Hemorrhagic fever symptoms
GL 6 can cause pathogens from the group of arboviruses spread by arthropods, a group of 4 Togaviridae flavovirusov and 3 representatives buniavirusov.
Pathogens GL frequently penetrate into the human body via vectors (mosquitoes, mosquitoes, ticks), but in some cases the infection can occur through contact with infected animals, their excrement, sick people (HFRS fever, Rift, Ebola and others.).GL Distribution is limited to certain regions, where there are favorable conditions for the virus to survive.So, the natural foci of KGL exist in the Crimea, the Rostov region, Astrakhan;Omsk GL is found in some areas of Omsk, Novosibirsk regions, Kyasanur forest disease - in the state of Mysore in India.
For GL, above all, characterized by increased bleeding.The beginning of the disease can be either acute or gradual.Often obsheinfektsionnaya symptomatology, continued for about 3 days, replaced by a short period of remission for a few hours, followed by a sudden rapid deterioration.Among the clinical manifestat
are bleeding tendency, especially skin hemorrhages, nosebleeds, bleeding from the gums, hemorrhagic conjunctivitis;typical internal bleeding, manifested bloody vomiting, melena, hematuria, metrorrhagia.
Another distinctive feature of the GL is a frequent occurrence in patients with cardiovascular syndrome, acute disorders of vascular tone, until the development of shock and collapse - reversible or irreversible.GL Among other manifestations may occur dehydration, uremia, hepatic coma, hemolysis, jaundice, nervous system damage, secondary bacterial infection.At the same time a certain organ specificity can be allocated at each of GL.So, for yellow fever is characterized by liver damage and jaundice for dengue - joints, muscles and tendons, fever Marburg - development of diarrhea, hemorrhagic fever with renal syndrome -.. Kidney disease, etc.
incidence GL person may be sporadic orepidemic.Among all known clinical forms of the greatest importance for Russia are haemorrhagic fever with renal syndrome, Crimean and Omsk hemorrhagic fever.
haemorrhagic fever with renal syndrome (HFRS) - an acute infectious viral disease of zoonotic nature, characterized by systemic lesion of small blood vessels (arteries and veins), hemorrhagic diathesis, disorders of hemodynamic and renal disease with the development of acute renal failure (ARF).
etiology. causative agents of HFRS are arboviruses (viruses Hunt) - Hantaan, Puumula, Seui, Dobrava.The most severe course peculiar virus Hantaan, popular in the Far East of Russia.Dobrava virus, detectable in South-Eastern Europe, genetically similar to Hantaan and also causes severe disease.
Puumula virus causes a mild illness called 'epidemic nephropathy ", distributed predominantly in a number of Scandinavian countries.In 1993, an outbreak of the Khanty-virus pulmonary syndrome with a high mortality rate (over 50%) in 4 states.The disease was caused by Sin Nombre - new serotype Hunt viruses.Then a number of other variations of the virus has been identified in the United States and South America.
Epidemiology. first clinical picture of HFRS was described in the early 30-ies.in the Far East.In the future, its pockets are found in Kaliningrad, Tula and Moscow regions and the Urals.
reservoir and source of transmission of the Khanty-viruses are different kinds of rodents (field and forest mice, rats), in which the infection is transmitted horizontally and vertically.
from rodents to man transmission of the virus is carried GLGPS aspiration, nutritional and contact methods.This vozdushnopylevoy path is considered as the main one.Alimentary way of infection caused by eating food contaminated with faeces of rodents.
Peak incidence is closely related to infection and the number of rodents.It can be observed as epidemic outbreaks and sporadic cases.
Ill HFRS people mostly young and middle-aged, employed in agricultural work.Described outbreaks among children.
pathogenesis. HFRS virus penetrating into the vascular endothelium, causing damage.This distinguished biologically active substances, dramatically alter vascular permeability and facilitate the exit liquid part of blood outside of the vascular bed.Developing a deficit of circulating plasma volume accompanied by decrease in blood pressure and the development of hypovolemic shock.Damage to the endothelium leads to activation of Hageman factor and running the blood coagulation system, the formation of DIC, which is exacerbated in liorgannye disorders in patients with HFRS.
Pathology. Pathological changes are characterized by a pronounced lesion of blood vessels - in the arterial wall-ol, capillaries and venules especially developed focal dystrophic, edematous and destructive necrobiotic changes.At the same time expressed inflammatory changes (vasculitis) they lack.
vascular disease accompanied by increased vascular permeability, hemorrhages and circulatory disorders in different organs.The most pronounced pathological changes are detected in the kidney, pituitary and adrenal glands, the right atrium and the central nervous system.
At autopsy the kidneys are increased in size, have a flabby consistency.In the section there is a sharp boundary between the cortical layer of pale and bright-red, packed blood brain matter.Microscopic examination of the morphological changes are regarded as acute tubulointerstitial nephritis.
Along with the changes in the kidneys legitimate disorder in the victims identified in the anterior pituitary (back almost does not suffer), although in some cases marked necrosis and hemorrhage in both lobes of the pituitary.Furthermore
pituitary changes are found in the adrenal glands, thyroid gland, pancreas insular system, CNS, myocardium, lung, gastro-intestinal tract.
classification. In daily practice, you can use the classification of HFRS proposed ZVSirotina and VFUchaikin (1998):
Classification of HFRS in children
Example of diagnosis:
Complications: acute renal failure, right-sided pneumonia polysegmental, Nam II degree.
Clinic. incubation period for HFRS is an average of 2 to 4 weeks.
Disease begins acutely and is accompanied by fever, chills, headache, severe general weakness, aches throughout the body.There are complaints of blurred vision ( "fog" in front of the eyes), abdominal pain, especially back pain, nausea, painful hiccups, vomiting.Patients may notice a decrease in urination.
Characteristic appearance of patients - puffy congested face, scleritis, conjunctivitis.
After the third day, rarely since the early days of the disease, may cause erratic or strictly linear punctate hemorrhagic rash on the skin of the breast side surfaces, the inner surface of the shoulder, in the supraclavicular and subclavian areas.May appear nosebleeds, bleeding at the injection site in the sclera.
If there is bleeding into the brain, adrenal glands, patients die.
the part of the cardiovascular system at the height of the disease are observed bradycardia, ventricular arrythmia, sometimes atrial fibrillation, lower blood pressure, up to the collapse or hypovolemic shock.
development of acute renal failure is accompanied by a rise in urea levels, Crea-tinina in the blood, acid-base balance shift towards acidosis, hyponatremia, increase of magnesium content in the blood serum.In this case the potassium content is normal or slightly increased.
By the end of the 2nd week of the disease oliguria polyuria replaced.As the magnitude of diuresis recovery condition of the patients improved.Disappear flushing of the skin, melkotochechnye hemorrhages in the skin, dissolve hemorrhages in the subcutaneous tissue, increased blood pressure, bradycardia disappears.Because of fluid loss decreases and the gain catabolism of body weight.In addition, nekorrigiruemye loss of sodium and potassium in the urine can appear clinically and general muscle weakness, nausea, abdominal pain, muscle twitching, and paresthesias, tachycardia and hypotension.
convalescence period begins with a noticeable improvement in general condition of patients, accompanied by the disappearance of azotemia.Recovery of renal function occurs within 1-3 months, and sometimes much longer.Within a year of the disease in convalescents there may be signs of asthenic syndrome, headaches, memory loss, vascular disorders, revealed focal neurological symptoms.
Changes in the blood count during the first days of the disease characterized by leukopenia, leukocytosis less, the appearance of plasma cells, the presence of which has important diagnostic value.
in urine sediment revealed a small amount of fresh or leached red blood cells, some protein and renal epithelial cells.
In severe forms of infection in the acute period may increase the level of urea and creatinine in the blood.
progression of the pathological process is accompanied by the appearance of blood neutrophilic leukocytosis with a left shift to stab, less young forms and myelocytes.Elevated levels of plasma cells is maintained.
Urine amplified hematuria, cylindruria, many renal epithelial cells, indicated moderate proteinuria.In some patients urine protein loss can be significant.At the same time the urine revealed fibrin flakes, which sometimes causes a discharge of renal colic.
convalescence period is characterized by a decrease in the level of urea and creatinine, normalization of white blood cells, red blood cells and hemoglobin in the peripheral blood, the gradual disappearance of the pathological changes in urinalysis.
differential diagnosis .The presence of fever, hemorrhagic syndrome in HFRS requires the exclusion of infectious diseases such as:
algorithm of differential diagnosis of diseases associated with the syndrome of "haemorrhagic rash»
Laboratory diagnosis. Currently decipher the etiology of the disease in HFRS can using immunofluorescence assay (IFA).For diagnosis using paired sera taken with an interval of 5-7 days.This increase in titer of antiviral antibodies in 4 or more times to diagnose HFRS.With the appropriate clinic certain diagnostic value and may have a high initial titer as specific antibodies to the virus appear after only 3-4 days of onset.
using molecular cloning and expression of the viral protein Hunt created another diagnostic system - EL1SA and IgG and IgM ELISA kits with recombinant antigens, allowing the early and short time to identify viral subtypes.
Treatment of patients with HFRS is performed only in a hospital should be:
As causal treatment can be used anandin, specific immunoglobulin, hyperimmune plasma, drugs interferon and inducers (amiksin et al.).
Central takes pathogenetic therapy aimed at combating intoxication, hemorrhagic manifestations (tab. 10.2).This treatment is most effective in a multi-hospital, ensuring the provision of not only specialized nephrology care and resuscitation.
Due to the threat of serious complications (collapse, bleeding, tear or rupture kidney cortex) treatment measures should be initiated prehospital and transportation of patients to the hospital should be as gentle.
important place in the treatment of patients with HFRS covers diet therapy, envisaging appointment of easily digestible food, containing all the necessary ingredients.Limiting protein produced in severe azotemia.
To combat vomit subcutaneous injections can be used a 2.5% solution of chlorpromazine, 2.5% solution Pipolphenum, 0.1% atropine solution droperidol in age dosages.
When expressed in the initial period of the disease hypercoagulable heparin intravenously for hemostasis control.It should be remembered that the uncontrolled introduction of the drug in HFRS may exacerbate symptoms of hemorrhagic diathesis.In the phase of "consumption coagulopathy" frozen plasma is used.The positive effect of treatment provides intermittent selective plasmapheresis.
ARF treatment in most patients performed conservatively, with strict control of water-electrolyte metabolism and CBS.
Tactics complex therapy HFRS
With regard to the stimulation of diuresis with high doses of diuretics no consensus.Some authors say that in patients with severe renal tubulointerstitial lesion tissue, their propensity to spontaneous tears and ruptures cortex use of diuretics can lead to negative consequences.
active strategy is required only in severe, and where there is the greatest danger of exceeding adequate therapy.The appearance at the turn of oligouricheskogo and poliuricheskogo periods of spontaneous ruptures and tears kidney cortex is an indication for their surgery.
The ARF conditions constituting the basis of all clinical HFRS, and reduced renal excretory capacity of even a small excess of the volumes and doses of administered drugs can cause iatrogenic disorders not related to the disease itself.
outcomes. The majority of patients recover completely.No significant cases of the disease are not re-described.
Mortality from this disease is highest in Asian countries, where the infection is caused by a virus Hantaan.Currently, it has decreased in the Amur region from 10-15 to 7-8%.In European regions of Russia, where HFRS occurs less severe, mortality ranges from 0.1 - 1%.
main causes of death from this condition are:
majority of deaths due to these causes occur in the early stages, no later than 10-12 days of illness, and because they occur against the background of acute renal failure, it served as a basis to allocate as a cause of death of patientsHFRS and uremia.
In addition, some patients recovery may occur with residual effects in the form of chronic pyelonephritis, hypertension, encephalopathy.The frequency and severity of residual symptoms depends on the severity of HFRS form.
Clinical examination. Clinical supervision includes control over the recovery of renal function, central nervous system and other internal organs affected in the acute period.Monitoring should be a pediatrician and nephrologist.
complex survey should include, in addition to clinical data, blood tests and urine tests, bacteriological urine culture, the definition of a hidden leukocyturia Nechiporenko method, calculation of the daily amount of urine.Special mention should be renoradiografiyu and renal ultrasound, with which it is possible to obtain valuable information about the state of the kidneys.
first survey conducted a month after discharge from hospital.Then the person who have had mild illness, are inspected once every 3 months, and in the absence of disease - once a year.Convalescents moderate and severe forms of HFRS visit the doctor once a month, and in the absence of deviations - 2 times a year.
Clinical supervision is terminated after 3 years in the absence of violations of the kidneys and other organs.
Prevention. Specific prophylaxis involves the use of a vaccine against different serotypes Hantaan virus and immunization relevant population groups.The experience gained so preventing disease in South Korea, North Korea and China.
Nonspecific prevention is to prevent the contact of people with rodents, the strict observance of measures of personal hygiene, sanitary and educational work among the population living in areas of HFRS distribution.