Etiology and pathogenesis of hemorrhagic fever with renal syndrome. Hemorrhagic fever with renal syndrome Hemorrhagic fever ICD 10

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 the subsequent development of thrombohemorrhagic syndrome.

HFRS: classification

There is currently no unified classification of this infectious disease. Causes, factors of occurrence, methods of spread of the disease Etiology Pathogen

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.

Routes of transmission of HFRS In nature and rural areas, the virus is spread by several species of mice. The pathogen is excreted in their feces. Infection occurs through airborne dust or nutrition. A person becomes infected through direct contact with rodents, consumption of water and food containing their feces, as well as through inhalation of dust with microparticles of dried rodent feces. Infection through household items is possible. The peak incidence occurs in the autumn-winter period, when infection carriers move into residential and auxiliary buildings. In urban environments, the virus can be carried by rats. It is impossible to catch a fever from another person. To prevent the occurrence of outbreaks of epidemics, deratization is carried out, i.e. destruction of animals that are latent carriers of the virus. Note: up to 90% of cases are males aged 16 to 50 years. Pathogenesis The effect of the virus on organs and systems The virus enters the human body through the mucous membrane of the respiratory system. In some cases, the entrance gates of infection can be the mucous membranes of the digestive organs and damaged skin. No pathological changes are observed directly at the site of virus entry. Symptoms appear after the pathogen spreads throughout the body through the bloodstream and intoxication begins to increase. The virus is characterized by pronounced vasotropy; it has a pronounced negative effect on the vascular wall. Also an important role in the pathogenesis of hemorrhagic syndrome is the disruption of the functional activity of the blood coagulation system. In particularly severe cases of the disease, glomerular filtration is significantly reduced, although the structure of the glomeruli is not disturbed. The severity of thrombohemorrhagic syndrome directly depends on the severity of the disease. Immunity After once suffering from “Korean fever”, stable immunity remains; cases of re-infection have not been described in the medical literature.

Signs of HFRS

With HFRS, the incubation period can range from 7 to 45 days (most often about 3 weeks). It is customary to distinguish the following stages of disease development: 1. initial; 2. oliguric; 3. polyuric; 4. convalescence (recovery). With HFRS, the clinical picture depends on a number of factors, including the individual characteristics of the body and the timeliness of measures taken. For HFRS disease, the main symptoms are as follows: Initial period of HFRS

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

From 3-4 to 8-11 days (oliguric period)

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.

From 6-9 days

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.

The polyuric period begins from the 9-13th day from the first clinical manifestations. Vomiting disappears, as well as severe pain in the lower back and abdomen, appetite returns and insomnia disappears. Daily diuresis increases to 3-5 liters. Convalescence occurs from 20-25 days. If these symptoms appear, you should immediately seek medical help. Treatment should be carried out only in a specialized hospital.

Possible complications of HFRS

The disease can cause severe complications, including:

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

In some cases, HFRS, also known as Churilov's disease, may be accompanied by pronounced brain symptoms. In this case, it is customary to talk about either a complication or a special “meningoencephalitic” form of the course. The consequences of HFRS cannot be underestimated. Lack of adequate treatment against the background of developed complications can cause death.

Diagnostics

A differential diagnosis of HFRS with such infectious diseases as other hemorrhagic fevers, typhoid fever, leptospirosis, tick-borne rickettsiosis, tick-borne encephalitis and common flu is mandatory. The diagnosis of HFRS is made taking into account epidemiological data. The patient’s possible stay in endemic foci, the general level of morbidity in the area and seasonality are taken into account. Much attention is paid to fairly specific clinical symptoms. Laboratory diagnosis of HFRS reveals the presence of casts in the urine, as well as significant proteinuria. A blood test for HFRS shows an increase in plasma cells, an increase in the erythrocyte sedimentation rate and pronounced leukocytosis. Of the special laboratory methods, the detection of IgM by enzyme-linked immunosorbent assay is often used. If there are complications already during treatment, some types of instrumental studies may be needed: FGDS, ultrasound, CT and radiography.

HFRS treatment

There are no standard treatment regimens for HFRS. Therapy should be comprehensive and aimed at eliminating the most important pathogenetic syndromes. It is necessary to combat DIC syndrome, renal failure and general intoxication. Treatment involves early hospitalization and strict bed rest for 1 to 4 weeks, depending on the severity of the disease. Strict control of the volume of fluid consumed and lost by the patient is necessary. Monitoring of hemodynamics, hemogram, hematocrit is required; Urine tests and electrolyte balance are regularly examined.

Drug therapy.

During the febrile period, antiviral, antioxidant and detoxification therapy is carried out and measures are taken to prevent the development of DIC syndrome.

Etiotropic therapy

For etiotropic therapy, either immunobiological drugs (interferons, hyperimmune plasma, donor specific immunoglobulin, etc.) or chemotherapy drugs - ribavirin (nucleoside derivative), as well as amixin, cycloferon and iodantipyrine (interferon inducers) are used. The fight against intoxication involves infusions of glucose solutions and saline with vitamin C. Hemodez can be administered once. At body temperatures above 39°C, anti-inflammatory drugs with an antipyretic effect are administered. To prevent DIC syndrome, the patient is administered antiplatelet agents, angioprotectors, and in severe cases, protease inhibitors and fresh frozen plasma. Administration of antioxidants to patients (for example, ubiquinone and tocopherol) is indicated.

Antishock therapy

To prevent the development of infectious-toxic shock, early hospitalization and strict bed rest are indicated. If ITS has developed (more often this happens on days 4-6 from the onset of the disease), then the patient is given intravenous drips of rheopolyglucin (400 ml) with hydrocortisone (10 ml), glucocorticosteroid drugs, 4% sodium bicarbonate solution (200 ml intravenously), cardiotonic drugs and cardiac glycosides (cordiamin, strophanthin, korglykon) intravenously. If measures are ineffective or stage 3 shock develops, dopamine administration with glucose or saline is indicated. When disseminated intravascular coagulation develops against the background of shock, heparin, protease inhibitors and angioprotectors are indicated. After restoration of normal hemodynamics, the patient is administered diuretics (Lasix). Special instructions: In case of infectious-toxic shock, antispasmodics, sympathomimetics, hemodez and polyglucin should not be used. In the oliguric period, it is necessary to reduce protein catabolism, eliminate azotemia and reduce intoxication. Correction of acid-base and water-electrolyte balance, correction of disseminated intravascular coagulation, as well as prevention and treatment of possible complications are also necessary. Gastric and intestinal lavage with a weakly alkaline solution and intravenous infusions of glucose (with insulin) are used. Enterosorbents are prescribed orally. Protease inhibitors are also recommended. To combat overhydration, the administration of Lasix is indicated, and sodium bicarbonate is used to reduce acidosis. Correction of hyperkalemia involves glucose-insulin therapy and a potassium-free diet. The pain syndrome is relieved by analgesics with desensitizing agents, persistent vomiting is eliminated by taking a solution of novocaine (orally) or atropine. The development of convulsive syndrome requires the use of relanium, aminazine or sodium hydroxybutyrate. For infectious complications, antibiotics from the groups of cephalosporins and semisynthetic penicillins are prescribed. During the period of convalescence, the patient needs general restorative drug therapy (including vitamins and ATP preparations).

Additional Methods

If conservative methods are ineffective, the patient may be indicated for extracorporeal dialysis.

HFRS: prevention

To prevent infection, it is often enough to observe the rules of personal hygiene while in the forest or rural areas. Water from open sources and containers should be boiled before drinking, hands should be washed thoroughly, and food should be stored in airtight containers. Under no circumstances should you handle rodents. After accidental contact, it is recommended to disinfect clothing and skin. When working in dusty areas (including barns and haylofts), you need to use a respirator.

Diet for HFRS and after recovery

Nutrition for HFRS should be fractional. For mild to moderate illness, patients are recommended to use table No. 4 (without limiting table salt), and for severe forms and the development of complications, table No. 1 is recommended. Against the background of oliguria and anuria, animal and plant foods high in protein and potassium should be excluded from the diet. Meat and legumes, on the contrary, should be consumed during polyuria! The amount of fluid consumed should not exceed the volume excreted by more than 500-700 ml. The rehabilitation period after HFRS involves a nutritious diet with a limit on salty, fatty, fried and spicy foods.

Features in children

HFRS in children is especially severe. The principles of therapy do not differ from those in the treatment of adult patients.

Features in pregnant women

The disease poses a great danger to the fetus. If a woman falls ill during lactation, the infant is immediately transferred to artificial feeding.

Zoonotic hantavirus infection characterized by thrombohemorrhagic syndrome and predominant kidney damage. Clinical manifestations include acute fever, hemorrhagic rash, bleeding, interstitial nephritis, and in severe cases, acute renal failure. Specific laboratory methods for diagnosing hemorrhagic fever with renal syndrome include RIF, ELISA, RIA, and PCR. Treatment consists of administering specific immunoglobulin, interferon preparations, detoxification and symptomatic therapy, and hemodialysis.

ICD-10

A98.5

General information

Hemorrhagic fever with renal syndrome (HFRS) is a natural focal viral disease, the characteristic signs of which are fever, intoxication, increased bleeding and kidney damage (nephrosonephritis). On the territory of our country, endemic areas are the Far East, Eastern Siberia, Transbaikalia, Kazakhstan, European territory, therefore HFRS is known under various names: Korean, Far Eastern, Ural, Yaroslavl, Tula, Transcarpathian hemorrhagic fever, etc. Every year in Russia from 5 to 20 thousand cases of hemorrhagic fever with renal syndrome. The peak incidence of HFRS occurs between June and October; The main contingent of cases (70-90%) are men aged 16-50 years.

Causes of HFRS

The causative agents of the disease are RNA-containing viral agents of the genus Hantavirus (hantaviruses), belonging to the Bunyaviridae family. Four serotypes of hantaviruses are pathogenic for humans: Hantaan, Dubrava, Puumala, Seoul. In the external environment, viruses remain stable for a relatively long time at negative temperatures and are less stable at a temperature of 37°C. Viruses are spherical or spiral in shape, with a diameter of 80-120 nm; contain single-stranded RNA. Hantaviruses have tropism for monocytes, cells of the kidneys, lungs, liver, salivary glands and multiply in the cytoplasm of infected cells.

The carriers of the causative agents of hemorrhagic fever with renal syndrome are rodents: field and forest mice, voles, house rats, which become infected from each other through the bites of ticks and fleas. Rodents carry the infection in the form of latent virus carriage, releasing pathogens into the external environment with saliva, feces and urine. The entry of material infected with rodent secretions into the human body can occur by aspiration (by inhalation), contact (by contact with the skin) or alimentary (by eating) route. The high-risk group for the incidence of hemorrhagic fever with renal syndrome includes agricultural and industrial workers, tractor drivers, and drivers who are actively in contact with environmental objects. The incidence of human disease directly depends on the number of infected rodents in a given area. HFRS is recorded mainly in the form of sporadic cases; less often - in the form of local epidemic outbreaks. After an infection, persistent lifelong immunity remains; cases of repeated incidence are rare.

The pathogenetic essence of hemorrhagic fever with renal syndrome consists of necrotizing panvasculitis, disseminated intravascular coagulation syndrome and acute renal failure. After infection, primary replication of the virus occurs in the vascular endothelium and epithelial cells of internal organs. Following the accumulation of viruses, viremia and generalization of infection occur, which are clinically manifested by general toxic symptoms. In the pathogenesis of hemorrhagic fever with renal syndrome, an important role is played by the resulting autoantibodies, autoantigens, CIC, which have a capillary toxic effect, causing damage to the walls of blood vessels, impaired blood clotting, the development of thrombohemorrhagic syndrome with damage to the kidneys and other parenchymal organs (liver, pancreas, adrenal glands, myocardium) , CNS. Renal syndrome is characterized by massive proteinuria, oligoanuria, azotemia, and impaired CBS.

Symptoms of HFRS

Hemorrhagic fever with renal syndrome is characterized by a cyclic course with a succession of several periods:

incubation (from 2-5 days to 50 days - on average 2-3 weeks)
prodromal (2-3 days)
febrile (3-6 days)
oliguric (from 3-6 to 8-14 days of HFRS)
polyuric (from 9-13 days of HFRS)
convalescent (early - from 3 weeks to 2 months, late - up to 2-3 years).

Depending on the severity of symptoms, the severity of infectious-toxic, hemorrhagic and renal syndromes, typical, erased and subclinical variants are distinguished; mild, moderate and severe forms of hemorrhagic fever with renal syndrome.

After the incubation period, a short prodromal period begins, during which fatigue, malaise, headaches, myalgia, and low-grade fever are noted. The febrile period develops acutely, with an increase in body temperature to 39-41°C, chills and general toxic symptoms (weakness, headache, nausea, vomiting, sleep disorders, arthralgia, body aches). Characterized by pain in the eyeballs, blurred vision, flashing “spots”, seeing objects in red. At the height of the febrile period, hemorrhagic rashes appear on the mucous membranes of the oral cavity, skin of the chest, axillary areas, and neck. An objective examination reveals hyperemia and puffiness of the face, injection of blood vessels of the conjunctiva and sclera, bradycardia and arterial hypotension up to collapse.

During the oliguric period of hemorrhagic fever with renal syndrome, body temperature decreases to normal or low-grade levels, but this does not lead to an improvement in the patient’s condition. At this stage, the symptoms of intoxication intensify even more and signs of kidney damage appear: lower back pain increases, diuresis sharply decreases, and arterial hypertension develops. Hematuria, proteinuria, and cylindruria are detected in the urine. As azotemia increases, acute renal failure develops; in severe cases - uremic coma. Most patients experience uncontrollable vomiting and diarrhea. Hemorrhagic syndrome can be expressed to varying degrees and include gross hematuria, bleeding from injection sites, nasal, uterine, and gastrointestinal bleeding. During the oliguric period, severe complications may develop (hemorrhages in the brain, pituitary gland, adrenal glands), causing death.

The transition of hemorrhagic fever with renal syndrome to the polyuric stage is marked by subjective and objective improvements: normalization of sleep and appetite, cessation of vomiting, disappearance of lower back pain, etc. Characteristic signs of this period are an increase in daily diuresis to 3-5 l and isohyposthenuria. During polyuria, dry mouth and thirst persist.

The period of convalescence for hemorrhagic fever with renal syndrome can be delayed for several months and even years. In patients, post-infectious asthenia persists for a long time, characterized by general weakness, decreased performance, fatigue, and emotional lability. Autonomic dystonia syndrome is expressed by hypotension, insomnia, shortness of breath with minimal exertion, and increased sweating.

Specific complications of severe clinical variants of HFRS may include infectious-toxic shock, hemorrhages in parenchymal organs, pulmonary and cerebral edema, bleeding, myocarditis, meningoencephalitis, uremia, etc. When a bacterial infection is associated, the development of pneumonia, pyelonephritis, purulent otitis, abscesses, phlegmon is possible , sepsis.

Diagnosis of HFRS

Clinical diagnosis of HFRS is based on the cyclical course of the infection and the characteristic change of periods. When collecting an epidemiological history, attention is paid to the patient’s stay in an endemic area and possible direct or indirect contact with rodents. When conducting a nonspecific examination, the dynamics of changes in indicators of general and biochemical urine analysis, electrolytes, biochemical blood samples, CBS, coagulogram, etc. are taken into account. In order to assess the severity and prognosis of the disease, ultrasound of the kidneys, FGDS, chest radiography, ECG, etc. are performed.

Specific laboratory diagnosis of hemorrhagic fever with renal syndrome is carried out using serological methods (ELISA, RNIF, RIA) over time. Antibodies in the blood serum appear at the end of the 1st week of illness, reach their maximum concentration by the end of the 2nd week and remain in the blood for 5–7 years. Virus RNA can be isolated using a PCR assay. HFRS is differentiated from leptospirosis, acute glomerulonephritis, pyelonephritis and enterovirus infection, and other hemorrhagic fevers.

Treatment of HFRS

Patients with hemorrhagic fever with renal syndrome are hospitalized in an infectious diseases hospital. They are prescribed strict bed rest and diet No. 4; water balance, hemodynamics, indicators of the functioning of the cardiovascular system and kidneys are monitored. Etiotropic therapy for hemorrhagic fever with renal syndrome is most effective in the first 3-5 days from the onset of the disease and includes the introduction of donor specific immunoglobulin against HFRS, the prescription of interferon drugs, antiviral chemotherapy drugs (ribavirin).

In the febrile period, infusion detoxification therapy is carried out (intravenous infusions of glucose and saline solutions); prevention of DIC syndrome (administration of antiplatelet drugs and angioprotectors); in severe cases, glucocorticosteroids are used. In the oliguric period, diuresis is stimulated (administration of loading doses of furosemide), acidosis and hyperkalemia are corrected, and bleeding is prevented. With increasing acute renal failure, transfer of the patient to extracorporeal infectious disease specialist, nephrologist and ophthalmologist is indicated throughout the year. Severe course is associated with a high risk of complications; Mortality from HFRS ranges from 7-10%.

Prevention of hemorrhagic fever with renal syndrome consists of exterminating mouse-like rodents in natural foci of infection, preventing contamination of homes, water sources and food products with rodent secretions, and deratization of residential and industrial premises. No specific vaccination against HFRS has been developed.

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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 to the forest, fishing trips, agricultural work, etc., as well as in November - December, which associated with the migration of rodents into 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.

A pathological examination reveals dystrophic changes, serous-hemorrhagic edema, and hemorrhages in the internal organs. 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 with mild forms of the 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 in the 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 mild, 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 in the internal organs, acute adrenal insufficiency, and cerebrovascular accident are possible. 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 the acute period of the disease and until the onset of convalescence.

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

In the initial period, the complex of therapeutic agents includes isotonic solutions of glucose and sodium chloride, ascorbic acid, rutin, antihistamines, analgesics, and antiplatelet agents. There is positive experience with the use of 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 at high temperatures - by 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 a complex of anti-shock measures, prescribing large doses of glucocorticoids, broad-spectrum antibiotics, 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 in moderate and severe forms of the disease. 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 measures are aimed at destroying the sources of infection - mouse-like rodents, as well as interrupting the routes of its transmission from rodents to humans.

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 for the same 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:

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);

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;
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;
The main foci of virus activity in recent years have been observed in the 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 occurs in an 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 the 9-10th day of illness The body temperature drops, but the patient does not feel better.

Renal symptoms are added: 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, and nosebleeds are not uncommon. Characterized by loose stools, swelling of the face, and 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 general condition improves. 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 during the recovery period retain asthenia, increased anxiety, and shortness of breath for a long time. This can lead to the development of hypochondria and neuroses.

Differential diagnosis

If acute symptoms of HFRS appear, it 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 recently. 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 of 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;
Replenishing fluid losses and eliminating possible dehydration, as well as intoxication: intravenous glucose, sodium chloride, saline;
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;
It is possible to prescribe 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 number 4. You can take salt, but meat is even necessary during polyuria. You need to drink enough fluids, especially healthy mineral waters (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.

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