≥30 mL of crystalloid/kg in during the first 3 hours, with simultaneous monitoring for signs of hypervolemia. Some patients may require immediate (or later) large fluid transfusions. Large volumes of fluid (eg >30 ml/kg) should be administered in portions (eg 200–500 ml), and response to treatment should be assessed each time they are transfused (see also). The SSC (2016) recommendations do not provide evidence for the superiority of balanced crystalloids over 0.9% NaCl (but, as a rule, balanced solutions are preferred, especially when large volumes of IV administration are required →), but give preference to crystalloids over solutions gelatin. The latter, however, do not have the same contraindications as hydroxyethyl starch (HES) solutions. Transfusion of albumin solutions (usually 4% or 5% concentration) is recommended in addition to crystalloid transfusions initially and during subsequent solution therapy in patients requiring large volumes of crystalloid transfusions.

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 transfusion of an appropriate volume of fluid. It should be administered (as quickly as possible) through a catheter inserted into the vena cava and blood pressure monitored invasively (insert the catheter into the artery). It is suggested that the use of dopamine 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 hypoperfusion that persists despite appropriate hydration and use of vasopressors. When dosing (→131), it should be taken into account that the goal is to eliminate hypoperfusion. Administration should be discontinued if hypotension increases and/or arrhythmia occurs.

3. Treatment of respiratory failure→ . Mechanical ventilation is usually necessary. Treatment of pneumonia →.

4. Treatment of kidney failure: the main importance is stabilization 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 is likely not recommended if oliguria and hypercreatininemia are the only indicators for renal replacement therapy).

5. Treatment acidosis: aimed at eliminating the cause. Leaving the pathophysiological aspects, NaHCO3 can be prescribed intravenously at blood pH<7,15; но клинические эффекты не определены.

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

7. Glycemic control: in case of hyperglycemia caused by severe sepsis (>10 mmol/l in 2 consecutive measurements), insulin should be prescribed (usually intravenous infusion); the 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) red blood cell 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 the platelet count is 10,000–20,000/µL and there is a condition at increased risk of bleeding (including sepsis or septic shock); invasive procedures may require platelet counts ≥50,000/µL;

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

2) nutrition - whenever possible, by the enteral route, in an amount tolerated by the patient (it is not necessary to satisfy the full calorie requirement);

3) prevention of stress ulcers- proton pump inhibitor or H2 blocker in patients with risk factors for bleeding (in severely 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 unless there are contraindications due to bleeding or a high risk of bleeding; It is recommended to use LMWH rather than fractionated heparin, and, if possible, initiate mechanical prophylaxis (only if there are contraindications to pharmacological prophylaxis).

5) algorithm of actions during mechanical ventilation l light- including the use of sedatives in the smallest possible doses, ensuring the established (best tolerated) level of sedation, avoid muscle relaxants with the exception of 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.