Toxic shock syndrome. Causes and symptoms of TSS.

Septic shock is a systemic pathological response to severe infection. It is characterized by fever, tachycardia, tachypnea, and leukocytosis when identifying the source of primary infection. In this case, microbiological blood testing often reveals bacteremia. In some patients with sepsis syndrome, bacteremia is not detected. When arterial hypotension and multiple systemic failure become components of the sepsis syndrome, the development of septic shock is stated.

General information

The term “shock” is a collective concept used to characterize special (urgent) conditions of the body’s most important vital functions, manifested by a complex of pathological processes resulting from extreme exposure to various factors.
An emergency condition of the body that occurs as a result of bacteremia, caused both by the action of the bacteria themselves and by their biologically active substances (exo/endotoxins), is called infectious toxic shock (ITSH). It is based on a complex of pathological disorders of the vital functions of the body, caused by inadequate or excessive compensatory reactions, manifested by disorders of blood circulation, respiration, blood coagulation, endocrine regulation, metabolic disorders, and central nervous system function, leading to the development of multiple organ failure. Despite the achievements of modern medicine, ITS is a common syndrome that causes the emergency condition of patients admitted to the intensive care unit/infectious diseases hospital.

The importance of timely diagnosis and treatment of ITS remains a pressing problem to this day, since such conditions are accompanied by high mortality rates (25-30%). In terms of incidence, ITS ranks third after cardiogenic and hemorrhagic shock , and in terms of mortality - first.

ITS is a serious complication of a number of infectious diseases accompanied by persistently severe bacteremia. The most common infectious-toxic shock is pneumonia (lobar), especially pneumonia caused by pneumococci ; meningococcemia ; typhoid and typhus , salmonellosis ; hemorrhagic fevers ; shigellosis ; plague; hypertoxic form of diphtheria . Quite often, bacteremic (endotoxic) shock occurs with septic complications in various purulent diseases, postpartum complications, abortion , and inflammatory diseases of the urinary tract. It can also develop against the background of other infectious diseases with unreasonably large doses of prescribed antibiotics.

In the 80s of the last century, cases of the development of ITS when using vaginal tampons were first described. Infectious-toxic shock from tampons (menstrual toxic shock syndrome) in most cases develops as a result of long-term use of super-absorbent hygienic tampons, diaphragms and caps, which creates favorable conditions for the development of microflora and the production of toxins . It is most often caused by exotoxin-producing bacteria - group A pyogenic β-hemolytic streptococcus and Staphylococcus aureus. At the same time, endotoxic shock most often occurs against the background of chronic carriage of pathogens, and improper use of tampons (failure to replace them on time) is a predisposing factor that creates favorable conditions for the proliferation of microorganisms and their penetration into the blood.

Signs and symptoms of septic shock

Sepsis can progress to septic shock when certain changes occur in the body's circulatory system and cells that impair the delivery of oxygen and other substances to tissues. Septic shock is more likely to cause death than sepsis. To be diagnosed with septic shock, you must have a probable or confirmed infection and both of the following:

1. The need for medications to maintain blood pressure greater than or equal to 65 millimeters of mercury.
2. High levels of lactic acid in your blood (serum lactate). Having too much lactic acid in your blood means your cells are not using oxygen properly.

When to see a doctor

Sepsis most often occurs in people who are hospitalized or have recently been hospitalized. People in the intensive care unit are especially vulnerable to developing infections that can lead to sepsis. If you develop signs and symptoms of sepsis after surgery or after hospitalization, seek medical attention immediately.

Causes of sepsis

Although any type of infection - bacterial, viral or fungal - can lead to sepsis, the most likely options are:

• Pneumonia
• Digestive system infection (which affects the stomach and colon)
• Infection of the kidneys, bladder and other parts of the urinary system
• Blood infection (bacteremia)

Risk factors

Sepsis and septic shock are more common:

• At a very young age
• In old age
• With a weakened immune system
• For diabetes or cirrhosis
• With frequent hospitalizations
• For wounds or injuries, burns
• When using invasive devices such as intravenous catheters or breathing tubes
• Previously received antibiotics or corticosteroids

Pathogenesis

The mechanism of the damaging effect of ITS is quite complex and is determined primarily by the pathogenicity factors of the pathogen, which are individual for each type of bacteria. Thus, Salmonella has significantly fewer aggressive factors, and their shockogenic properties are weaker than those of the plague pathogen. The likelihood of developing ITS is determined both by the pathogenic properties of the pathogen and the state of the human immune system in whose body these pathological processes develop. The main interaction between external and internal factors occurs primarily in the microvasculature, the pathological changes of which predetermine the development of ITS in the future. The triggering factor for the cascade development of reactions is the entry into the blood of a large number of bacteria and bacterial toxins.

The basis of the endotoxin of gram-negative bacteria is the somatic antigen lipopolysaccharide (LPS). Endotoxin is released predominantly only after the death of the bacterial cell and exhibits pronounced biological activity. The toxic effect of LPS is based on massive stimulation of cells of the lymphoreticular system, promoting the release in large volumes of cytokines and other mediators of the inflammatory response and shock. It is they who, in ITS, play a critical role in the appearance of fever, tissue damage, and the development of severe arterial hypotension . LPS also have direct cardiodepressive and cytotoxic effects. ITS is developing relatively quickly.

Most gram-positive bacteria do not contain endotoxin, but have a liposaccharide capsule and specific antigens (including exotoxins). Such components of the bacterial cell stimulate the production of cytokines and change the activity of lymphocytes/mononuclear macrophages, so their action is to a certain extent determined by humoral factors.

The combination of aggressive factors causes a predominance of pro-inflammatory factors, which forms the systemic inflammatory response syndrome, which is the pathogenetic basis of infectious-toxic shock.

Under the influence of a complex of damaging factors, a cascade of pathological reactions is triggered (vasodilation develops, vascular permeability increases, blood cell aggregation is activated and active lysosomal enzymes and oxygen radicals enter the blood), leading to metabolic , microcirculation, damage to vascular endothelial cells and blood elements, and increased permeability capillaries.

Against this background, the total peripheral vascular resistance in the microvasculature decreases and the volume of blood supply decreases significantly. A spasm of pre/postcapillaries is formed, arteriovenous shunts open, which leads to the flow of blood from the arterial bed into the venous bed, bypassing the capillary network. Myocardial contractility is inhibited. As a compensatory response, the production of adrenocorticotropic hormone , aldosterone and cortisol , which temporarily optimizes hemodynamics. However, further deterioration of microcirculation contributes to the formation of progressive hypoxia . It is microcirculation disorders and tissue hypoxia that determine the further progression of ITS - redistribution of systemic blood flow, retention of water and salts by the kidneys, transfer of interstitial fluid from tissues to blood vessels, increased blood glucose levels, and increased myocardial work.

Effective therapeutic measures taken at this stage to eliminate the causes of ITS make it possible to restore microcirculation and circulating blood volume (CBV) in full, thereby stopping the development of the pathological process. In cases of insufficiency/ineffectiveness of therapeutic measures and with the continued entry of toxic agents into the blood, the development of ITS continues.

The onset of rheological disorders worsen, DIC and sludge syndrome develop, acidosis in tissues worsens, tissue metabolites accumulate, causing expansion of the precapillaries while the postcapillaries remain spasmodic. At the same time, blood is pumped into the microvasculature with increased permeability (depositing up to 10% of the bcc), which contributes to the exudation of serum proteins and blood plasma into the extravascular space and, accordingly, additional losses of circulating blood volume. Against this background, blood circulation is centralized so that vital organs (brain, heart, liver) receive it first.

In a state of tissue hypoxia and deep acidosis , blood circulation significantly worsens and all vascular reactions change, intracellular potassium is replaced by sodium, which causes cellular hyperhydration and fluid leaving the intravascular bed. Further, aggregation of blood elements, microthrombosis of blood vessels develop and peripheral blood circulation is practically blocked, coagulation is disrupted, irreversible degenerative changes occur in tissues and organs and multiple organ failure develops.

Against this background heart failure , severe shortness of breath , inhibition of various parts of the central nervous system, including the vasomotor center, increases, cerebral edema , interstitial pulmonary edema , oliguria begins, cardiac and respiratory reflexes are inhibited, disturbances of consciousness appear and often end in death. The causes of death are irreversible multiple organ failure (50%), severe arterial hypotension (40%), and decompensated heart failure (10%).

Course of septic shock

In septic shock, hypercytokinemia increases the activity of nitric oxide synthetase in endothelial and other cells. As a result, the resistance of resistive vessels and venules decreases. A decrease in the tone of these microvessels reduces overall peripheral vascular resistance. During septic shock, some of the body's cells suffer from ischemia caused by peripheral circulatory disorders. Peripheral circulation disorders in sepsis and septic shock are consequences of systemic activation of endothelial cells, polymorphonuclear neutrophils and mononuclear phagocytes.

Inflammation of this origin is purely pathological in nature and occurs in all organs and tissues. A critical drop in the number of structural and functional elements of most effector organs is the main link in the pathogenesis of the so-called multiple system failure.

According to traditional and correct ideas, sepsis and a systemic inflammatory response are caused by the pathogenic action of gram-negative microorganisms.

In the occurrence of a systemic pathological reaction to invasion into the internal environment and blood of gram-negative microorganisms, the decisive role is played by:

• Endotoxin (lipid A, lipopolysaccharide, LPS). This heat-stable lipopolysaccharide forms the outer coating of gram-negative bacteria. Endotoxin, acting on neutrophils, causes the release of endogenous pyrogens by polymorphonuclear leukocytes.

• LPS-binding protein (LPBP), traces of which are determined in plasma under physiological conditions. This protein forms a molecular complex with endotoxin that circulates in the blood.

• Cell surface receptor of mononuclear phagocytes and endothelial cells. Its specific element is a molecular complex consisting of LPS and LPSSB (LPS-LPSSB).

Currently, the frequency of sepsis caused by invasion of gram-positive bacteria into the internal environment is increasing. The induction of sepsis by Gram-positive bacteria is usually not associated with their release of endotoxin. Peptidoglycan precursors and other wall components of Gram-positive bacteria are known to trigger the release of tumor necrosis factor-alpha and interleukin-1 by immune cells. Peptidoglycan and other components of the walls of gram-positive bacteria activate the complement system through the alternative pathway. Activation of the complement system at the whole body level causes systemic pathogenic inflammation and contributes to endotoxicosis in sepsis and the systemic inflammatory response.

It was previously thought that septic shock was always caused by endotoxin (a lipopolysaccharide of bacterial origin) released by gram-negative bacteria. It is now generally accepted that less than 50% of cases of septic shock are caused by Gram-positive pathogens.

Disorders of peripheral circulation during septic shock, adhesion of activated polymorphonuclear leukocytes to activated endothelial cells - all this leads to the release of neutrophils into the interstitium and inflammatory alteration of cells and tissues. At the same time, endotoxin, tumor necrosis factor-alpha, and interleukin-1 increase the formation and release of tissue coagulation factor by endothelial cells. As a result, mechanisms of external hemostasis are activated, which causes fibrin deposition and disseminated intravascular coagulation.

Arterial hypotension in septic shock is mainly a consequence of a decrease in total peripheral vascular resistance. Hypercytokinemia and an increase in the concentration of nitric oxide in the blood during septic shock causes dilatation of arterioles. At the same time, through tachycardia, the minute volume of blood circulation increases compensatoryly. Arterial hypotension in septic shock occurs despite a compensatory increase in cardiac output. Total pulmonary vascular resistance increases during septic shock, which can be partly attributed to the adhesion of activated neutrophils to activated endothelial cells of the pulmonary microvessels.

The following main links in the pathogenesis of peripheral circulatory disorders in septic shock are distinguished:

1) increased permeability of the microvascular wall;

2) an increase in microvascular resistance, which is enhanced by cell adhesion in their lumen;

3) low response of microvessels to vasodilating influences;

4) arteriolo-venular shunting;

5) drop in blood fluidity.

Hypovolemia is one of the factors of arterial hypotension in septic shock.

The following causes of hypovolemia (a drop in cardiac preload) in patients in a state of septic shock are identified:

1) dilatation of capacitive vessels;

2) loss of the liquid part of the blood plasma in the interstitium due to a pathological increase in capillary permeability.

It can be assumed that in most patients in a state of septic shock, the drop in oxygen consumption by the body is mainly due to primary disorders of tissue respiration. In septic shock, moderate lactic acidosis develops with normal oxygen tension in the mixed venous blood.

Lactic acidosis in septic shock is considered to be a consequence of decreased pyruvate dehydrogenase activity and secondary accumulation of lactate, rather than a decrease in blood flow in the periphery.

Peripheral circulatory disorders in sepsis are systemic in nature and develop with arterial normotension, which is supported by an increase in minute volume of blood circulation. Systemic microcirculation disorders manifest themselves as a decrease in pH in the gastric mucosa and a decrease in oxygen saturation of blood hemoglobin in the hepatic veins. Hypoergosis of intestinal barrier cells, the action of immunosuppressive links in the pathogenesis of septic shock - all this reduces the protective potential of the intestinal wall, which is another cause of endotoxemia in septic shock.

Classification

There is a reversible ITS, which includes 3 stages:

• Early reversible - characterized by spasm in the microvasculature and with initial symptoms of tissue hypoxia.
• Late reversible - characterized by expansion of the microcirculatory bed with the deposition of blood in it; increased hypoxia, initial control of enzymatic metabolism in the tissues of the most sensitive organs.
• Sustained reversible (decompensated shock) - development of disseminated intravascular coagulation (stage 1-2), severe hypoxia, signs of dysfunction of individual organs.

Irreversible ITS is DIC syndrome (stage 3-4) with severe disorders of microcirculation and blood coagulation. Severe intracellular acidosis. Symptoms of irreversible multiple organ failure.

Causes

The most common cause of the development of ITS are gram-negative enterobacteria (70% of cases) - pneumococcus , Escherichia coli , salmonella , meningococcus , Proteus , Klebsiella , Pseudomonas aeruginosa . Less commonly - gram-positive microflora - enterococci , streptococci , staphylococci or viruses (herpes, CMV), protozoa, fungi.

In addition to the presence of an infectious agent in the body, the development of ITS requires a combination of two additional factors:

• Opportunities for massive penetration of the pathogen and/or its toxins into the bloodstream.
• Reducing the general resistance (immunodeficiency) of the body.

Risk factors for the development of ICT are:

• Incorrect antibiotic .
• Complicated abortion/puerperal sepsis .
• Diseases of the ENT organs (sinusitis, tracheitis), closed wounds (in the nose).
• Open wounds, burns .
• Postoperative purulent complications.
• Improper use of tampons during menstruation and means of preventing pregnancy (intravaginal contraceptives - diaphragms/caps).
• Immunodeficiency states of the body.

Symptoms of toxic shock syndrome

Clinical symptoms of ICT include symptoms of acute circulatory failure and generalized infection. Specific manifestations are determined by the stage of development of the pathological process.

Stage 1.1. The phase of early reversible shock is not always clinically diagnosed and is short-lived. It is characterized by spasm in the microvasculature with initial manifestations of tissue hypoxia with the development of symptoms of peripheral vasodilation and a hyperdynamic state, which are manifested by anxiety. Pronounced motor and speech excitement, moderate thirst.

Vascular tone is not affected; sometimes there is generalized arteriolospasm , which causes pallor of the skin and mucous membranes. The skin is warm to the touch, sometimes moist. The pupils are constricted, breathing is rhythmic and deep, but against the background of fever it can become more frequent. The pulse rate is rapid, the pulse is tense, the blood pressure level is normal or slightly elevated. Diuresis is slightly reduced (hourly urine output is at least 40 ml/h). In the blood - hypercoagulation , hyperglycemia , slight metabolic acidosis . As already indicated, the vast majority of doctors almost never diagnose this phase.

Starting from stage 1.2 , a gradual decrease in cardiac output, an increase in spasm of peripheral vessels and the beginning of the functioning of arteriovenous shunts are characteristic. Tachycardia increases , blood pressure decreases (systolic blood pressure is below the level of 70-60 mm Hg, at which renal filtration almost stops and hypoxia of the kidney tissue increases).

In the absence of adequate medical care, the countdown of time begins from this stage, the duration of which subsequently determines the potential possibility of removing the patient from shock. The pulse is frequent (over 100 beats/min) and weak, heart sounds are muffled, breathing is rapid, severe lethargy and apathy. The pallor of the skin increases, it becomes cold and damp, acquires a marbled tint, acrocyanosis , and the facial skin has a gray-cyanotic color.

Stage 1.3 . Characterized by a further slowdown in capillary blood flow, an increase in hypovolemia , the development of disseminated intravascular coagulation syndrome, metabolic disorders, and inhibition of the sympathetic nervous system. Breathing in the lungs is harsh, and obvious increasing shortness of breath develops (respiratory rate more than 30/min). Partial pressure sharply decreases (below 50 mm Hg), diuresis decreases, hypoxia/hypercapnia sharply increases, cyanosis of the skin and mucous membranes increases, signs of multiple organ functional failure (pulmonary, renal and hepatic failure) appear, which is manifested by a decrease in urination (oliguria ), shortness of breath, jaundice.

Due to the progression of DIC syndrome (second stage), some patients develop a rash, often hemorrhagic in nature. Body temperature drops to subfebrile. The patient's condition is rapidly deteriorating, the pulse is soft and thready, there is severe tachycardia, and blood pressure may not be determined.

Irreversible shock phase - symptoms of systemic severe irreversible multiple organ failure develop: breathing is greatly accelerated, becomes shallow and ineffective (sometimes Cheyne-Stokes breathing). Signs of pulmonary edema appear - increasing moist rales, initially in the lower parts of the lungs, and then spreading to all the lungs. Severe cyanosis often becomes total. Body temperature reaches subnormal levels. brain hypoxia increase (a soporous state develops, turning into a coma). Subsequently, respiratory and cardiac activity stops. It should be noted that the symptoms of infectious toxic shock rapidly progress and it is not always possible to clinically clearly and timely differentiate all phases of ITS.

Symptoms of toxic shock syndrome from tampons appear more often on the 3rd-5th day of menstruation.

The disease begins acutely, and less often occurs with prodromal symptoms such as headache , general malaise, and nausea. The first sign of TSS is severe chills, the temperature rises to 39°C, after which full clinical symptoms develop over the course of 2-5 days. Most women experience diffuse muscle pain and muscle weakness, predominantly in the muscles of the proximal lower extremities, back and abdominals. Sometimes joint pain occurs. Characterized by persistent vomiting, watery diarrhea, decreased diuresis.

Dizziness, headache, paresthesia and fainting against the background of a sharp decrease in blood pressure. In the acute stage (the first 2 days), women are inhibited and partially disoriented. A specific manifestation of the syndrome is the appearance of skin rashes in the form of diffuse redness, spots or small nodular rashes, followed by peeling and peeling of the skin epithelium of the palms, fingers, toes, and soles. In 75% of patients, conjunctival hyperemia and redness of the mucous membrane and mouth of the posterior pharyngeal wall are detected. Most of them experience swelling in the area of ​​the external genitalia and their soreness.

In the future, in the absence of treatment, symptoms of toxic damage to the respiratory and cardiovascular systems, liver, kidneys occur with shortness of breath, pain in the abdomen, right hypochondrium, lower back, and a sharp drop in blood pressure. Much less often, ITS from tampons occurs in a mild (erased) form. At the same time, against the background of chills , fever, nausea, vomiting, diarrhea and general malaise, blood pressure does not decrease, and the pathological condition often resolves without any treatment.

Shock

Which doctors should I contact?

At the first signs of shock, you should immediately call an ambulance.

Treatment of shock

A patient with shock of any type should be taken to the intensive care unit according to the expected profile of the disease. In case of injury, in the presence of signs of internal bleeding, as well as in situations where the cause of shock could not be determined at the prehospital stage, hospitalization in an anti-shock operating room (or another operating room intended for the treatment of victims with shock) is indicated.

Main goals of therapy:

• interrupt pain impulses;
• normalize the volume of circulating blood and the rheological properties of blood;
• correct metabolism;
• eliminate the causes of organ disorders.

1. Ensuring airway patency.
Oxygen therapy is carried out through a mask. In cases of severe shock or inadequate ventilation, intubation of the airway with mechanical ventilation is necessary. 2. Installation of intravascular catheters for rapid infusion of solutions and blood components, and, if necessary, administration of large quantities of medications (including catecholamines).

3. Etiological treatment.

4. Support the circulatory system and oxygen transport:

• discontinuation of antihypertensive drugs, if any were used;
• in most types of shock, the main importance is to replenish the intravascular volume by infusion of plasma substitutes and plasma expanders, solutions of crystalloids and colloids;
• infusion of vasopressor drugs to eliminate hypotension;
• patients with low cardiac output in the absence of cardiac arrhythmias are prescribed a continuous intravenous infusion of dobutamine; with concomitant hypotension, vasoconstrictor drugs are simultaneously used;
• oxygen therapy to reduce hemoglobin oxygen saturation.

5. The main method of correcting lactic acidosis is etiotropic treatment that supports the functions of the circulatory system.
6. Monitoring vital signs.

7. Prevention of bleeding from the gastrointestinal tract and thromboembolic complications.

8. Correction of hyperglycemia.

After resuscitation, specific treatment for the underlying disease is prescribed.
Additional supportive care depends on the type of shock. Complications
The danger of shock is a decrease in blood supply to vital tissues. The prognosis depends on the cause of shock and the timeliness of treatment.

If left untreated, shock is fatal.

The development of hypovolemic shock is accompanied by a mortality rate of up to 70%, depending on its severity. With timely assistance provided in full, the mortality rate does not exceed 25%. Distributive shock is characterized by varying mortality rates, depending on the etiological factor, and can reach 70% in the case of septic shock. Obstructive shock associated with fairly effectively removable causes is accompanied by a mortality rate not exceeding 15%. With pulmonary embolism, the mortality rate exceeds 30%. Even with treatment, mortality from cardiogenic shock after myocardial infarction remains very high and reaches 70%.

Prevention of shock

Shock is a condition, a process that cannot be considered separately from known nosological forms. Therefore, shock cannot be the cause of death; the cause of death becomes the factor that caused the state of shock. Prevention of shock involves timely treatment of diseases that can lead to its development.

Sources:

1. Great Medical Encyclopedia (BME), edited by Petrovsky B.V., 3rd edition, volume 27.
2. Clinical guidelines (protocol) for providing emergency medical care for shock in children. Russian Society of Emergency Medical Care Union of Pediatricians of Russia, 2015, p. 21.
3. Moroz V.V., Bobrinskaya I.G., Vasiliev V.Yu. et al. Shock. Educational and methodological manual for students, residents, graduate students and doctors. - Moscow, 2011.

IMPORTANT!

The information in this section cannot be used for self-diagnosis and self-treatment. In case of pain or other exacerbation of the disease, diagnostic tests should be prescribed only by the attending physician. To make a diagnosis and properly prescribe treatment, you should contact your doctor.

Tests and diagnostics

The main diagnostic criteria for ITS are the dynamics of indicators of the state of the cardiovascular and respiratory systems, blood parameters, and the diagnosis of metabolic disorders. General clinical methods for diagnosing stages of ITS are of secondary importance.

The diagnostic criteria for ITS are:

• Chills and hyperthermia (>38-39 °C), in the later stages paradoxical hypothermia (<36 °C).
• Microcirculation disorders (pale, cold skin).
• Hypoxemia / tachypnea (acrocyanosis, partial pressure <32 mm Hg; heart rate >20 per minute).
• Circulatory disorders (hypodynamic syndrome): Systolic blood pressure <90 mm Hg. tachycardia (heart rate 100-120/min) in the absence of other reasons for the development of hypotension. At the same time, infusion therapy does not restore hemodynamics.
• Neuropsychiatric disorders (euphoria, agitation, disorientation, stupor).
• Oligoanuria (less than 30 ml/h), diarrhea , vomiting.
• Blood parameters: accelerated ESR, leukocytosis (>12.0•109/l), neutrophilia >10%, LII >9; level of hematocrit, lactate (>2 mmol/l).

The diagnosis of ITS is made when there is a focus of infection in the body and two or more of the above symptoms.

Infectious-toxic shock in children

ITS in children is especially severe, with dynamically increasing symptoms. In addition to the listed diseases in adults, which are often complicated by ITS in children, it often develops against the background of dysentery , scarlet fever , diphtheria and meningococcal infection . Infectious-toxic shock is also often caused by the introduction of an infectious pathogen during scratches or scratching abrasions. The disease in children is characterized by active development of the process within 1-2 days. This is characterized by a sharp increase in body temperature to 39-41 C.

The child's condition is serious and is accompanied by severe chills, motor agitation, vomiting, convulsions, pallor of the mucous membranes and skin, increased heart rate, a significant and sharp drop in blood pressure, and confusion. With meningococcal infection, numerous hemorrhages of various shapes appear on the skin of children. Increasing microcirculation disorders can provoke an earlier development of acute renal failure .

Treatment of infectious-toxic shock in children should begin as quickly as possible and is carried out only in the intensive care unit according to a scheme similar to the treatment of ITS in adults with adjustment of drugs for the age/body weight of the child. Without adequate timely treatment, there is a high risk of death.

When to see a doctor

Of course, all of the listed symptoms of TSS rarely occur at the same time. It also happens that the first signs of shock appear only 20 days after menstruation1. Therefore, always monitor your health and be sure to call a doctor at home if you develop fever, body aches, weakness, dizziness or skin rash. Even if the cause of the illness turns out to be a common ARVI, it is better to play it safe. Be sure to tell your doctor that you use tampons during your period. This will help diagnose TSS. With timely seeking medical help and proper treatment, complications can be avoided1.

Diet

Early initiation of nutritional support is recommended (in the first 24–36 hours), which is based on the following recommendations:

• The energy value of the diet is based on 25–30 kcal/kg body weight/day.
• Protein component: 1.3–2.0 g/kg/day.
• Lipids: 15–20% non-protein calories.
• Glucose: 50–60% non-protein calories, maintaining glycemic levels no higher than 6.1 mmol/L.

After relief of ITS, nutrition according to the recommendations for a specific infectious disease or Table No. 15 .

Prevention

To prevent infectious-toxic shock, it is recommended:

• Timely and adequate treatment of infectious diseases, especially accompanied by high bacteremia and high alertness to the possibility of developing ITS in patients with salmonellosis , lobar pneumonia , hypertoxic form of diphtheria , shigellosis , sepsis , meningococcemia , Legionnaires' disease , out-of-hospital abortions, complicated childbirth, purulent diseases, bacterial obstructive urinary tract diseases.
• Timely treatment of bruises and wounds with violation of the integrity of the skin with antiseptic drugs.

To prevent toxic shock syndrome from tampons, it is recommended for women to:

• alternate hygiene products (pads and tampons) every menstrual cycle, and if necessary - during one menstrual cycle (tampons during the day, and pads at night);
• carefully select tampons whose adsorbing capabilities correspond to the volume of discharge;
• change tampons every four hours, even if it is not yet completely saturated with discharge;
• Avoid using mechanical means of preventing pregnancy (intravaginal contraceptives - diaphragms/caps).

How to reduce your risk of developing TSS

In 97% of cases, TSS is treatable, but the disease can develop again1. Therefore, if you have had toxic shock, don't use tampons - choose sanitary pads.

To reduce your risk of developing TSS from tampons, follow these guidelines:

1. do not use a tampon with damaged individual packaging;
2. open the wrapper only with clean hands;
3. do not place the tampon on a surface that may be contaminated with bacteria - hold it in your hand;
4. tampons are intended only for menstrual flow; for normal flow, replace them with panty liners;
5. change the hygiene product every 4 hours, do not leave it in the vagina at night, and also if you do not have the opportunity to quickly replace it;
6. choose only high-quality hygiene products, such as ob®;
7. Always consider the amount of menstrual blood and do not use highly absorbent tampons if there is little discharge.

Everything we've told you about TSS isn't a reason to stop using tampons. ob® tampons are a modern, safe hygiene product that makes life easier for millions of women. Among ob® tampons you can find convenient options with different absorbent capacities. Use them and follow safety rules.