Etiology and pathogenesis of hemorrhagic fever with renal syndrome. Hemorrhagic fever with renal syndrome - Symptoms, Diagnosis, Treatment Hemorrhagic fever with renal syndrome ICD 10

Initially, the diagnosis of HFRS is established on the basis of the clinical picture of the infection with a set of certain symptoms of the early (first week) stage of the disease: acute onset, fever, syndrome of general toxicosis and hemodynamic disorders, then pain in the abdomen and lumbar region. The stage at the height of the disease is characterized by the dominance of hemorrhagic syndrome and manifestations of acute renal failure (ARF). At the same time, the polymorphism and variability of symptoms, the lack of standardized characteristics of the leading syndromes do not allow the primary diagnosis of HFRS to be established clinically with reliable accuracy.
The clinical picture of HFRS, described by numerous authors from different regions of the world and associated with different hantaviruses, demonstrates the similarity of the main manifestations of the disease. The generalized nature of the infection with the involvement of various organs and systems in the pathological process determines the polymorphism of symptoms regardless of the etiological agent (hantavirus serotype).
The disease is characterized by a cyclical course and a variety of clinical variants from abortive febrile forms to severe forms with massive hemorrhagic syndrome and persistent renal failure.
The following periods of illness are distinguished. Incubation (from 1 to 5 weeks, on average 2-3 weeks), febrile (initial, general toxic), lasting on average from 3 to 7 days; oliguric (on average 6-12 days), polyuric (on average 6-14 days), convalescence period (early - up to 2 months and late - up to 2-3 years).
In the clinical picture of the disease, 6-7 main clinical and pathogenetic syndromes are distinguished:
1) general toxic;
2) hemodynamic (central and microcirculatory disorders);
3) renal;
4) hemorrhagic;
5) abdominal;
6) neuroendocrine;
7) respiratory syndrome.
Various combination of these syndromes characterizes each of the four periods of the disease. Symptoms of dysfunction of various organs involved in the infectious process are observed during all periods of the disease.
The incubation period lasts from 4 to 49 days (most often from 14 to 21 days), with no clinical manifestations No. During this period, the HFRS virus enters the body through the epithelium respiratory tract, gastro- intestinal tract, as well as through damaged skin. The virus then reproduces in the cells of the macrophage system. It causes activation of specific and nonspecific defense factors, the adequacy of which, as well as the infectious dose, pathogenicity and virulence of the pathogen, determines both the fate of the virus itself and the severity of pathological changes in the patient’s body.
1.3.1 Initial (febrile) period of HFRS.
The pathogenetic basis of the initial (febrile) period of HFRS is viremia, intoxication, activation of hormonal and immune systems, production of pro-inflammatory cytokines, massive vasopathy (associated with the tropism of hantavirus to the endothelium of microcirculatory vessels), coagulopathy, microcirculation disorders, tissue destruction, formation of autoantigens with the formation of autoantibodies (in severe HFRS).
In most patients, HFRS begins acutely. Chills appear headache, pain in muscles, joints, dry mouth, thirst, sometimes a slight cough, severe general weakness. In a small proportion of patients, the appearance of pronounced signs of the disease is preceded by a prodromal period: general malaise, fatigue, low-grade fever.
Fever in most patients reaches high levels on the first day of illness and lasts from 5-6 to 10-11 days, on average 6-7 days. The temperature curve does not have a specific pattern; in most cases it decreases lytically over two to three days. In mild forms of the disease, there is a slight short-term fever, which is often visible to the patient.
An objective examination reveals pronounced hyperemia of the skin of the face, neck, upper half of the body, associated with autonomic disorders at the level of the cervical and thoracic spinal cord. Particularly noticeable is the injection of blood vessels in the sclera and conjunctiva, hyperemia of the oropharyngeal mucosa, and the appearance of spotted enanthema of the upper palate. It is possible to develop hemorrhagic syndrome in the form of a petechial rash in the area of ​​the inner surfaces of both shoulders, the lateral surfaces of the torso, on the chest (the “scourge” symptom), ecchymosis at the injection sites, and short-term nosebleeds. Positive endothelial symptoms (cuffs, pinch, tourniquet) are determined. Blood pressure is normal or tends to hypotension, and relative bradycardia is characteristic. Some patients note a feeling of heaviness in the lower back.
At the end of the initial period, the frequency of urination decreases and diuresis decreases slightly. Laboratory changes are characterized by a slight increase in serum levels of creatinine and urea, a decrease in the relative density (RD) of urine and the appearance of single fresh red blood cells and proteinuria in its sediment. The blood test in most patients is characterized by moderate leukopenia and, less often, slight leukocytosis and band shift to the left, signs of blood thickening against the background of plasmorrhea and hypovolemia in the form of an increase in the number of red blood cells and hemoglobin. The pathognomonic symptom of HFRS in the early period is thrombocytopenia, caused by the damaging effect of the virus, the development of immunopathological reactions, an increase in the adhesive properties of platelets and the formation of cellular aggregates with their retention in microcirculation vessels, and a violation of the rheological properties of blood.
1,3,2 Oligouric period of HFRS.
During the oligouric period of HFRS (the height of the disease), systemic circulatory disorders, hypovolemia and hemoconcentration, hypoperfusion and hypoxia of organs, tissue acidosis and damage to vital body systems continue. The hypocoagulation phase of DIC predominates. Edema, hemorrhages, dystrophic and necrobiotic changes occur in the pituitary gland, adrenal glands, kidneys, myocardium and other parenchymal organs.
The greatest changes are observed in the kidneys, which is accompanied by a decrease in glomerular filtration and impaired tubular reabsorption. AKI in HFRS is caused by damage to the renal parenchyma, acute interstitial nephritis. On the one hand, disruption of microcirculation and increased permeability of the vascular wall contribute to plasmorrhea and serous-hemorrhagic edema of the interstitium of the kidneys, mainly pyramids, with subsequent compression of the tubules and collecting ducts, leading to dystrophy, desquamation of the tubular epithelium, sweating of protein and fibrin with obstruction of the tubules and collecting ducts tubes with fibrin clots and impaired reverse reabsorption of urine. On the other hand, an immunopathological factor is the fixation of immune complexes on the glomerular basement membrane, which reduces glomerular filtration. Interstitial edema increases the impairment of renal microcirculation, up to ischemia, in some cases to necrosis of the renal tubules, and contributes to a further decrease in glomerular filtration and tubular reabsorption. Tubular cells are especially sensitive to hypoxia, a lack of energy material that occurs during ischemia. IN pathological process autoantibodies to damaged tissue structures may also be involved. Disorders in central hemodynamics (hypovolemia, decreased cardiac output, blood pressure) aggravate renal blood flow disorders.
The oligouric period is the most striking period when it unfolds clinical picture, inherent in HFRS. Body temperature drops to normal, sometimes rising again to subfebrile levels - a “two-humped” curve. However, a decrease in temperature is not accompanied by an improvement in the patient’s condition; as a rule, it worsens. General toxic effects reach a maximum, signs of hemodynamic disturbances, renal failure, and hemorrhagic diathesis intensify. The most constant sign of transition to the oliguric period is the appearance of lower back pain of varying intensity: from discomfort heaviness to sudden, painful nausea, vomiting not associated with food or medication intake, in severe cases - hiccups. Asthenia and adynamia increase. Many patients experience abdominal pain, mainly in the umbilical and epigastric region. The face is hyperemic, as renal failure increases, the blush gives way to pallor, hemorrhagic manifestations intensify, mainly in severe cases of the disease - hemorrhages in the sclera, ecchymosis, nosebleeds and gross hematuria, hematomas at injection sites, less often - intestinal bleeding, blood in the vomit, hemoptysis. When making a diagnosis, it is important to identify visual impairment (decreased visual acuity, “flying spots”, a feeling of fog before the eyes), caused by impaired microcirculation in the retina of the eyes, which appears on days 2-7 of the disease and continues for 2-4 days.
In most patients at the beginning of the oligouric period arterial pressure within normal limits, and in severe cases, arterial hypotension develops, reaching the degree of severe collapse or infectious-toxic shock. In the second half of this period, blood pressure (BP) increases in 1/3 of patients; the duration of hypertension rarely exceeds 5 days. Absolute or relative bradycardia is characteristic. Vesicular hard breathing is heard over the lungs, isolated dry rales, wet rales can be detected, in especially severe cases a picture of pulmonary edema or distress syndrome is observed.
On days 2-5 of illness, 10-15% of patients experience diarrhea. The tongue is dry, covered with a gray or brown coating. The abdomen is moderately swollen, there is pain on palpation in the epigastric and periumbilical areas, especially in the projection of the kidneys and sometimes of a diffuse nature. There may be phenomena of peritonism. The liver is enlarged and painful in 20-25% of patients. In isolated cases, signs of meningism may appear. Most specific complications of HFRS develop during this period.
Kidney syndrome is one of the leading ones. Pasternatsky's symptom is positive or strongly positive, so check this symptom must be carried out with extreme caution, by applying light pressure in the area of ​​the costovertebral points to avoid tearing the renal cortex. The full picture of acute renal failure is characterized by progressive oligoanuria, increasing uremic intoxication, water and electrolyte imbalance, and increasing metabolic acidosis.
Disturbances in the activity of the central nervous system are observed in almost all patients, both as manifestations of cerebral symptoms associated with intoxication, and as a consequence of focal lesions. It is possible to develop symptoms of meningism, encephalitic reactions with the appearance of meningeal symptoms (stiff neck, Kernig, Brudzinski symptoms), focal symptoms (corresponding to areas of brain damage), and mental disorders are also observed (from sleep disturbances to various disorders of consciousness).
The hemogram naturally reveals neutrophilic leukocytosis (up to 15-30×109/l of blood), plasmacytosis, and thrombocytopenia. In severe cases, the blood picture is characterized by a leukemoid reaction. Due to blood thickening, the level of hemoglobin and red blood cells may increase, but with bleeding these indicators decrease. The ESR gradually accelerates. Characterized by an increase in the level of residual nitrogen, urea, creatinine, as well as hyperkalemia, hypermagnesemia, hyponatremia and signs metabolic acidosis. A general urine test reveals massive proteinuria (up to 33-66 g/l), the intensity of which varies throughout the day (“protein shot”), hematuria, cylindruria, and the appearance of renal epithelial cells (the so-called Dunaevsky cells). From the second half of the oliguric period, hyposthenuria develops.
Significant changes occur in the state of the blood coagulation system. While hypercoagulation persists in some patients, hypocoagulation develops in severe cases of the disease. It is caused by the consumption of plasma clotting factors due to the formation of microthrombi in small vessels. It is in the oliguric period of HFRS that hemorrhagic manifestations reach their apogee and often become the cause of death.
1,3,3 Polyuric period of the disease.
The period of polyuria begins from 9-13 and lasts until 21-24 days of illness. As a result of the formation of specific immunity, elimination of the pathogen, immune complexes, pathological changes in the kidneys and other organs regress, and there is a tendency towards normalization of their functions. In the stage of polyuria, glomerular filtration increases first of all. In conditions of damaged tubular apparatus, even a slight increase in filtration contributes to an increase in diuresis. Polyuria is caused by osmotic diuresis. Nitrogenous wastes accumulated in the body during oliguria, with the restoration of the functional capacity of the kidneys, exhibit their osmodiuretic effect, and the amount of urine excreted does not depend on the state of hydration of the body; excessive fluid loss with urine with insufficient replenishment can lead to dehydration, hypovolemia and re-development of oliguria . Slow restoration of the reabsorption function of the tubules leads to loss of potassium, sodium, and chlorine.
Vomiting stops, pain in the lower back and abdomen gradually disappears, sleep and appetite normalize, the daily amount of urine increases (up to 3-10 l), nocturia is characteristic. Against the background of hypokalemia, weakness, muscle hypotonia, intestinal paresis, and atony persist Bladder, tachycardia, arrhythmia, dry mouth, thirst. Duration of polyuria and isohyposthenuria depending on severity clinical course illness can range from several days to several weeks. However, the rate of improvement does not always parallel the increase in diuresis. Sometimes in the first days of polyuria, azotemia still increases, dehydration, hyponatremia, hypokalemia may develop, and hypocoagulation persists, so this stage is often called the stage of “uncertain prognosis.”
Laboratory changes during this period consist of a slight decrease in the number of red blood cells, hemoglobin, and an increase in the number of platelets. The erythrocyte sedimentation rate (ESR) accelerates somewhat. Blood serum urea and creatinine levels gradually decrease, and hypokalemia often develops.
Changes in urine (Zimnitsky test) are characterized by extremely low relative density, not exceeding 1001-1005. A small amount of protein, moderate hematuria and cylindruria, sometimes leukocyturia, and small amounts of renal epithelial cells are detected in the urine sediment.
1,3,4 Period of convalescence.
The recovery period is pathogenetically characterized by the formation of stable post-infectious immunity with high level specific IgG, restoration of hemostasis, microcirculation, glomerular filtration of urine, but with long-term persistence of tubular disorders (tubular insufficiency). There is a noticeable improvement in the general condition, restoration of daily diuresis, normalization of urea and creatinine levels. Convalescents exhibit asthenic syndrome: general weakness, fatigue, decreased performance, emotional lability. Along with this, vegetative-vascular syndrome is observed in the form of hypotension, muffled heart sounds, shortness of breath with slight physical activity, tremor of fingers, increased sweating, insomnia. During this period, heaviness in the lower back, a positive Pasternatsky sign, nocturia may be noted, and isohyposthenuria may persist for a long time (up to 1 year or more). It is possible to connect a secondary bacterial infection with the development of pyelonephritis, most often observed in survivors of acute renal failure.

Hemorrhagic fever with renal syndrome (hemorrhagic nephrosonephritis) is an acute viral natural focal disease that occurs in the European part of Russia and the Far East. This disease is characterized by a febrile reaction, severe intoxication of the body, specific damage to the kidneys and damage to small blood vessels with subsequent development of thrombohemorrhagic syndrome.

HFRS: classification

The Manchurian hemorrhagic or Tula fever virus was isolated only in 1976, although the viral etiology of HFRS (ICD-10 code - A98.5) became known three decades earlier. The pathogen that causes HFRS was found in the lungs of rodents (the main carrier is the bank vole mouse). These small mammals are intermediate hosts (natural reservoir) of the infectious agent. Microbiology classifies the causative agent of HFRS as belonging to the Bunyanvirus family. The virus dies when heated to +50°C for half an hour. At temperatures from 0 to +4°C, it can remain active in the external environment for 12 hours. At temperatures from +4° to +20°, the virus in the external environment is quite stable, i.e. can remain viable for a long time.

Signs of HFRS

• high temperature (39°-40°C);
• chills;
• Strong headache;
• sleep disorders;
• blurred vision;
• hyperemia skin neck and facial area;
• dry mouth;
• weakly positive Pasternatsky symptom.

• rash in the form of small hemorrhages (petechiae);
• vomiting 6-8 times a day;
• pain in the lumbar region;
• hyperemia of the pharynx and conjunctiva;
• dry skin;
• injection of scleral vessels;
• 50% of patients have thrombohemorrhagic syndrome.

• pain in the abdominal area;
• hemoptysis;
• vomiting blood;
• tarry stools;
• nosebleeds;
• lower back pain;
• blood in urine;
• positive Pasternatsky symptom;
• puffiness of the face;
• pastiness of the eyelids;
• oliguria to anuria.

Possible complications of HFRS

• acute vascular insufficiency;
• focal pneumonia;
• pulmonary edema;
• kidney rupture;
• azotemic uremia;
• eclampsia,
• acute interstitial nephritis;
• acute renal failure.

Diagnostics

HFRS treatment

Drug therapy.

Etiotropic therapy

Antishock therapy

Additional Methods

HFRS: prevention

Diet for HFRS and after recovery

Features in children

Features in pregnant women

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Disease code A98.5 (ICD-10)

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral natural focal disease that occurs with high fever, severe general intoxication, hemorrhagic syndrome and peculiar kidney damage in the form of nephrosonephritis.

Historical information

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Under various names (Manchurian gastritis, hemorrhagic nephrosonephritis, Songo fever, etc.), the disease has been recorded in the Far East since 1913.

In 1938–1940 in complex studies by virologists, epidemiologists and clinicians, the viral nature of the disease was established, the basic patterns of epidemiology and the features of its clinical course were studied. In the 50s, HFRS was identified in Yaroslavl, Kalinin (Tver), Tula, Leningrad,

Moscow regions, the Urals, and the Volga region. Similar diseases have been described in Scandinavia, Manchuria, and Korea. In 1976, American researchers G. Lee and P. Lee isolated the virus from rodents Apodemus agrarius in Korea, and in 1978 they isolated the virus from a sick person.

Since 1982, by decision of the WHO Scientific Group, various variants of the disease have been united under the common name “hemorrhagic fever with renal syndrome.”

Etiology

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Pathogens of HFRS – viruses of the genus hantaan (Hantaan pymela, seoul, etc.), family bunyaviridae – belong to spherical RNA-containing viruses with a diameter of 85–110 nm.

Epidemiology

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HFRS is a natural focal virus.

A reservoir of viruses On the territory of Russia there are 16 species of rodents and 4 species of insectivorous animals, in which latent forms of infection are observed; enzootics with the death of animals occur less frequently. The virus is released into the external environment mainly through the urine of rodents, less often with their feces or saliva. Among animals, transmissible transmission of the virus by gamas ticks and fleas is observed.

From rodents to humans under natural or laboratory conditions, the virus is transmitted through airborne dust, nutritional and contact routes. There are no known cases of HFRS infection from a sick person.

The incidence is sporadic, and group outbreaks are also possible. Natural foci are located in certain landscape-geographical zones: coastal areas, woodlands, wet forests with thick grass, which contributes to the preservation of rodents.

The incidence has a clear seasonality : the largest number of cases of the disease is recorded from May to October - December with a maximum rise in June - September, which is due to an increase in the number of rodents, frequent visits forests, fishing trips, agricultural work, etc., as well as in November - December, which is associated with the migration of rodents to residential premises.

Most often, rural residents aged 16–50 years old, mostly men (loggers, hunters, field farmers, etc.), are affected. The morbidity of urban residents is associated with their stay in the suburban area (visiting the forest, relaxing in holiday camps and sanatoriums located near the forest), and working in vivariums.

Immunity After an illness, he is quite persistent. Recurrent diseases are rare.

Pathogenesis and pathological picture

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After entering the human body through damaged skin and mucous membranes and replication in the cells of the macrophage system, the virus enters the blood. The viremia phase develops, which causes the onset of the disease with the development of general toxic symptoms.

Providing a vasotropic effect, the virus damages the walls of blood capillaries both directly and as a result of increased hyaluronidase activity with depolarization of the main substance of the vascular wall, as well as due to the release of histamine and histamine-like substances, activation of the kallikrein-kinin complex, which increase vascular permeability.

Immune complexes play a large role in the genesis of capillary toxicosis. There is damage to the vegetative centers that regulate microcirculation.

As a result of damage to the vascular wall, plasmorrhea develops, the volume of circulating blood decreases, its viscosity increases, which leads to a disorder of microcirculation and contributes to the formation of microthrombi. An increase in capillary permeability in combination with disseminated intravascular coagulation syndrome causes the development of hemorrhagic syndrome, manifested by hemorrhagic rash and bleeding.

The greatest changes develop in the kidneys. The impact of the virus on the renal vessels and microcirculatory disorders cause serous-hemorrhagic edema, which presses the tubules and collecting ducts and contributes to the development of desquamative nephrosis. Glomerular filtration decreases, tubular reabsorption is disrupted, which leads to oligoanuria, massive proteinuria, azotemia and electrolyte imbalances and acidotic changes in the acid-base state.

Massive desquamation of the epithelium and fibrin deposition in the tubules cause the development of obstructive segmental hydronephrosis. The occurrence of renal damage is facilitated by autoantibodies that appear in response to the formation of cellular proteins that acquire the properties of autoantigens, circulating immune complexes and fixed on the basement membrane.

During pathological examination, internal organs reveal dystrophic changes, serous-hemorrhagic edema, hemorrhages. The most pronounced changes are found in the kidneys. The latter are enlarged in volume, flabby, their capsule is easily removed, and there are hemorrhages underneath. The cortex is pale, bulges above the cut surface, the medulla is purplish-red with multiple hemorrhages in the pyramids and pelvis, and there are foci of necrosis. On microscopic examination, the urinary tubules are dilated, their lumen is filled with cylinders, and the collecting ducts are often compressed. The glomerular capsules are dilated, and individual glomeruli have dystrophic and necrobiotic changes. In areas of hemorrhage, the tubules and collecting ducts are grossly altered destructively, their lumen is absent due to compression or filled with cylinders. The epithelium is degenerated and desquamated. Widespread dystrophic changes in the cells of many organs, endocrine glands (adrenal glands, pituitary gland) and autonomic ganglia are also revealed.

As a result of immune reactions (increased antibody titers, IgM and IgG classes, changes in lymphocyte activity) and sanogenic processes, pathological changes in the kidneys regress. This is accompanied by polyuria due to a decrease in the reabsorption capacity of the tubules and a decrease in azotemia with a gradual restoration of renal function over 1 to 4 years.

Clinical picture (Symptoms)

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The main symptoms of HFRS are high fever, hyperemia and puffiness of the face, the appearance of hemorrhagic syndrome and renal dysfunction in the form of oliguria, massive proteinuria and azotemia from the 3rd–4th day of illness, followed by polyuria.

The disease is characterized cyclical course and variety of clinical variants from abortive febrile forms to severe forms with massive hemorrhagic syndrome and persistent acute renal failure.

Incubation period of HFRS 4–49 days, but more often 2–3 weeks. During the course of the disease, 4 periods are distinguished: 1) febrile (1st–4th day of illness); 2) oliguric (days 4–12); 3) polyuric (from 8–12 to 20–24 days); 4) convalescence.

The febrile period, or the initial phase of infection , is characterized by an acute increase in temperature, the appearance of painful headaches and muscle pain, thirst, and dry mouth.

Temperature rises to 38.5–40 °C and remains at high levels for several days, after which it decreases to normal (short lysis or delayed crisis). The duration of the febrile period is on average 5–6 days. After a decrease in temperature, a few days later it may rise again to low-grade levels - a “two-humped” curve.

Excruciating headache from the first days of the disease it is concentrated in the forehead and temples. Patients often complain of blurred vision and the appearance of a “mesh” before the eyes. On examination, puffiness and hyperemia of the face, injection of blood vessels in the sclera and conjunctiva, and hyperemia of the pharynx are naturally noted.

Hemorrhagic enanthema appear from the 2nd–3rd day of illness on the mucous membrane of the soft palate,

and from the 3rd–4th day – petechial rash in the armpits; on the chest, in the collarbone area, sometimes on the neck and face. The rash may appear in stripes that resemble a whiplash.

Along with this there appear major hemorrhages into the skin, sclera, and injection sites.

Subsequently, nasal, uterine, gastric bleeding which can cause deaths. In some patients light forms disease, hemorrhagic manifestations are absent, but the symptoms of “tourniquet” and “pinch”, indicating increased capillary fragility, are always positive.

Pulse at the beginning of the disease it corresponds to temperature, then pronounced bradycardia develops. The boundaries of the heart are normal, the tones are muffled. Blood pressure is reduced in most cases. In severe cases of the disease, the development of infectious-toxic shock is observed. Signs of bronchitis and bronchopneumonia are often detected.

When palpating the abdomen, pain is determined, more often in the hypochondrium, and in some patients - tension abdominal wall. Pain in the abdominal area can subsequently be intense, which necessitates differentiation from surgical diseases of the abdominal cavity.

Liver usually enlarged, the spleen – less often.

effleurage lower back painful.

Chair delayed, but diarrhea with the appearance of mucus and blood in the stool is possible.

In the hemogram in this period of the disease - normocytosis or leukopenia with a neutrophilic shift to the left, thrombocytopenia, increased ESR. A general urine analysis revealed leukocytes and erythrocytes, slight proteinuria.

Oliguric period . From the 3rd–4th day of illness, against the background of high temperature, the oliguric period begins. The condition of the patients noticeably worsens. Severe pain occurs in the lumbar region, often forcing the patient to take a forced position in bed. There is an increase in headache, repeated vomiting occurs, leading to dehydration. The manifestations of hemorrhagic syndrome increase significantly: hemorrhages in the sclera, nasal and gastrointestinal bleeding, hemoptysis.

The amount of urine decreases to 300–500 ml per day; in severe cases, anuria occurs.

Bradycardia, hypotension, cyanosis, and rapid breathing are noted. Palpation of the kidney area is painful (examination should be carried out carefully due to the possible rupture of the renal capsule with rough palpation). From the 6th–7th day of illness, body temperature decreases significantly and less critically, but the condition of the patients worsens. Characterized by pale skin combined with cyanosis of the lips and limbs, severe weakness. Signs of hemorrhagic syndrome persist or increase, azotemia progresses, manifestations of uremia, arterial hypertension, pulmonary edema are possible, and in severe cases coma develops. Peripheral edema is rare.

The hemogram naturally reveals neutrophilic leukocytosis (up to 10-30 * 10^9 /l of blood), plasmacytosis (up to 10-20%), thrombocytopenia, an increase in ESR to 40-60 mm/h, and in case of bleeding - signs of anemia. Characterized by increased levels of residual nitrogen, urea, creatinine, hyperkalemia and signs of metabolic acidosis.

A general urine analysis reveals massive proteinuria (up to 20–110 g/l), the intensity of which varies throughout the day, hypoisosthenuria (relative density of urine 1.002–1.006), hematuria and cylindruria; Casts containing tubular epithelial cells are often found.

From the 9th–13th day of illness, the polyuric period begins. The condition of the patients noticeably improves: nausea and vomiting stop, appetite appears, diuresis increases to 5–8 l, nocturia is characteristic. Patients experience weakness, thirst, and are troubled by shortness of breath and palpitations even with little physical exertion. Lower back pain decreases, but is weak, aching pain may persist for several weeks. Long-term hypoisosthenuria is characteristic.

During the period of convalescence polyuria decreases, body functions are gradually restored.

There are mild, moderate and severe forms of the disease.

• The mild form is considered those cases when the fever is low, hemorrhagic manifestations are mild, oliguria is short-lived, and there is no uremia.
• For moderately severe forms All stages of the disease develop sequentially without life-threatening massive bleeding and anuria, diuresis is 300–900 ml, the residual nitrogen content does not exceed 0.4–0.8 g/l.
• In severe form a pronounced febrile reaction is observed, infectious-toxic shock, hemorrhagic syndrome with bleeding and extensive hemorrhages during internal organs, acute adrenal insufficiency, cerebrovascular accident. Anuria and progressive azotemia (residual nitrogen more than 0.9 g/l) are noted. Death may occur due to shock, azotemic coma, eclampsia, or rupture of the renal capsule. There are known forms of HFRS that occur with encephalitis syndrome.

Complications. Specific complications include infectious-toxic shock, pulmonary edema, uremic coma, eclampsia, kidney rupture, hemorrhages in the brain, adrenal glands, heart muscle (clinical picture of myocardial infarction), pancreas, massive bleeding. Pneumonia, abscesses, phlegmon, mumps, and peritonitis are also possible.

The patient must remain in bed during acute period illness and before the onset of convalescence.

Easily digestible food is prescribed without restrictions on table salt () .

In the initial period in the complex medicinal products include isotonic solutions of glucose and sodium chloride, ascorbic acid, rutin, antihistamines, analgesics, antiplatelet agents. Available positive experience applications antiviral drugs(ribamidil).

Against the background of oliguria and azotemia, limit the intake of meat and fish dishes, as well as foods containing potassium. The amount of fluid drunk and administered to the patient should not exceed the daily volume of excreted urine and vomit by more than 1000 ml, and if high temperature– for 2500 ml.

Treatment of patients with severe forms of HFRS with severe renal failure and azotemia or infectious-toxic shock is carried out in intensive care units using the complex anti-shock measures, prescribing large doses of glucocorticoids, antibiotics wide range actions, methods of blood ultrafiltration, hemodialysis, and in case of massive bleeding - blood transfusions.

Patients are discharged from the hospital after clinical recovery and normalization of laboratory parameters, but not earlier than 3–4 weeks from the onset of the disease with moderate severity and severe forms diseases. Those who have recovered are subject to dispensary observation for 1 year with quarterly monitoring of a general urine test, blood pressure, examination by a nephrologist, and an ophthalmologist.

Prevention

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Preventive actions are aimed at destroying the sources of infection - mouse-like rodents, as well as interrupting the routes of its transmission from rodents to humans.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols Ministry of Health of the Republic of Kazakhstan - 2018

Hemorrhagic fever with renal syndrome (A98.5)

Short description

Approved
Joint Commission on Quality medical services
Ministry of Health of the Republic of Kazakhstan
dated March 29, 2019
Protocol No. 60

Hemorrhagic fever with renal syndrome(GLPS)- an acute viral natural focal disease characterized by fever, general intoxication, and a kind of kidney damage similar to acute interstitial nephritis and the development of thrombohemorrhagic syndrome.

INTRODUCTORY PART

Protocol name: Hemorrhagic fever with renal syndrome

ICD-10 code(s):

Date of development of the protocol: 2018

Abbreviations used in the protocol:

Classification

Table 1. Clinical classification HFRS

Diagnostics

DIAGNOSTIC METHODS, APPROACHES AND PROCEDURES

Diagnostic criteria

Complaints and anamnesis:
initial period (duration 1-3 days)
- fever (38-40°C);
- chills;
- Strong headache;
- weakness;
- sleep disturbance;
- deterioration of vision (decreased visual acuity, “flying spots”, a feeling of fog before the eyes - appears on days 2-7 of illness and continues for 2-4 days ;
- dry mouth;
- weakly positive Pasternatsky symptom.
oliguric period (from 3-4 to 8-11 days of illness)
- body temperature drops to normal, sometimes rising again to subfebrile levels - a “two-humped” curve;
- headache;
- weakness;
- lower back pain;
- stomach ache;
- diarrhea (on days 2-5 of illness in 10-15% of patients)
- oliguria (300-900 ml/day);
- anuria (in severe cases);
- vomiting up to 6-8 times a day or more;
- thrombohemorrhagic syndrome (in severe form in 50-70% of patients, in moderate form - 30-40%, in mild form - 20-25%)

From 6-9 days
- nose bleed;
- blood in urine;
- tarry stools.

polyuric period(from 9-13 days of illness)
- pain in the lower back and abdomen disappears;
- vomiting stops;
- the daily amount of urine increases (up to 3-10 l);
- weakness persists.

Physical examination:
- hyperemia of the skin of the face, neck, upper chest (symptom of “hood”);
- the mucous membrane of the oropharynx is hyperemic; from the 2-3rd day of illness, in most patients, hemorrhagic enanthema appears on the mucous membrane of the soft palate;
- vessels of the sclera and conjunctiva are injected;
- there may be a hemorrhagic rash on the conjunctiva and sclera;
- puffiness of the face, pastiness of the eyelids;
- moderate bradycardia
- in the lungs there is vesicular hard breathing, isolated dry rales, wet rales can be detected, in especially severe cases - pulmonary edema or distress syndrome;
- the tongue is dry, covered with a gray or brown coating;
- the abdomen is moderately swollen, pain in the epigastric and peri-umbilical areas, especially in the projection of the kidneys and sometimes of a diffuse nature. There may be phenomena of peritonism;
- the liver is enlarged and painful in 20-25% of patients;
- in isolated cases, signs of meningism may appear;
- positive Pasternatsky symptom;
- positive tourniquet test;
- 3-5 days (in 10-15% of patients) - petechial rash in the armpits, on the chest, in the collarbone area, sometimes on the neck, face. The rash is not abundant, is grouped in nature and lasts from several hours to 3-5 days;
- gross hematuria (in 7-8%);
- intestinal bleeding (up to 5%);
- bruising at injection sites;
- nosebleeds, hemorrhages in the sclera.

Anamnesis It is necessary to clarify the following risk factors for infection:
. poor personal hygiene
. use fresh vegetables without heat treatment from storage (cabbage, carrots, etc.);

HFRS and pregnancy.
A newborn can become infected in utero, but more often during childbirth or immediately after it. The outcome depends on the virulence of the particular circulating serotype, the mode of transmission, and the presence or absence of passively transmitted maternal antibodies.
The life of a pregnant woman is threatened by the development of specific and nonspecific complications, in particular infectious-toxic shock, disseminated intravascular coagulation syndrome, pulmonary and cerebral edema, hemorrhages in the brain, myocardium, adrenal glands, eclampsia, acute cardiovascular failure, sepsis, etc.

Laboratory research:
- UAC: neutrophilic leukocytosis (up to 15-30x10 9 l), plasmacytosis, thrombocytopenia, due to blood thickening, the level of hemoglobin and red blood cells may increase, but with bleeding these indicators decrease, moderate increase in ESR
- OAM: proteinuria (up to 66 g/l), cylindruria (gealine and granular), hematuria
- Determination of blood group and Rh factor.
- Coagulogram.
- Blood chemistry: total protein, albumin, increase in the level of residual nitrogen, urea, creatinine, also hyperkalemia, hypermagnesemia, hyponatremia, bilirubin, ALT, AST.
- Stool analysis to detect intraintestinal bleeding.
- Serological diagnostics: (RNIF, ELISA, RPGA), paired sera are used, obtained with an interval of 10-12 days (the first on the 4-5th day of illness, the second - after the 14th day of illness). Diagnostic criterion- increase in antibody titer by 4 times or more.
- Determination by ELISA of AT class Ig M, IgG
- PCR method: isolation of virus RNA from nasopharyngeal mucus, CSF, feces, blood and other secretions

Instrumental studies (according to indications):

Table 2. Methods instrumental diagnostics

Indications for consultation with specialists:

Table 3. Indications for specialist consultations

Picture 1.Algorithm for diagnostic search in the initial periodhemorrhagic fever with renal syndrome

Diagnostic algorithm for HFRS:




Figure 2. Algorithm for diagnostic search for hemorrhagic fever with renal syndrome according to hemorrhagic syndrome

Differential diagnosis

Differential diagnosis and rationale for additional studies

Table 4. Criteria differential diagnosis HFRS

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Treatment

Drugs ( active ingredients), used in the treatment

Treatment (outpatient clinic)

OUTPATIENT TREATMENT TACTICS: no.

Treatment (inpatient)

TREATMENT TACTICS AT THE INPATIENT LEVEL

Patient observation card: inpatient card;

Patient routing:

Non-drug treatment:

• Bed rest - until polyuria stops, on average: for mild form - 7-10 days, moderate - 2-3 weeks and severe - at least 3-4 weeks from the onset of the disease.
• Diet: Table No. 4 without salt restriction is recommended; for severe forms and complications - table No. 1. Meals should be complete, fractional, warm. With oligoanuria, foods rich in protein (meat, fish, legumes) and potassium (vegetables, fruits) are excluded. In polyuria, on the contrary, these products are most necessary. The drinking regime should be dosed, taking into account the allocated liquid. The amount of liquid drunk and injected should not exceed the volume excreted (urine, vomit, stool) by more than 500-700 ml.

1. Ribavirin: first dose 2000 mg once (10 capsules), then 1000 mg every 6 hours for 4 days, then 500 mg every 6 hours for 5 days, course of treatment is 14 days.
2. Ribavirin(intravenous form) - initially 33 mg/kg (maximum 2 g) is administered diluted in 0.9% NaCl solution or 5% dextrose solution, then 16 mg/kg (maximum single dose 1 g) every 6 hours for the first 4 days , then the next 3 days 8 mg/kg (maximum 500 mg) every 8 hours, treatment course is 14 days.

• If hypoproteinemia develops (a decrease in total blood protein below 52 g/l, albumin below 20 g/l), albumin 20% - 200-300 ml or plasma preparations should be included in the infusion program.
• If signs of hypercoagulation appear, heparin up to 10,000-15,000 units/day, hypocoagulation (decrease in coagulation rates by 1/3 of the norm), heparin up to 5,000 units/day, fresh frozen plasma (FFP) at a dose of 15 ml/kg intravenous drip are indicated.
• Hemostatic therapy (etamzilate) 250 mg every 6 hours.
• Nutritional support is provided through enteral nutrition and, if necessary, artificial nutritional mixtures. If enteral nutrition is not possible, parenteral nutrition is performed.
• For hyperthermia, the drug of choice is paracetamol 500 mg, orally; rectal suppositories 0.25; 0.3 and 0.5 g (for hyperthermia above 38°C). Drugs are absolutely contraindicated acetylsalicylic acid(aspirin), which is associated with irreversible inhibition of cyclooxygenase in circulating platelets and endothelium.
• If there is a history peptic ulcer stomach and duodenum, already during this period of the disease, hydrogen pump inhibitors or H2 histamine receptor blockers are recommended.
• Diuretics should be prescribed after hemodynamic normalization (or CVP > 120 mmH2O); in case of HFRS, administration of mannitol is contraindicated;
• For cupping pain syndrome non-narcotic analgesics are recommended; in cases of their ineffectiveness, antipsychotics and narcotic analgesics should be prescribed;
• For persistent vomiting and hiccups, gastric lavage, novocaine (peros), metoclopramide, atropine, chlorpromazine are indicated;
• At arterial hypertension(ACE inhibitors, beta blockers and etc.).
• Antibacterial therapy in the first two periods of the disease is carried out only in the presence of bacterial complications (pneumonia, abscesses, sepsis, etc.); it is recommended to use semi-synthetic penicillins and cephalosporins.
• Desensitizing therapy.
• If conservative measures are ineffective, extracorporeal hemodialysis is indicated, the need for which may arise on days 8-12 of illness.

• ITS decompensated,
• hemorrhagic stroke,
• hemorrhagic infarction of the adenohypophysis,
• massive bleeding
• spontaneous kidney rupture.

• body temperature;

• diuresis;
• azotemia indicators;
• hemograms;
• absence of pyuria and microhematuria;
• isohyposthenuria is not a contraindication for discharge.

• mild form - no earlier than the 12th day of illness;
• moderate - no earlier than the 16th day of illness;
• severe form - no earlier than 21 days of illness.

Hospitalization

INDICATIONS FOR HOSPITALIZATION, INDICATING THE TYPE OF HOSPITALIZATION:

Indications for planned hospitalization: No

Indications for emergency hospitalization:

• fever,
• intoxication,
• hemorrhagic syndrome.

Information

Sources and literature

1. Minutes of meetings of the Joint Commission on the Quality of Medical Services of the Ministry of Health of the Republic of Kazakhstan, 2018
   1. 1. Sirotin B.Z. Hemorrhagic fever with renal syndrome.-Khabarovsk, 1994.-302 p. 2. Classifications of main infectious diseases Reference materials for students of the 5th and 6th years, in the discipline " Infectious diseases» Ivanovo 2014, S43-44 3. Lobzin Yu.V. Guide to Infectious Diseases- Tutorial. - St. Petersburg: 2000. - 226 p. 3. Infectious diseases: national guidelines / Ed. N.D.Yushchuk, Yu.Ya.Vengerova. - M.: GEOTAR-Media, 2009. - 1040 p. 4. Ma C, Yu P, Nawaz M, Zuo S, Jin T, Li Y, Li J, Li H, Xu J. J. 2012. Hantaviruses in rodents and humans, Xi’an, PR China. Vol. 93(10):2227-2236 doi:10.1099/vir.0.043364-0 5. Krautkramer, E., Zeier, M. and Plyusnin, A. 2012. Hantavirus infection: an emerging infectious disease causing acute renal failure. Kidney International (2012) 83, 23–27; doi:10.1038/ki.2012.360 6. Fulhorst F, C., Koster T, F., Enria A, D., Peters C, J. 2011. Hantavirus Infections. In: Tropical Infectious Diseases: Principles, Pathogens and Practice, Third Ed., Philadelphia: Elsevier. p. 470-480 7. Jonsson B, C., Figeiredo T M, L. and Vapalathi, O. 2010. A Global Perspective on Hantavirus Ecology, Epidemiology, and Disease, Clinical Microbiology Reviews, Vol. 23. p. 412-441 8. Wichmann, D., Josef Grone, H., Frese, M., Pavlovic, J. Anheier, B. 2002. Hantaan Virus Infection Causes an Acute Neurological Disease That Is Fatal in Adult Laboratory Mice, Journal of Virology , Vol. 76, No. 17. p. 8890-8899. doi: 10.1128/JVI.76.17.8890–8899.2002 9. Xu ZY, et al. Epidemiological studies of hemorrhagic fever with renal syndrome: analysis of risk factors and mode of transmission. Journal of Infectious Diseases1985; 152: 137–144. 10. Denecke, B., Bigalke, B., Haap, M., Overkamp, ​​D., Lehnert, H., and Haas, C. S. (2010). Hantavirus infection: a neglected diagnosis in thrombocytopenia and fever? Mayo Clin. Proc. 85, 1016–1020. doi: 10.4065/mcp.20 09.0040 11. Kruger DH, Figueiredo LT, Song JW, Klempa B. Hantaviruses are globally emerging pathogens. J Clin Virol 2015; 64:128.

Information

ORGANIZATIONAL ASPECTS OF THE PROTOCOL

List of protocol developers with qualification information:
1. Kosherova Bakhyt Nurgalievna - Doctor of Medical Sciences, Professor, Vice-Rector for Clinical Work and Continuing Professional Development of NAO " Medical University Karaganda".
2. Dmitrovsky Andrey Mikhailovich - Doctor of Medical Sciences, Professor of the Department of Infectious and Tropical Diseases of JSC National Medical University;
3. Egemberdieva Ravilya Aitmagambetovna, Doctor of Medical Sciences, Professor of the Department of Infectious and Tropical Diseases of JSC National Medical University, highest medical category;
4. Kurmangazin Meirambek Saginaevich - Candidate of Medical Sciences, Head of the Department of Infectious Diseases of the NAO West Kazakhstan Medical University named after. Marat Ospanov";
5. Yukhnevich Ekaterina Aleksandrovna - clinical pharmacologist, acting associate professor of the department clinical pharmacology And evidence-based medicine NJSC "Medical University of Karaganda".

Disclosure of no conflict of interest: No.

Reviewers:
Begaidarova Rozalia Khasanovna - Doctor of Medical Sciences, Professor of the NAO Department of Infectious Diseases and Phthisiology of the NAO "Medical University of Karaganda", a doctor of the highest category.

Indication of the conditions for reviewing the protocol:
revision of the protocol after 5 years and/or when new diagnostic and/or treatment methods with a higher level of evidence become available.

Attached files

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A severe disease of natural origin affects not only the kidneys, but also adjacent vessels.

It has several names, the main one of which is HFRS, which stands for “hemorrhagic fever with renal syndrome.” The virus is widespread in the European part of Russia and the Far Eastern District, as well as in Siberia and Transbaikalia. The disease is widespread throughout the world.

What is it - disease clinic

Manchurian gastritis, Far Eastern hemorrhagic fever, hemorrhagic nephrosonephritis, Songo fever are synonyms of the same thing viral disease – hemorrhagic fever with renal syndrome (HFRS). The source of infection is sick small rodents, for example, the field mouse. In cities, rats can serve as carriers.

In ICD-10 hemorrhagic nephrosonephritis is under code A98.5. Here the pathology has a classification:

• Crimean hemorrhagic fever A98.0;
• Omsk hemorrhagic fever A98.1;
• Kyasanur forest disease A98.2;
• Disease caused by Marburg virus A98.3;
• Ebola A98.4 virus disease;
• Hemorrhagic fever with renal syndrome A 98.5.

In turn, hemorrhoidal fever with renal syndrome divided into several types: Korean, Russian, Tula, Scandinavian epidemic.

Causes of infection and routes of transmission of the virus

The hemorrhagic nephrosonephritis virus is known to have a diameter of approximately 90–100 nm. The medical history begins since 1976, when it was first discovered in the lungs of mice. Then the official name was given: the genus Hantanaan of the family Bunyaviridae. And now HFRS has not lost its relevance.

The virus is quite tenacious and active: it ceases to act only at a temperature of +50 C, but even in this case it remains viable for almost an hour. And the external temperature of +20 C is generally the most comfortable. That is why the peak of cases occurs in the summer. At zero degrees, viruses are active for 13 hours.

What you need to know about hemorrhagic fever with renal syndrome:

1. Method of transmission of the virus to humans: rodents, or rather their feces. People can get the disease through airborne transmission, that is, by inhaling dusty air that contains the virus.

The risk of transmission is present through direct contact with carriers, as well as through consumption of contaminated food or water, as well as through household objects (for example, when spending time in nature);

2. Who is susceptible to infection: agricultural workers, farmers, agrarians, foresters, hunters, ordinary vacationers who spend time in nature. Men 17 – 40 years old are more prone to this disease;
3. There is a tendency for the disease to be seasonal: in the winter months the virus is not active, and the risk of infection tends to zero. From the beginning of summer to the end of October, the probability increases several times;
4. The main foci of virus activity in last years observed in Samara, Saratov, Ulyanovsk regions, as well as in Udmurtia, Bashkiria and Tatarstan.

The disease is not transmitted from person to person. The patient is completely safe for others.

It is worth noting that the disease always flows in acute form . There is no chronic course. After suffering from the disease, lifelong immunity is acquired.

Symptoms and signs

HFRS has a fairly long incubation period. It can last more than a month - up to 50 days. But most often the pathogen begins to show its activity after two weeks. This time is enough for the virus to break through the body’s defenses and enter the bloodstream, quite severely affecting the blood vessels.

On initial stage symptoms develop quickly and violently:

• The temperature rises sharply to high levels - 39.5–40 C;
• The person has a fever and a severe headache;
• Vision is impaired: pain in the eyes, feeling of fainting, decreased clarity of vision. False sensation of seeing the surroundings in red;
• From the 3rd day of illness, reddish rashes appear in the mouth, in the collarbone area, on the neck and armpits;
• Nausea and then vomiting up to 9 times a day;
• Pain in the lower back during the Pasternatsky test, which indicates possible kidney damage;
• Development of conjunctivitis;
• Feeling of dryness both in the mouth and throughout the body;
• Oliguria;
• Blood pressure is low, which leads to possible dizziness.

Approximately on day 9-10 of illness The body temperature drops, but the patient does not feel better.

Join kidney symptoms: arterial hypotension is replaced by high blood pressure, the patient cannot find a place for himself due to lower back pain, and the amount of urine increases, nosebleeds appear. Characteristic loose stool, swelling of the face, increased blood clotting.

From 15-16 days of illness the patient’s condition begins to gradually return to normal: vomiting and diarrhea stop, pain subsides, and improvement general state. Blood clotting indicators also improve.

In general, the course of hemorrhagic fever with renal syndrome is usually divided into several degrees: mild, moderate and severe.

The most dangerous is the severe degree, in which case coma may develop, which can be fatal.

Patients of any severity in recovery period Asthenia, increased anxiety, and shortness of breath persist for a long time. This can lead to the development of hypochondria and neuroses.

Differential diagnosis

When acute symptoms HFRS is necessary consult a doctor immediately, because the signs of this disease are very similar to other equally dangerous diseases: typhoid fever, influenza, pyelonephritis, leptospirosis.

The doctor collects the patient's medical history, as well as finds out his whereabouts Lately . This is a mandatory item if HFRS is suspected, because in this way possible contact with infected animals is revealed.

Difficulties for diagnosis are erased and atypical forms HFRS.

First, an external examination is carried out. The doctor pays attention to the persistent cyclical nature of the disease, symptoms characteristic of hemorrhagic fever, such as muscle pain, vision problems, rashes, oliguria, etc.

Special methods - enzyme immunoassay - ELISA, immunofluorescence reaction - RNIF, RIA - radioimmunoassay must be done dynamically. After all, the effect of antibodies in HFRS is not constant, and their maximum concentration is achieved only by the 13th day of illness.

The RNIF method must be applied as early as possible and repeated after 6 days of disease activity. Such a study will definitely confirm the diagnosis if antibody titers increase at least 3 times.

In severe cases and in the presence of complications, the doctor prescribes to the patient additional research : FGDS, x-ray or.

After the diagnosis has been formulated, treatment of hemorrhagic nephrosonephritis is carried out only in a hospital setting. As a rule, this is an infectious diseases hospital.

Moreover, a late visit to a doctor or self-medication can end in disaster.

In the hospital, doctors carry out complex therapy , which includes:

• Mandatory bed rest;
• Replenishment of fluid losses and elimination possible dehydration, as well as intoxication: intravenous glucose, sodium chloride, saline solution;
• Fighting the virus: prescribing antiviral drugs: “Vitaferon”, “Grippferon”, “Ingraverin” and others;
• Anti-inflammatory drugs: Nurofen;
• Control of blood clotting: “Aspirin”, “Thromboass”;
• For renal syndrome, diuretics are prescribed: Furosemide, Tolvaptan;
• Vitamin preparations: any;
• Appointment possible antibacterial agents: “Ceftriaxone”, “Flemoxin”, “Ampicillin”;
• Antispasmodics: “Ketorol”, “”;
• Antishock therapy for toxic shock.

It must be remembered that in case of shock, painkillers and hemodesis should not be used.

When severe kidney damage is observed, it is carried out. Extracorporeal dialysis is used when the patient’s condition is very serious, when other means do not help.

If the HFRS virus found in children, then, as a rule, special monitoring is established for such patients, because their course of the disease is especially severe. The principles of therapy do not differ from adults, the only differences are in adjusting the doses of drugs.

Patients are prescribed mandatory diet No. 4. You can take salt, but meat is even necessary during polyuria. You need to drink enough fluids, especially healthy ones mineral water(“Essentuki”, etc.) If oliguria is present, then it is necessary to exclude foods high in protein.

In severe forms of the disease, the patient table number 1 is prescribed. During the recovery period, you must also adhere to a diet. Try to eat well, limit fried, salty and smoked foods.

With properly organized treatment, the patient recovers completely, although “echoes” of the disease may persist for some time.

Complications after illness

Hemorrhagic fever with renal syndrome is a serious disease that threatens the development of such complications, How:

• various pneumonias,
• acute vascular insufficiency,
• lung problems
• gap,
• bleeding,
• acute renal failure and others.

Prevention of infection

At the beginning of the summer season, during the period of activity of the HFRS virus (May-October), SanPin introduces control over the activities of individual entrepreneurs, agricultural workers, agricultural enterprises and other organizations working in one way or another in agriculture. They must comply with all sanitary and epidemiological rules.

In hotspots measures are being taken to exterminate dangerous rodents.

Summer residents and vacationers are recommended to thoroughly clean the house (necessarily wearing protective gloves); when being in nature, they should be careful: wash your hands especially thoroughly and hide food, do not touch wild animals with your hands!

If you suspect a developing fever, you should immediately call an ambulance!

Hemorrhagic fever with renal syndrome is a common disease, but nevertheless, the risk of contracting it is not so great. It is important, if possible, not to travel to areas where the virus is active and to try maintain personal hygiene.

Find out how to protect yourself from this virus from the video: