Signs of hemorrhagic fever with renal syndrome. Hemorrhagic fever with renal syndrome in children HFRS symptoms incubation period

Hemorrhagic fevers

Hemorrhagic fevers (febres haemorrhagica) is a group of acute viral zoonotic diseases with various mechanisms of transmission of pathogens, characterized by the development of universal capillary toxicosis and hemorrhagic syndrome against the background of an acute febrile state and occurring with symptoms of general intoxication.

Currently, 13 hemorrhagic fevers have been described in humans, most of which are endemic to tropical regions. Crimean-Congo hemorrhagic fever, Omsk hemorrhagic fever and hemorrhagic fever with renal syndrome are described in Russia.

The causative agents of hemorrhagic fevers belong to the ecological group of arboviruses (families of togaviruses and bunyaviruses), arenaviruses and filoviruses.

Hemorrhagic fevers are natural focal infections. The main reservoirs of pathogens are animals - primates, rodents, large and small cattle, ticks, etc., in the body of which a latent infection usually develops with long-term persistence of viruses, which ensures intense environmental contamination in enzootic foci. In some cases, the infection can become anthroponotic in nature.

The mechanisms of infection with hemorrhagic fevers are diverse: transmissible - with arbovirus hemorrhagic fevers; aerogenic, alimentary and contact - with arenavirus hemorrhagic fevers, parenteral transmission of some pathogens of hemorrhagic fevers is possible.

Susceptibility to hemorrhagic fevers is high, high-risk contingents of infection are persons who have close professional contact with animals or wildlife (lumberjacks, geologists, agricultural workers, vivarium workers, etc.). The most severe forms of the disease are observed in people visiting the foci of infection for the first time. Local residents often have mild and subclinical forms of hemorrhagic fevers. Mortality in hemorrhagic fevers ranges from 1-5 to 50-70%.

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

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

In 1938-1940. in complex studies of virologists, epidemiologists and clinicians, the viral nature of the disease was established, the main patterns of epidemiology and the features of its clinical course were studied. In the 1950s, HFRS was detected in Yaroslavl, Kalinin (Tver), Tula, Leningrad,

Moscow regions, in the Urals, in 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 the rodents Apodemus agrarius in Korea; in 1978, they isolated the virus from a sick person.

Since 1982, according to the decision of the WHO Scientific Group, various variants of the disease have been united under the general name "hemorrhagic fever with renal syndrome".

Etiology. The causative agents of HFRS are viruses of the genus hantaan (Hantaan pymela, seoul, etc.), of the bunyaviridae family, and belong to spherical RNA-containing viruses with a diameter of 85-110 nm.

Epidemiology. HFRS - natural focal virosis. The reservoir of viruses on the territory of Russia is 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 environment mainly with the urine of rodents, less often with their feces or saliva. Among animals, transmissible transmission of the virus by gamasid mites and fleas is observed.

From rodents to humans in natural or laboratory conditions, the virus is transmitted by airborne, alimentary and contact routes. Cases of infection with HFRS from a sick person are unknown.

The incidence is sporadic, and group outbreaks are possible. Natural foci are located in certain landscape-geographical zones: coastal areas, woodlands, wet forests with dense grass, which contributes to the conservation 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, 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 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.) get sick. The incidence of urban residents is associated with their stay in the suburban area (visiting the forest, resting in holiday camps and sanatoriums located near the forest), work in vivariums.

Immunity after an illness is quite persistent. Recurrences are rare.

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

Having a vasotropic effect, the virus damages the walls of blood capillaries both directly and as a result of an increase in the activity of hyaluronidase 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.

A large role in the genesis of capillary toxicosis is assigned to immune complexes. There is a defeat of 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 occurrence of microthrombi. An increase in capillary permeability in combination with a syndrome of disseminated intravascular coagulation causes the development of a hemorrhagic syndrome, manifested by a hemorrhagic rash and bleeding.

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

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

Pathological anatomical 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, there are hemorrhages under it. The cortical substance is pale, bulges above the cut surface, the medulla is purple-red with multiple hemorrhages in the pyramids and pelvis, 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, some glomeruli have dystrophic and necrobiotic changes. In the foci of hemorrhages, the tubules and collecting ducts are grossly destructively altered, their lumen is absent due to compression or is filled with cylinders. The epithelium is regenerated and desquamated. Widespread dystrophic changes in the cells of many organs, endocrine glands (adrenal glands, pituitary gland) and autonomic ganglia are also detected.

As a result of immune reactions (increase in antibody titer, 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 within 1 to 4 years.

clinical picture. The main symptoms of HFRS are high fever, flushing and puffiness of the face, the occurrence of hemorrhagic syndrome from the 3rd-4th day of illness and impaired renal function in the form of oliguria, massive proteinuria and azotemia, followed by polyuria. The disease is characterized by a cyclic course and a variety of clinical variants from abortive febrile forms to severe forms with massive hemorrhagic syndrome and persistent acute renal failure.

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

The feverish period, or the initial phase of the infection, is characterized by a sharp rise in temperature, the appearance of excruciating headache and muscle pain, thirst, and dry mouth. The temperature rises to 38.5-40 ° C and remains at high levels for several days, after which it drops 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 subfebrile figures - a “two-humped” curve.

An excruciating headache from the first days of the disease is concentrated in the forehead, temples. Often, patients complain of visual impairment, the appearance of a "grid" before the eyes. On examination, puffiness and flushing of the face, injection of vessels of the sclera and conjunctiva, and hyperemia of the pharynx are naturally noted.

From the 2nd-3rd day of the disease, a hemorrhagic enanthema appears on the mucous membrane of the soft palate, and from the 3rd-4th day - a petechial rash in the armpits; on the chest, in the region of the collarbones, sometimes on the neck, face. The rash may be in the form of stripes, resembling a "whiplash". Along with this, large hemorrhages appear in the skin, sclera, and injection sites. Subsequently, nasal, uterine, gastric bleeding is possible, which can be the cause of death. In some patients with mild forms of the disease, hemorrhagic manifestations are absent, but the symptoms of a “tourniquet” and “pinch”, indicating an increased fragility of capillaries, are always positive.

The pulse at the onset of the disease corresponds to the temperature, then severe bradycardia develops. The borders of the heart are normal, the tones are muffled. Arterial pressure in most cases is lowered. In a severe course of the disease, the development of infectious-toxic shock is observed. Often there are signs of bronchitis, bronchopneumonia.

On palpation of the abdomen, pain is determined, more often in the hypochondrium, and in some patients, tension in the abdominal wall. Pain in the abdomen can be intense in the future, which makes it necessary to differentiate from surgical diseases of the abdominal cavity. The liver is usually enlarged, the spleen is less common. Tapping on the lower back is painful. The chair is delayed, but diarrhea is possible with the appearance of mucus and blood in the stool.

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

From the 3rd-4th day of illness, against the background of high temperature, the oliguric period begins. The patient's condition is deteriorating markedly. There are severe pains 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 the hemorrhagic syndrome are significantly increased: 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 6-7th day of the disease, the body temperature drops lytically and less often critically, but the condition of the patients worsens. Pallor of the skin in combination with cyanosis of the lips and extremities, severe weakness are characteristic. Signs of hemorrhagic syndrome persist or increase, azotemia progresses, manifestations of uremia, arterial hypertension, pulmonary edema are possible, 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 up to 40-60 mm/h, and signs of anemia in case of bleeding. Characterized by an increase in the level of residual nitrogen, urea, creatinine, hyperkalemia and signs of metabolic acidosis.

In the general analysis of urine, massive proteinuria (up to 20-110 g / l) is noted, the intensity of which changes during the day, hypoisostenuria (relative density of urine 1.002-1.006), hematuria and cylindruria; the cylinders including cells of a tubular epithelium are quite often found.

From the 9th-13th day of illness, a polyuric period begins. The condition of patients noticeably improves: nausea, vomiting stop, appetite appears, diuresis increases to 5-8 liters, nocturia is characteristic. Patients experience weakness, thirst, they are disturbed by shortness of breath, palpitations even with little physical exertion. Lower back pain improves, but mild, aching pain may persist for several weeks. Prolonged hypoisostenuria is characteristic.

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

Allocate mild, moderate and severe forms of the disease. The mild form includes those cases when the fever is low, hemorrhagic manifestations are mild, oliguria is short-term, there is no uremia. In the form of moderate severity, all stages of the disease develop sequentially without life-threatening massive bleeding and anuria, diuresis is 300-900 ml, the content of residual nitrogen 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 internal organs, acute adrenal insufficiency, and cerebrovascular accident are possible. Anuria, progressive azotemia (residual nitrogen more than 0.9 g/l) are noted. Possible death due to shock, azotemic coma, eclampsia, or rupture of the renal capsule. There are known forms of HFRS that occur with the syndrome of encephalitis.

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

Forecast. Mortality in HFRS in the Far East has reached 6-8% in recent years, in the European part of Russia - 1-3.5%, but it is also possible up to 10%.

Diagnostics. Recognition of HFRS is based on the identification of characteristic clinical signs. From epidemiological data, contact with environmental objects infected with rodent secretions should be taken into account.

Of great diagnostic importance are changes in the hemogram in the form of leukopenia followed by neutrophilic hyperleukocytosis, thrombocytopenia, and an increase in ESR. An essential diagnostic feature is massive and alternating proteinuria, persistent hypoisostenuria. The diagnosis is confirmed by MFA, RIA and ELISA with the antigen of Hantaan viruses in cryostat sections of the lungs of rodents (bank voles Apodemus agrarius) and antibodies to it in NRIF.

It is carried out with influenza, typhoid and cheese fever, leptospirosis, encephalitis, acute pyelonephritis, surgical diseases of the abdominal cavity (acute appendicitis, cholecystitis, pancreatitis, perforated stomach ulcer), etc.

Treatment. Patients with HFRS are subject to mandatory hospitalization in an infectious diseases hospital in compliance with the requirements of the most gentle transportation. Therapeutic measures are carried out taking into account the period and form of the severity of the disease with constant monitoring of the main biochemical parameters. The patient must comply with bed rest in the acute period of the disease and before the onset of convalescence. Easily digestible food is prescribed without table salt restrictions (table No. 4 according to Pevzner).

In the initial period, the complex of therapeutic agents includes isotonic solutions of glucose and sodium chloride, ascorbic acid, rutin, antihistamines, analgesics, antiplatelet agents. There is a positive experience with the use of antiviral drugs (ribamidil).

Against the background of oliguria and azotemia, the intake of meat and fish dishes, as well as foods containing potassium, is limited. The amount of fluid drunk and administered to the patient should not exceed the daily volume of urine and vomit by more than 1000 ml, and at high temperature - 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, blood ultrafiltration methods, 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 and severe forms of the disease. Those who have been ill are subject to dispensary observation for 1 year with quarterly control of the general analysis of urine, blood pressure, examination by a nephrologist, ophthalmologist.

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

Synonym: acute infectious capillary toxicosis, hemorrhagic fever, Crimean Congo fever

Hemorrhagic Crimean-Congo fever - viral natural focal disease, the causative agent of which is transmitted through the bites of ixodid ticks; characterized by severe intoxication and a pronounced hemorrhagic syndrome.

Historical information. The disease was first described by M.P. Chumakov et al. in 1944-1945 in the Crimea and later in the republics of Central Asia. In 1956-1969. foci of similar diseases have been identified in Bulgaria, Yugoslavia, Hungary, East and West Africa, Pakistan and India. The disease is common in the Crimea, Donetsk, Astrakhan, Rostov and Kherson regions, Krasnodar and Stavropol territories, Kazakhstan, Uzbekistan, Turkmenistan and Azerbaijan.

Etiology. The causative agent is a virus of the nairovirus genus, Bunyaviridae family.

Epidemiology. Crimean-Congo hemorrhagic fever is a natural focal virus. The reservoir of viruses is wild (hares, African hedgehogs, etc.) and domestic (cows, sheep, goats) animals, ticks of more than 20 species from 8 genera with transovarial transmission of pathogens.

The mechanism of infection is usually transmissible through the bite of an infected tick Hyaloma plumbeum (in the Crimea), Hyaloma anatolicum (in Central Asia, Africa) and midges - Culicoideus. Perhaps aerogenic infection (in laboratory conditions) and in contact with the blood of sick people (nosocomial infection).

In endemic areas, the incidence is seasonal and increases during agricultural work (in our country in June-August), often acquiring a professional character. In non-immune individuals, the disease is severe with high mortality. After illness, immunity is maintained.

Pathogenesis and pathological anatomical picture. Pathological reactions in Crimean hemorrhagic fever are characterized by a cyclic course. After the introduction of the virus and its replication in the elements of the macrophage system, the phase of viremia develops, which determines the occurrence of a general toxic syndrome. The subsequent phase of hematogenous dissemination leads to the development of universal capillary toxicosis, intravascular coagulation syndrome and various injuries (bridging necrosis in the liver, degenerative changes in the myocardium, kidneys and adrenal glands), which is clinically manifested by massive hemorrhages and signs of organ pathology.

clinical picture. The incubation period lasts 2-14 days (average 3-5 days). The disease can occur in mild, mild, moderate and severe forms. In addition to the incubation period, there are 3 periods of the disease: initial, peak, or hemorrhagic phase, and outcomes.

The initial period lasts 3-6 days and is characterized by a sudden onset of chills, a rapid increase in body temperature to 39-40 ° C, widespread myalgia and arthralgia, severe headache, often pain in the abdomen and lumbar region. In a number of patients, a positive symptom of Pasternatsky is determined. Common symptoms are dry mouth, dizziness, and repeated vomiting.

Patients are usually excited, their face, mucous membranes, neck and upper chest are hyperemic, lips are dry, herpetic rash is often noted. Arterial hypotension is characteristic, the pulse often corresponds to body temperature or is somewhat slowed down. Hematological changes during this period are manifested by leukopenia with a neutrophilic shift to the left, thrombocytopenia, and an increase in ESR.

The peak period of the disease lasts 2-6 days, often develops after a short-term, within 1-2 days, decrease in body temperature. In this phase of the disease, a pronounced hemorrhagic syndrome is revealed in the form of a petechial rash on the lateral parts of the trunk, in the area of large folds and limbs. In severe forms of the disease, purpura, ecchymosis are observed, bleeding from the gums, nose, stomach, uterus, intestines, and lungs is possible.

Patients are depressed, pale; they have acrocyanosis, tachycardia and arterial hypotension; bullshit is possible. In 10-25% of cases, meningeal symptoms, agitation, convulsions are observed, followed by the development of coma. The liver is usually enlarged, some patients show signs of hepatargia. Often develop oliguria, microhematuria, hypoisostenuria, azotemia. Sometimes there are complications in the form of pneumonia, pulmonary edema, thrombophlebitis, acute renal failure, shock. The duration of the fever is 4-8 days.

The period of convalescence is long, up to 1-2 months, characterized by asthenic symptom complex. In some patients, working capacity is restored over the next 1-2 years.

In endemic areas, abortive forms of the disease are often observed without a pronounced hemorrhagic syndrome.

In laboratory studies, in addition to characteristic hematological changes, an increase in hematocrit, residual nitrogen, aminotransferase activity, and signs of metabolic acidosis are detected. Significant thrombocytopenia and high hematocrit values may indicate a poor prognosis.

Forecast. Serious, mortality can reach 40%.

Diagnostics. Recognition of the disease is based on the identification of typical signs of the disease: an acute onset of the disease with high fever, facial flushing, a rapid increase in hemorrhagic manifestations, vascular insufficiency, nephropathy and hepatopathy in high-risk patients (livestock breeders, hunters, geologists, etc.).

Specific diagnosis includes the isolation of the virus from the blood during the period of viremia, the use of serological tests: NRIF, RTNGA, RSK.

Differential diagnosis. It is carried out with meningococcal infection, influenza, leptospirosis, typhus, thrombocytopenic purpura and Schonlein-Henoch disease, in tropical countries with yellow fever and other hemorrhagic fevers.

Treatment. It is carried out in accordance with the general principles of therapy for patients with hemorrhagic fevers. A positive effect was obtained from the use of 60-100 ml of immune serum (proposed by M.P. Chumakov in 1944) or hyperimmune immunoglobulin.

Prevention. During hospitalization of patients, prevention of nosocomial infection, including parenteral route, should be provided. In the foci of the disease, a complex of deratization and disinfection measures is carried out. According to the indications, vaccination, the introduction of immunoglobulin are necessary.

Hemorrhagic Omsk fever

Historical information. Hemorrhagic Omsk fever was first described in 1945-1948. during an epidemic outbreak in the Omsk and Novosibirsk regions. Since 1958, due to carrier depression, case reports have been rare.

Etiology. The causative agent is the Omsk fever virus of the genus Flavivirus, family Togaviridae.

Epidemiology. Omsk hemorrhagic fever is a natural focal virus. The reservoir of viruses is muskrats, water rats and other rodents. The vectors are Dermacentor pictus mites, possibly other mites of this genus, gamasid mites and fleas.

Human infection occurs through contact with infected muskrats, through tick bites, by airborne dust in the laboratory.

The highest frequency of disease is usually observed in the summer months during the period of activity of ticks.

Pathogenesis and pathological anatomical picture. Not studied enough. As a result of viremia and hematogenous dissemination of viruses, characteristic capillary toxicosis develops, damage to the central and autonomic nervous system, endocrine system (adrenal glands). In the course of the disease, a strong immunity is formed.

clinical picture. The incubation period is 3-10 days. The initial period of the disease is acute, with high fever, tremendous chills, headache and myalgia. Diffuse hyperemia of the face and neck, a bright injection of the vessels of the sclera and conjunctiva are noted. From the first days of the disease, petechial elements can be detected on the mucous membrane of the oral cavity, in the pharynx and on the conjunctiva.

Unlike the Crimean hemorrhagic fever, hemorrhagic exanthema in Omsk fever is observed intermittently (in 20-25% of patients), massive bleeding from the gastrointestinal tract and other organs is less common.

During the height of the disease, the development of meningoencephalitis is possible. In 30% of patients, atypical pneumonia or bronchitis is detected; hepatomegaly is often found. In some patients, transient proteinuria can be noted.

The feverish period is 4-12 days, in the latter cases the fever is often two-wave.

In the hemogram - leukopenia with a neutrophilic shift to the left, thrombocytopenia, the absence of eosinophils. During the second temperature wave, neutrophilic leukocytosis is possible.

Forecast. The disease is characterized by a favorable course and relatively low mortality (0.5-3%).

Diagnosis and treatment. Similar to those in the Crimean-Congo hemorrhagic fever.

Yellow fever

Yellow fever (febres flava) is an acute viral natural focal disease with transmissible transmission of the pathogen through a mosquito bite, characterized by a sudden onset, high biphasic fever, hemorrhagic syndrome, jaundice and hepatorenal insufficiency. The disease is common in tropical regions of America and Africa.

Yellow fever belongs to the diseases provided for by the International Health Regulations and is subject to registration with WHO.

Historical information. Yellow fever has been known in America and Africa since 1647. In the past, the infection often took on the character of severe epidemics with high mortality. The viral nature and transmission of the virus by Aedes aegypti mosquitoes was established by K. Finlay and the W. Reed Commission in 1901 in Cuba. The eradication of this species of mosquito ensured the disappearance of urban foci of infection in the Americas. The yellow fever virus was isolated in 1927 in Africa.

Etiology. The causative agent, yellow fever virus (flavivirus febricis), belongs to the genus flavivirus, family Togaviridae.

Epidemiology. There are two epidemiological types of yellow fever foci - natural, or jungle, and anthropourgical, or urban.

The reservoir of viruses in the case of the jungle form are marmoset monkeys, possibly rodents, marsupials, hedgehogs and other animals.

The carrier of viruses in natural foci of yellow fever are mosquitoes Aedes simpsoni, A. africanus in Africa and Haemagogus sperazzini and others in South America. Human infection in natural foci occurs through the bite of an infected A. simpsoni or Haemagogus mosquito, capable of transmitting the virus 9-12 days after infecting bloodsucking.

The source of infection in urban foci of yellow fever is a sick person in the period of viremia. Virus carriers in urban outbreaks are Aedes aegypti mosquitoes.

The incidence in jungle foci is usually sporadic and is associated with human stay or economic activity in tropical forests. The urban form proceeds in the form of epidemics.

Currently, sporadic incidence and local group outbreaks are recorded in the tropical forest zone in Africa (Zaire, Congo, Sudan, Somalia, Kenya, etc.), South and Central America.

Pathogenesis and pathological anatomical picture. The inoculated yellow fever virus hematogenously reaches the cells of the macrophage system, replicates in them for 3-6, less often 9-10 days, then re-enters the blood, causing viremia and clinical manifestation of the infectious process. Hematogenous dissemination of the virus ensures its introduction into the cells of the liver, kidneys, spleen, bone marrow and other organs, where pronounced dystrophic, necrobiotic and inflammatory changes develop. The most characteristic are the occurrence of foci of colliquation and coagulation necrosis in the mesolobular sections of the hepatic lobule, the formation calf Councilman, development of fatty and protein degeneration of hepatocytes. As a result of these injuries, cytolysis syndromes develop with an increase in ALT activity and a predominance of AST activity, cholestasis with severe hyperbilirubinemia.

Along with liver damage, yellow fever is characterized by the development of cloudy swelling and fatty degeneration in the epithelium of the tubules of the kidneys, the appearance of areas of necrosis, which cause the progression of acute renal failure.

At pathoanatomical examination, the purple-cyanotic color of the skin, widespread jaundice and hemorrhages in the skin and mucous membranes attract attention. The size of the liver, spleen and kidneys are enlarged, they show signs of fatty degeneration. In the mucous membrane of the stomach and intestines, multiple erosions and hemorrhages are determined. In addition to changes in the liver, dystrophic changes in the kidneys and myocardium are naturally detected. Hemorrhages are often detected in the perivascular spaces of the brain; the cardiovascular system is also affected.

With a favorable course of the disease, stable immunity is formed.

clinical picture. During the course of the disease, 5 periods are distinguished. The incubation period lasts 3-6 days, rarely extended to 9-10 days.

The initial period (hyperemia phase) lasts for 3-4 days and is characterized by a sudden increase in body temperature to 39-41 ° C, severe chills, intense headache and diffuse myalgia. As a rule, patients complain of severe pain in the lumbar region, they have nausea and repeated vomiting. From the first days of the disease, most patients experience pronounced hyperemia and puffiness of the face, neck and upper chest. The vessels of the sclera and conjunctiva are brightly hyperemic (“rabbit eyes”), photophobia, lacrimation are noted. Often you can observe prostration, delirium, psychomotor agitation. The pulse is usually rapid, and bradycardia and hypotension develop in the following days. Preservation of tachycardia may indicate an unfavorable course of the disease. In many, the liver is enlarged and painful, and at the end of the initial phase one can notice icterus of the sclera and skin, the presence of petechiae or ecchymosis.

The phase of hyperemia is replaced by a short-term (from several hours to 1-1.5 days) remission with some subjective improvement. In some cases, recovery occurs later, but more often a period of venous stasis follows.

The patient's condition during this period noticeably worsens. The temperature rises again to a higher level, jaundice increases. The skin is pale, in severe cases cyanotic. A widespread hemorrhagic rash appears on the skin of the trunk and extremities in the form of petechiae, purpura, and ecchymosis. Significant gum bleeding, repeated vomiting with blood, melena, nasal and uterine bleeding are observed. In severe cases, shock develops. The pulse is usually rare, weak filling, blood pressure is steadily decreasing; develop oliguria or anuria, accompanied by azotemia. Often there is toxic encephalitis.

The death of patients occurs as a result of shock, liver and kidney failure on the 7-9th day of illness.

The duration of the described periods of infection averages 8-9 days, after which the disease enters the convalescence phase with a slow regression of pathological changes.

Among local residents of endemic areas, yellow fever can occur in a mild or abortive form without jaundice and hemorrhagic syndrome, which makes it difficult to timely identify patients.

In laboratory studies, in the initial phase of the disease, leukopenia is usually noted with a shift of the leukocyte formula to the left to promyelocytes, thrombocytopenia, and during the peak period - leukocytosis and even more pronounced thrombocytopenia, increased hematocrit, hyperkalemia, azotemia; in urine - erythrocytes, protein, cylinders.

Hyperbilirubinemia and an increase in the activity of aminotransferases, mainly AST, are detected.

Forecast, Currently, the mortality rate from yellow fever is approaching 5%.

Diagnostics. Recognition of the disease is based on the identification of a characteristic clinical symptom complex in individuals belonging to the high-risk category of infection (unvaccinated people who visited the jungle foci of yellow fever for 1 week before the onset of the disease).

The diagnosis of yellow fever is confirmed by the isolation of the virus from the patient's blood (in the initial period of the disease) or antibodies to it (RSK, NRIF, RTPGA) in the later periods of the disease.

Differential diagnosis. Carried out with other types of hemorrhagic fevers, viral hepatitis, malaria.

Treatment. Yellow fever patients are hospitalized in mosquito-proof hospitals; prevent parenteral infection.

Therapeutic measures include a complex of anti-shock and detoxification agents, correction of hemostasis. In cases of progression of hepatic-renal failure with severe azotemia, hemodialysis or peritoneal dialysis is performed.

N. V. Gavrilova Tamara Vladimirovna Pariyskaya

author P. Vyatkin

From the book Complete Medical Diagnostic Handbook author P. Vyatkin

From the book Modern Home Medical Reference. Prevention, treatment, emergency care author Viktor Borisovich Zaitsev

From the book The Big Protective Book of Health author Natalya Ivanovna Stepanova

Hemorrhagic fever with renal syndrome (HFRS) or mouse fever should be familiar to every inhabitant of Russia.

The disease is dangerous with the likelihood of severe complications. The number of deaths among patients in Russia reaches 8%.

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The site provides background information. Adequate diagnosis and treatment of the disease is possible under the supervision of a conscientious physician. All drugs have contraindications. You need to consult a specialist, as well as a detailed study of the instructions! .

What causes HFRS

This is a viral disease that affects the blood vessels and kidneys. The causative agent of the disease is the Hantaan virus, belonging to the Bunyavirus family.

Between animals, this virus is spread by flea or tick bites. Rodents are latent carriers of the virus and will release it into the environment with faeces, urine and saliva.

The virus is characterized by resistance to negative temperatures and dies within half an hour at a temperature of 50 degrees. The peculiarity of the virus is that it infects the inner lining of blood vessels (endothelium).

There are 2 types of virus:

Eastern type. The type prevails in the Far East; the Manchurian field mice are the carrier of the infection.
The Western type is common in the European part of Russia. The peddler is a red and red-backed vole.

It is noted that the first type is more dangerous and causes from 10 to 20% of deaths, the second - up to 2%. There are several ways to get this disease.

Infection occurs when a person comes into contact with secretions of infected rodents by inhalation, ingestion, or when they come into contact with damaged areas of the skin. The disease has an autumn-winter seasonal character.

Symptoms of this disease

The course of HFRS is divided into several periods.

Depending on the stage of the course of the disease, the patient manifests symptoms of the disease.

incubation period. This stage lasts about 20 days. At this stage, the disease does not manifest itself. The patient may not be aware of the infection.
The initial (febrile) period lasts 3 days.
Oligoanuric lasts about a week.
Polyuric (early convalescence) - from 2 to 3 weeks.
Late convalescence begins approximately from the second month of the course of the disease and lasts up to 3 years.

The initial stage of the disease is characterized by a significant jump in body temperature in the morning and afternoon. The patient is accompanied by insomnia, body aches, fatigue, lack of appetite.

There is a headache, a painful reaction to light stimuli, conjunctivitis. A white coating forms on the tongue. There is redness of the upper body.

In the third stage of the disease, the temperature decreases somewhat, but other pronounced symptoms appear.

Characteristic for this period are pain in the lower back, which in severe form of the disease may be accompanied by nausea, vomiting, aching pain in the abdominal part.

The volume of urine excreted is reduced. Due to this, the level of potassium and urea in the blood increases, and the level of calcium and chlorides decreases.

A small rash appears on the patient's skin (hemorrhagic syndrome). The most commonly affected areas are the chest, armpits and shoulders. This is accompanied by nasal and gastrointestinal bleeding.

The patient's cardiovascular system malfunctions: the pulse becomes less frequent, blood pressure in a short period grows from low to high and vice versa.

A characteristic symptom of hemorrhagic fever with renal syndrome is damage to the nervous system. Hemorrhages in the patient's brain can provoke hallucinations, deafness, fainting. At the stage of oliguria, the patient has complications - acute renal and adrenal insufficiency.

At the stage of early convalescence, the patient feels relief. Initially, there is an abundant excretion of urine (up to 10 liters per day), then diuresis gradually returns to normal.

Late convalescence is characterized by residual manifestations of symptoms. The patient feels a general malaise - dizziness, weakness, increased sensitivity in the legs, need for fluid, increased sweating.

Features of the development of HFRS

The development of HFRS in a patient begins with an incubation period in the first 2-3 weeks from the moment of infection. The infection enters the body through the mucous membrane of the respiratory tract or digestive system, less often through open wounds on the skin.

If a person has strong immunity, the virus dies. It starts to multiply.

Then the infection enters the bloodstream and the patient begins to manifest an infectious-toxic syndrome. Once in the blood, the virus settles on the endothelium.

To a greater extent, the vessels of the kidneys are affected. From the patient's body, the infection is excreted in the urine.

At this time, the patient may experience acute renal failure. Regression sets in, and body functions are restored. The recovery process is complex and proceeds slowly, this period can last up to 3 years.

Diagnosis of pathology

The first symptoms of the disease are similar to SARS, so the patient often hesitates to seek help from a medical institution. Consider the features in the symptoms of HFRS in the early stages of the disease.

Firstly, with ARVI, the patient's temperature rises in the evening, while with HFRS this occurs mainly in the morning. Another feature of the disease is the reddening of the skin of the upper body of a person, the eyeballs.

In the later stages of the development of the disease, clearer symptoms appear. This is a hemorrhagic rash, a decrease in the volume of urine excreted, pain in the lumbar region.

At the first suspicion of the development of hemorrhagic fever, you should consult a doctor. When making a diagnosis, the seasonal factor, the likelihood of the patient staying in endemic foci and other epidemiological characteristics are taken into account.

To make an accurate diagnosis, differential and laboratory diagnostics are used. During differential research methods, specialists exclude other diseases, SARS, influenza, tonsillitis, pyelonephritis.

The patient is constantly monitored to identify new symptoms of the disease.

Laboratory diagnostic methods include urinalysis, general and biochemical analysis of the patient's blood. With HFRS, fresh erythrocytes are found in the patient's urine, the protein level is significantly reduced.

In the blood, the level of urea and creatine increases, and the level of hemoglobin and red blood cells decreases. In the blood serum, the concentration of fats increases and the level of albumin decreases.

The diagnosis of HFRS is confirmed by the detection of antibodies of the IgM and G class in the body. For this, enzyme-linked immunosorbent assay is used.

An important feature of the diagnosis of this disease is not the very fact of ongoing research, but their frequency.

The patient must be under constant observation, and the diagnosis is made on the basis of changes that are observed in the results of studies during the course of the disease.

Instrumental diagnostic methods (X-ray, computed tomography, and others) are carried out to identify the degree of damage to internal organs.

Video

Effective treatment of the disease

When a disease is detected, the patient is strictly shown hospitalization as soon as possible. Due to the fact that the disease is not transmitted from person to person, the treatment of hemorrhagic fever with renal syndrome is carried out in infectious hospitals, in surgical, therapeutic.

Transportation of the patient in the later stages of development is carried out with extreme caution, fearing hemorrhages and rupture of the kidneys.

The patient needs bed rest, diet. During the patient's stay in the hospital, preventive measures are taken to prevent complications.

Drug treatment of the disease includes taking antibacterial drugs. To save energy, glucose solutions with insulin are prescribed.

Curantil and eufillin normalize microcirculation. To relieve the symptoms of the disease, antipyretic and analgesic drugs are used.

Features of the therapeutic diet

Recovery requires a strict diet. For patients with HFRS, diet No. 4 of 15 therapeutic nutrition systems, developed by the Soviet doctor M.I. Pevzner.

You need to eat often and in small portions. Food should be at medium temperature. Fermentation products (cabbage, plum, sour cream, cheese) should be completely excluded from the diet.

Diet number 4 is aimed at limiting the amount of fat and carbohydrates. Hard-to-digest foods that increase gastric secretion are also excluded from it.

These include:

Fatty varieties of fish and meat;
Smoked products;
Pickles;
Sausages;
Sauces;
Canned food;
Bakery products;
Dried fruits;
Carbonated drinks;
Sweets.

Dishes should not be spicy or spicy.

Low-fat boiled meat and fish, low-fat cottage cheese, wheat crackers are acceptable for consumption. From cereals you need oats, rice, buckwheat, semolina, jelly decoctions from these cereals are useful.

Raw fruits and vegetables are not allowed. Compotes, jelly, jelly are prepared from fruits, vegetables are consumed in the form of mashed potatoes.

Help of folk remedies

Effective treatment of the disease is impossible without medical assistance.

Self-medication of this disease leads to serious consequences and death. Before taking this or that folk remedy, you should consult with your doctor.

Doctors advise taking various decoctions aimed at normalizing the functioning of the kidneys. In herbal medicine, many medicinal plants are known, the use of which has a diuretic and anti-inflammatory effect.

The most common decoctions used for HFRS disease:

1 teaspoon of flax seeds and 200 ml of water must be brought to a boil. You need to drink a decoction of 100 ml every 2 hours.
50 g of young birch leaves should be infused for 5 hours in 200 ml of warm water, take 100 ml 2 times a day.
Add 2 tablespoons of lingonberry leaves to 200 ml of hot water. Infuse the decoction in a water bath for half an hour, you need to take 100 ml 2 times a day.
Add 3 g of dry leaves of orthosiphon (kidney tea) to a glass of boiling water and boil for another 5 minutes. The decoction is insisted for 4 hours and drunk 100 ml before meals.

Herbal preparations are considered the most effective; they are already available in pharmacies in ready-made proportions.

In most of these collections, bearberry leaves are used, they can be brewed separately as a tea.

The composition of fees with bearberry:

Bearberry leaves, licorice root, cornflower inflorescences in proportions 3:1:1;
Bearberry leaves, licorice root, juniper fruits in proportions 2:1:2;
Bearberry leaves, orthosiphon leaves, lingonberry leaves in proportions 5:3:2.

A tablespoon of the collection is brewed in a glass of water. You need to take a decoction of half a glass 3 times a day. To normalize the functioning of the cardiovascular system, currant juice and a decoction of fragrant geranium roots are used.

Currant juice is taken 100 ml 3 times a day. Geranium roots (about 4 pieces) are poured into 1 liter of water and boiled for 20 minutes. You need to drink this decoction in a warm form every 20 minutes.

The use of folk remedies is also possible to relieve the symptoms of the disease. To lower body temperature, they take baths with cool water (about 30 degrees) and drink decoctions of raspberries, honeysuckle and strawberries.

Possible complications of the disease

It has been proven that the most dangerous in terms of complications is the oligoanuric stage of the disease. The period runs from 6 to 14 days of illness.

The complications that hemorrhagic fever can cause are specific and non-specific.

Various complications include:

Infectious-toxic shock;
DIC (disseminated vascular coagulation);
Edema of the brain and lungs;
Acute cardiovascular failure;
Various hemorrhages (in the brain, adrenal glands and others) and bleeding;
Kidney rupture.

Infectious-toxic shock is characterized by acute circulatory failure. The patient's arterial pressure drops, insufficiency of internal organs develops.

This complication of the disease is the most common cause of death in HFRS.

With DIC, there is a violation of normal blood circulation in the patient's body. This leads to the development of serious dystrophic changes.

Hypocoagulation develops - the patient's blood clotting ability decreases, thrombocytopenia - the level of platelets in the blood decreases. The patient is bleeding.

Among non-specific complications, diseases are distinguished - pyelonephritis, purulent otitis media, abscesses, pneumonia. Complications of HFRS are dangerous and can often lead to death of the patient.

Patients who have had this disease develop strong immunity to the virus. This statement is substantiated by the fact that there were no cases of re-infection in patients who underwent HFRS.

Timely diagnosis of the disease is important, which will provide effective and qualified treatment.

Disease prevention

In order to prevent hemorrhagic fever with renal syndrome, you must follow the rules of personal hygiene.

You need to thoroughly wash your hands and consumed fruits and vegetables, do not leave food in the reach of rodents.

Use a gauze bandage to protect your respiratory tract from dust that can carry infection.

The main measures of general prevention of the disease is the destruction of the population of murine rodents in the foci of HFRS.

It is necessary to ensure the improvement of territories adjacent to residential buildings, crowded places, food warehouses, and the like. Weeds and thickets should not be allowed to spread.

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Hemorrhagic fever with renal syndrome (HFRS) is a rare severe disease that spreads mainly in the European part of Russia and in the Far Eastern regions. It affects not only blood vessels, but also internal organs, mainly the kidneys, which can lead to serious consequences in the form of kidney failure and death.

The causative agent is the Hantaan virus, localized mainly in the lungs of rodents and is characterized by the fact that it affects the inner lining of blood vessels. Allocate eastern and western types of the disease. The eastern type is the most toxic, is able to change, and carries the highest percentage of death.

Ways of infection

The source of infection is the habitat of small rodents (mainly field mice). There are several routes of infection with the virus:

when inhaling air, which contains dust from dried rodent excrement;
when using dirty products that contain particles of field mice feces;
during contact with hay, straw, feed or infected rodents.

A person can only become infected from an animal, the virus does not pass from person to person. People are very susceptible to the causative agent of HFRS, infection mainly occurs in autumn or winter. In urban environments, the virus can be carried by rats. The risk group includes people who:

periodically visit the forest in order to collect berries, mushrooms;
living in forest areas or near a forest belt;
gardeners and gardeners;

working on drilling rigs, deforestation and oil pipelines;
vacationers in the bosom of nature, in rest houses and sanatoriums, especially those located in the forest;
agricultural workers.

Children and the elderly are most susceptible to infection, this is due to weak immunity, among patients - mostly men. If a person has been ill with HFRS once, he develops strong immunity and cannot get sick again.

Symptoms

The syndrome virus enters the human body through the mucous membrane of the respiratory system or the oral cavity, entering the esophagus.

Often, with good immunity, the virus dies. But in a weakened body, it begins to multiply, the incubation period lasts 5–35 days, it can pass latently and manifest itself in an acute form, when a large-scale intoxication of the body has already occurred.

Getting into the blood, the Hantaan virus affects the vessels from the inside, which causes hemorrhagic fever, then it enters the kidneys with urine. For 7-9 days, renal failure develops, and it is this period of the disease that can become critical.

Then, a positive dynamics of the syndrome can be observed, blood clots resolve, swelling of the kidneys decreases and urine outflow is restored. A person can fully recover only after 1-3 years.

Hemorrhagic fever with renal syndrome has a cyclic course:

the latent period (incubation) of the disease can last from 5 to 35 days, depending on the age and body of the person;
the febrile (initial) period of the syndrome is characterized by a sharp rise in temperature up to 40 0 C, which is accompanied by a severe headache, chills, weakness, aching joints and the whole body, usually lasts no more than three days;
the oligoanuric period of the disease is manifested by some relief of symptoms, the temperature decreases, but the patient continues to feel unwell. In parallel, there is a sharp pain in the kidney area, this period lasts up to 10 days from the onset of the disease;
the polyuric period is a period of regression of the disease, urine begins to drain, the patient becomes better, lasts mainly up to a month from the onset of the disease;
recovery period - lasts up to three years.

In hemorrhagic fever with renal syndrome, the symptoms depend on the period of illness and the presence of chronic diseases.

It often happens that before the initial period of the disease, weakness, fatigue, discomfort in the larynx, pain in the joints may appear, this lasts for three days. The symptoms are very similar to SARS, so not everyone attaches importance to them. The peculiarity of the reproduction of the virus in the human body is a violation of the system that is responsible for blood clotting.

Fever period

It is characterized by a high temperature throughout the week, differs from other diseases in that the maximum increase occurs in the morning or afternoon. In parallel, signs of general intoxication of the body appear:

loss of appetite;
constant feeling of thirst;
sleep disturbance;
lethargy, headache, spreading throughout the head;

reaction to light, as in migraine;
visual impairment in the form of a veil;
swelling of the face and neck, redness of the skin;
bursting vessels of the eyes;
white coating on the tongue.

With severe intoxication, vomiting appears, a decrease in the pulse rate, a sharp decrease in blood pressure and loss of consciousness.

Oliguric period

During this period of HFRS, pains appear in the kidney area, they can be sharp or debilitating. In a severe course of the disease, vomiting and pain in the abdominal region occur, as in case of poisoning.

Then comes oliguria (violation of the outflow of urine), laboratory tests in the urine reveal the presence of protein, erythrocytes, and the level of urea in the blood increases, as in diabetes mellitus. A hemorrhagic rash spreads on the chest, armpits and shoulders. Some may develop nosebleeds, as well as internal gastrointestinal bleeding.

Characteristic for this period of the disease is a significant change in the work of the cardiovascular system:

decrease in heart rate;
lowering blood pressure followed by an increase to a hypertensive crisis;
the tone of heart contractions becomes muffled;
tachycardia or bradycardia develops.

Such a patient needs close attention, this period of the disease is the most dangerous, and in one day pressure surges can be very significant.

Severe nausea and vomiting that does not bring relief can be triggered by a small sip of liquid. Severe pain in the intestines and diarrhea with blood indicate a serious intoxication of the body.

Become vivid symptoms that indicate damage to the central nervous system:

intense diffuse headache that does not affect only the eye area;
loss of consciousness, in this case it is safe to say that the vessels of the brain burst and blood enters the medulla;

the patient is in a state as if he had been stunned;
feverish delirium, hallucinations may appear.

It is during this period of the disease that renal failure can develop.

Early convalescence

Early convalescence (polyuric period) is a period of regression of HFRS, in which the patient begins to experience relief, the symptoms of the disease gradually recede. Urination normalizes, first 10 liters per day, then a normal amount of urine is reached.

Urine and blood tests show an improved result, renal function returns to normal. The patient's condition returns to normal after a month from the onset of the disease, but general weakness persists.

body recovery period

Hemorrhagic fever with renal syndrome is a serious disease in which the human body is exposed to large-scale intoxication. For the restoration of all organs, especially the kidneys, a long time period is required, at least 2-3 years. During this time, some symptoms may still persist:

low efficiency, rapid fatigue;
poor appetite;
increased sweating;
itching of the skin;

decrease in sexual desire;
pain in the kidney area;
increased urination, especially at night;
constant feeling of thirst.

Symptoms can persist for six months, gradually receding. Full recovery of the body from such a serious illness requires a lot of effort and patience.

Childhood

Children can get sick, regardless of age, there have been cases of infection in infants. The disease begins suddenly, acutely, without any precursors.

The fever lasts for a week, accompanied by a severe headache, drowsiness. The child involuntarily tries to stay in bed, complains of pain in the lower back.

For a child, calling an ambulance should not be delayed for a minute if there is a high temperature.

The general list of warning signs for adults and children is:

redness and swelling of the face and neck;
headache;
pain syndrome of muscles and limbs;
general weakness;
heat;

hemorrhagic rash of the skin;
pain in the kidney area;
urinary retention;
bursting vessels of the sclera;
confusion.

In the presence of such symptoms, urgent hospitalization is necessary. If the patient does not receive timely adequate treatment, hemorrhagic fever with renal syndrome can cause serious complications, which in turn will lead to death.

Treatment

This disease can be treated only in a clinic with a specialized inpatient department. Therapeutic actions are primarily aimed at cleansing the body of toxins and stopping kidney failure.

The patient needs to observe bed rest for 2-4 weeks and control the amount of fluid he drinks, as well as the amount of fluid released.

As a drug therapy for hemorrhagic fever with renal syndrome, use:

antibiotic treatment (penicillin group);
drip inject a solution of glucose with insulin;
taking prednisone;
as part of drugs to eliminate intoxication, ascorbic acid, calcium gluconate are used;
dopamine is prescribed to improve urine output;
eufillin, chimes;
hemodialysis is used for severe intoxication;
medicines to lower the temperature;
antispasmodics;
specific antiviral drugs and immunomodulators - amixin, immunoglobulin, virazole.

The drugs are used in a complex, intensive therapy lasts 5-7 days, then the doctor can selectively cancel the drugs when the desired effect is achieved and the patient's condition is alleviated.

In hemorrhagic fever with renal syndrome, treatment should be accompanied by proper nutrition. The diet must be divided into 5-6 doses and limited to portions of no more than 300 grams. Food should not be heavy or coarse, it is better to cook soups and mashed potatoes.

If an infectious-toxic shock has developed, antispasmodics and gemodez are not prescribed. First, intoxication is reduced by washing the stomach, as well as the intestines. In case of illness, it is necessary to take absorbents.

With the development of a convulsive syndrome during the illness, Relanium or chlorpromazine is prescribed. When the patient begins to recover, he is prescribed fortifying agents and vitamins.

Preventive measures

Prevention of hemorrhagic fever with renal syndrome is an important measure. Such a serious disease is much easier to prevent than to cure. Preventive measures are as follows:

compliance with the rules of personal hygiene, especially while being in the bosom of nature or in the countryside;
water from any natural source must be boiled;
you can not pick up rodents, especially for children;
all products intended for outdoor consumption must be hermetically sealed;
Wash hands thoroughly with soap and water before drinking or eating.

if accidental contact with an animal occurs, measures must be taken to disinfect skin and clothing;
if you have to work in the hayloft, in the barn or in the field, you must use a respirator;
it is necessary to conduct preventive conversations with children and monitor their behavior in the forest and rural areas, to prevent eating berries, fruits and vegetables in an unwashed form.

In children, hemorrhagic fever with renal syndrome is much more severe than in adults. Infection of a pregnant woman can have terrible consequences of the disease, the danger to the fetus is obvious. If a woman becomes ill during breastfeeding, the baby is urgently transferred to artificial nutrition to reduce the risk of infection.

With timely intensive treatment, the prognosis may be favorable, as a consequence of the illness, chronic pyelonephritis and hypertension may develop. Lethal cases of the disease make up no more than 8% of sick people.

Hemorrhagic fever is a disease whose history began in 1935 in the Far East. Later and to this day, outbreaks of the disease in Russia began to be observed in the regions in the Central region of the country and the Urals.

Hemorrhagic fever with renal syndrome

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease transmitted by small rodents, which is characterized by vascular damage and negatively affects primarily renal function.

The causative agent of hemorrhagic renal fever is Hantavirus from the Bunyavirus family. There are 4 varieties of this type of infection, but only one is found in Russia - Puumala.

Any person is susceptible to Hantavirus, that is, getting Puumala into the bloodstream becomes a catalyst for the pathological process in all people who have not had hemorrhagic fever earlier. But, according to statistics, the vast majority of people who have encountered HFRS are men aged 18 to 50 years.

There are two types of HFRS, divided according to the principle of the source of infection:

Type I (eastern) is spread by the field mouse, the clinical picture is severe, the statistics of death as a result of therapy is 20%;
Type II (Western) is spread by the bank vole, the symptoms of the disease are milder than in type I, and the mortality rate during treatment is less than 2%.

Basic information about hemorrhagic renal fever with renal syndrome

Etiology

There are six ways of infection, but all of them are united by human contact with a virus that enters the environment from the saliva and feces of rodents:

The forest type is most common, with it a person becomes infected during hiking trips in the forest, searching for mushrooms, picking berries.
Household type means that the source of Hantavirus is inside the person's home - this is found in private houses located next to the forest.
Production type - occurs during drilling, oil pipeline and other works in the forest.
Garden type - relevant among summer residents.
The camp type of infection is recorded among children and adolescents vacationing in suburban summer camps.
The agricultural route is marked by activity in autumn and winter.

In the vast majority of cases, the virus enters the body by contact with the mucous membrane of the upper respiratory tract, less often through damage to the skin.
On the video, the etiology of hemorrhagic fever:

Pathogenesis

After entering the body, the virus begins to infect the walls of blood vessels from the inside, destroying the inner layer - the endothelium. The vessels become permeable, the plasma leaves the vascular system through perforations, and the blood thickens.

Damage to the vessels negatively affects the activity of absolutely all systems, but the kidneys suffer the most with HFRS: as the stages of this disease proceed, the rate (GFR) decreases, the risk of chronic renal failure increases, requiring hemodialysis in the terminal stage.

Clinical picture

Incubation period

The incubation period of HFRS lasts from 1 to 7 weeks, more often - 3 weeks. At this stage, the patient does not feel the symptoms of the disease, but the pathology in the body already takes place: the walls of the vessels are affected, the composition of the blood changes, and disturbances in the functioning of all systems begin.

Prodromal manifestations

The prodromal period does not always occur and lasts no more than 3 days.

It occurs after the incubation period of HFRS and has the following symptoms:

weakness;
headache;
chills;
aches in the bones;
subfebrile condition.

Fever

hemorrhagic fever with renal syndrome is characterized by a sharp onset of fever, with an increase in body temperature to 39-40 degrees. It lasts from 2 to 8 days, the peak of the thermometer is not in the evening and night hours, as with influenza or SARS, but in the morning.

High temperature serves as a source of intoxication, because of which a person experiences nausea, pain, chills. Approximately 3 out of 10 patients have visual impairment.

Hemorrhagic period

The hemorrhagic period begins from the moment of appearance on the skin of traces of rash and hemorrhages of the sclera of the eyes. This stage occurs simultaneously with the oliguric stage.

With hemorrhagic syndrome, the following phenomena occur:

red cherry syndrome - hemorrhages on the whites of the eyes;
infectious-toxic shock - the reaction of the body in the presence of a virus in it, expressed in a decrease in blood pressure and pathological work of several systems at once;
internal bleeding.

The photo shows the main manifestations of hemorrhagic fever

Oliguria

It develops from the third day from the onset of HFRS symptoms and, statistically, can last up to 1 month, but usually disappears after 9-12 days.

Oliguria - a decrease in the quantitative indicator of urine excreted during the usual drinking regimen. During this period, changes in the blood are actively taking place: substances previously excreted by the urinary system remain in the blood, poisoning the body.

At the same time, pathological processes in the systems are fixed:

cardiovascular (hypotension, bradycardia, extrasystole);
digestive (nausea, vomiting, sometimes with blood);
nervous (delusions, hallucinations, fainting).

Polyuria

Polyuria begins after the oliguric period, that is, after 9-12 days from the onset of HFRS, and lasts up to 4 weeks.

During this period, the amount of urine, on the contrary, increases dramatically, and diuresis can reach 10 liters. Due to the large amount of urine, its density decreases, and protein and cylinders are also found in it.

A day after the onset of the process of polyuria, the dynamics of restoration of the filtration capacity of the kidneys becomes positive.

convalescence period

After the completion of polyuria, a person recovers. But deviations in laboratory tests can persist for up to three years.

During the recovery period of the body, a person may experience fatigue, face functional disorders of the nervous and endocrine systems, and in the activity of the kidneys.

On the video, the symptoms and pathogenesis of hemorrhagic fever:

Diagnostics

Differential diagnosis in hemorrhagic fever with nephrological syndrome is required to exclude pathologies:

flu;
typhoid fever;
leptospirosis;
glomerulonephritis;
tick-borne rickettsiosis;
encephalitis;
pyelonephritis.

To make a diagnosis, the main tool can be called observation of the patient, questioning and examination, with the help of which they fix:

strict alternation of the described stages in this order;
the fact of a decrease in the amount of urine excreted after temperature stabilization;
the presence of hemorrhages on the skin.

The second factor confirming HFRS is epidemiological data on the fact of the possibility of HFRS infection in a given area.

To confirm the diagnosis, laboratory tests are performed:

a general urine test to detect (the presence of traces of protein in the urine), cylindruria;
a general blood test to detect an increase in leukocytes, erythrocyte sedimentation rate, plasma cells;
a biochemical blood test to detect an increase in the level of creatinine and urea, a decrease in albumin;
, which determines the GFR;
detection of IgM antibodies.

At the stage of nephrological symptoms, ultrasound of the kidneys and radiography with contrast are prescribed.

Treatment

HFRS therapy is carried out in a hospital under strict bed rest and therapeutic nutrition, which reduces the load on the kidneys. The amount of urine drunk and excreted per day is controlled.

Drug therapy is used primarily to relieve symptoms:

to relieve intoxication, intravenous glucose infusions (20-40%) and saline are prescribed;
to restore kidney function and improve microcirculation of the glomeruli, the drugs Curantil, Trental, Eufillin are used; in severe cases of the disease, hormonal drugs (glucocorticosteroids) - Prednisolone, Metipred can be prescribed;
with severe internal hemorrhages, blood and albumin transfusions are performed;
during the period of oliguria, a hemodialysis machine is used to normalize the composition of the blood and remove excess fluid from the body;
to reduce body temperature, antipyretics are used: "Paracetomol", "Nise".

If the patient was hospitalized in a hospital in the first 3-5 days from the onset of symptoms, the appointment of immunomodulators and antiviral drugs is recommended.

Complications and consequences

Infectious-toxic shock and azotemic uremia - poisoning of the body with decay products during a decrease in kidney GFR or cessation of urination, resulting in multiple organ failure, and then - uremic coma.
Rupture of the kidney capsule, which occurs against the background of vascular damage and a high load on the cardiovascular system due to the accumulation of fluid during oliguria.
Pulmonary and cerebral edema also occurs with oliguria, when a large amount of fluid remains in the body that is not excreted by inactive kidneys.
Lethal outcome - on average, is recorded in 8 percent of cases and depends on the fact of the presence of concomitant somatic pathologies, age, the moment of initiation of adequate therapy.
Infectious processes (pyelonephritis, sepsis) belong to a non-specific category of complications, since their development requires the penetration of bacteria into the body, which are catalysts for the described pathologies, during HFRS.

On the video about the prevention of hemorrhagic renal fever:

Causes of the disease
Complications and prevention
Treatment of hemorrhagic fever

Hemorrhagic fever with renal syndrome is an acute infectious disease that selectively affects the blood vessels. The disease is accompanied by intoxication, fever and affects the kidneys. Representatives of different sexes and ages suffer from the disease. The disease is quite rare, but serious.

The main carrier of the disease are rodents: field mouse, gray mouse, black rat. In animals, the disease occurs without symptoms. The main sources of transmission of the virus are urine, feces, saliva. Infection is rare. Patients with fever are not contagious. Hemorrhagic fever with renal syndrome can be transmitted from carrier to person in various ways:

air-dust;
food;
contact.

Between rodents, the virus is transmitted during crossing, a long stay in the same room. Direct contact is required to transmit the virus. For rodents, there is another way of transmitting the disease (aspiration). Infection occurs by inhalation of dust, dry excrement. For humans, infection can mean eating meat from an infected rodent, direct contact with animal feces, a bite, contact with saliva.

Most often, hemorrhagic fever with renal syndrome spreads in the summer. At this time, there is a high probability of contact with infected secretions. Even if you previously caught animals, one of them turned out to be a carrier of infection, after contact with it you did not wash your hands, then there is a high probability of infection. Getting rodent saliva into cuts and abrasions can be the cause of infection.

In winter, infection can occur through aspiration contact. Farm workers, owners of private houses (if there is a possibility that mice or rats live in the house) may be at risk. Hemorrhagic fever with renal syndrome can be transmitted through ticks that are on the body of rodents. But these ticks do not attack people.

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Symptoms of the disease from 1 to 11 days

The development of the disease can take up to 1 month. In the first 2 weeks, the patient experiences the initial and oliguric stages of disease progression. Hemorrhagic fever with renal syndrome begins to manifest from day 1 of infection. The patient has a very high temperature (up to 40 ° C), which is accompanied by chills. After that, symptoms appear:

Weakness all over the body.
Great thirst and dry mouth.
Headache.
Swelling of the neck, face and chest.

A rash similar to an allergic one sometimes appears on the skin of patients. On day 2, the patient may begin swelling of the airways, severe malaise, and back pain. Usually, there is no change in the functioning of internal organs at the initial stage of infection. Rarely, patients may have pain in the region of the heart, difficulty in breathing.

The feverish period begins on the 4th day of the incubation period and lasts until the 11th day of illness. A person continues to have a high temperature for 2-3 days, but usually on the 7th day it subsides. Following this, there are no significant changes in the patient's condition. The main symptom that manifests itself the most is lower back pain.

If the pain disappears on the 5th-6th day of the incubation period, then this may mean that the diagnosis was made incorrectly. Patients on the 6th day begin prolonged causeless vomiting, which can be repeated many times throughout the day. The person begins to swell and ache in the stomach. The swelling of the mucosa begins to increase, no manifestations of the lesion are noted on the skin.

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Symptoms of the disease from 12 to 26 days

On day 12, the patient's temperature may gradually decrease. But this is not a sign of improvement in his condition. During this period, internal inflammation of the organs can develop. The patient develops an irresistible thirst, dry skin, dry mouth, severe headaches and lethargy. The patient cannot sleep, and the pain in the lumbar back begins to spread to the entire abdominal cavity.

In the blood of the patient, the level of nitrogenous slags begins to rise sharply. This happens due to the breakdown of proteins and a violation of the amount of nitrogen that is excreted by the kidneys. The patient has a significant decrease in the amount of urine produced. The more severe the disease is tolerated, the less urine is excreted by the body per day.

Renal syndrome may be accompanied by isohyposthenuria. This disease develops in almost all patients due to fever and provokes a sharp decrease in urine density. A study of the blood of patients at this stage of the development of the disease shows an increased content of leukocytes in the plasma.

From the 13th day, the patient may stop vomiting and nausea, appetite and the ability to move normally appear. During this time, there may be a significant increase in the amount of daily urine, gradually it reaches a normal value. The person has dry mouth, weakness throughout the body and malaise.

After this stage, a slow recovery begins. The final recovery period can take a very long time. This usually takes 4 to 12 months. Accompanied by recovery pathologies from the kidneys, dry mouth, polyuria. If these symptoms continue for too long or are very severe, the patient may need to be readmitted to the hospital.

Often, the disease contributes to the violation of the excretory-secretory function of the tubules and other less pronounced disorders. Such processes can continue in the human body for a very long time, and it may take up to 10 years to fully restore all body functions. However, during this time, the disease will not turn into a chronic form of renal failure.

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Complications and prevention

Patients sometimes experience complications after illness. They are expressed through:

development of infectious-toxic shock;
renal failure;
edema of the respiratory tract;
internal hemorrhages;
frequent seizures;
loss of consciousness;
pupil dilation;
partial loss of pulse.

As the disease progresses, many patients may experience vomiting and nausea. Often the consequences are expressed through hiccups and increased fatigue, drowsiness. Often, patients develop a nervous tic and involuntary movement of the muscles of the face. When examining a blood test in plasma, the content of urea and creatinine sharply increases. Complications can be accompanied by severe back pain and heavy bleeding.

Prevention of hemorrhagic fever with renal syndrome implies careful behavior of people in parks, forests, and plantations. It is important to observe the rules of personal hygiene. On the territory of private sectors, preventive work should be carried out to eliminate rodents from the territory of a populated area. People need to be extremely careful when in contact with rodents.