Infectious diseases. Hemorrhagic fever. Etiology, epidemiology, pathogenesis, clinical picture, diagnosis, treatment (lecture notes)

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Infectious diseases. Hemorrhagic fever. Etiology, epidemiology, pathogenesis, clinical picture, diagnosis, treatment (lecture notes)

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LECTURE No. 21. Hemorrhagic fever. Etiology, epidemiology, pathogenesis, clinic, diagnostics, treatment

Hemorrhagic fever with renal syndrome (hemorrhagic nephrosonephritis) is an acute viral disease that occurs with a peculiar renal syndrome and symptoms of intoxication, fever, hemorrhagic manifestations. This is a natural focal disease.

Etiology. The causative agent belongs to the group of arboviruses, spherical RNA-containing viruses.

Epidemiology. HFRS is a typical zoonotic natural focal infection. The reservoir of viruses on the territory of Russia is rodents and insectivores, which have latent forms of infection. The virus is excreted into the external environment mainly with urine (less often with feces, saliva). The transmission of infection from rodent to rodent is carried out through ticks and fleas. Transmission of the virus to humans is carried out by aspiration by inhalation of air containing suspended infectious excretions of rodents. There may be a contact route - when an infected material gets on abrasions, cuts, scratches, an alimentary route - when eating food contaminated with infected secretions of rodents. After the illness, a strong immunity is acquired. Relapses are extremely rare.

Pathogenesis. After entering the human body through damaged skin and mucous membranes, the virus is localized in the vascular endothelium, where it replicates and accumulates intracellularly. Then comes the viremia phase, which coincides with the onset of the disease and the appearance of general toxic symptoms. The virus has a capillary toxic effect in the form of destructive arteritis with increased permeability of the vascular wall, impaired microcirculation, development of disseminated intravascular coagulation syndrome, and organ failure, especially of the kidneys. During the febrile period of the disease, the virus is in the blood, causing infectious-toxic damage to the nervous system and severe hemorrhagic capillary toxicosis. Kidney damage with the development of acute renal failure is typical.

Clinic. The incubation period is from 11 to 23 days. There are four stages of the disease: febrile, oliguric, polyuric, convalescent stage. The febrile stage begins acutely. Fever (38-40 °C), headache, insomnia, myalgia, and photophobia appear. The face, neck, and upper parts of the body are hyperemic, the vessels of the sclera are injected. By the 3-4th day of illness, the patient’s condition worsens, vomiting, abdominal pain, hemorrhages in the form of a rash, nosebleeds, and hemorrhages at the injection sites appear. The rash may appear in stripes that resemble a whiplash. Subsequently, nasal, uterine, and stomach bleeding are possible, which can cause death. From the cardiovascular system, bradycardia, muffled heart sounds, and decreased blood pressure are observed. In severe cases of the disease, the development of infectious-toxic shock is observed. Pain appears in the abdomen and lower back, intensifies to unbearable, palpation of the abdomen reveals pain (usually in the hypochondrium), the liver is enlarged, tapping on the lower back is sharply painful.

The oliguric period begins on the 3-4th day of illness; against the background of high temperature, the patient’s condition worsens: severe pain in the lower back appears, forcing the patient to take a forced position. Headaches and vomiting appear, leading to dehydration. Palpation of the kidney area is painful. Spontaneous kidney rupture may occur. The amount of urine decreases, its relative density is low (up to 1,004), urinary retention may occur, azotemia increases, and the resulting renal failure in some cases ends in uremic coma. From the 6-7th day of illness, the body temperature begins to decrease to normal, but the patient’s condition does not improve. Toxicosis progresses (nausea, vomiting, hiccups), insomnia, and meningeal symptoms appear. Characterized by the absence of jaundice, enlarged liver and spleen. Transporting the patient during this period must be very careful. The polyuric stage occurs from the 9-13th day of illness. The patient's condition improves: nausea and vomiting stop, appetite appears, diuresis increases to 5-6 l, nocturia is characteristic. Lower back pain becomes less intense, but persists for several weeks, sometimes several months. During the recovery process, the symptoms of the disease are gradually reduced, but asthenia in the body may persist for a long time. During the period of convalescence, polyuria decreases and body function is restored. The convalescent period lasts up to 3-6 months. Recovery comes slowly. Complications: infectious-toxic shock, pulmonary edema, uremic coma, eclampsia, kidney rupture, hemorrhages in the brain, adrenal glands, heart muscle, pancreas.

Diagnosis is based on characteristic clinical symptoms; specific methods of laboratory diagnostics are not widely used.

Differential diagnosis should be made with leptospirosis, Q fever, pseudotuberculosis.

Treatment. There is no etiotropic therapy. Bed rest, a dairy-vegetable diet, and vitamins are recommended. Hormone therapy is prescribed, prednisolone from 50 to 120 mg/day. After normalization of body temperature, the dose is gradually reduced. Course duration is 8-15 days. In the first days, a 5% glucose solution or an isotonic sodium chloride solution is administered intravenously with the addition of a 1% potassium chloride solution (50 ml per 1 liter of isotonic solution), a 5% ascorbic acid solution (20 ml/day. ) and 4% sodium bicarbonate solution (50 ml per 1 liter of solution). 1-1,5 liters are administered per day. In the absence of arterial hypotension in the oliguria phase, mannitol or furosemide (Lasix) is prescribed. Gastric lavage with a 2% solution of sodium bicarbonate and siphon enemas are advisable. During attacks of intense pain, pantopon is prescribed. If signs of renal failure increase, the patient needs extracorporeal hemodialysis.

The prognosis is favorable, sometimes there are complications in the form of ruptured kidneys, uremic coma, meningoencephalitis. Ability to work returns slowly, sometimes after several months.

Prevention. Destruction of rodents, protection of foodstuff from their penetration. Patients are isolated. Current and final disinfection is carried out in the wards.

Author: Gavrilova N.V.

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