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Hemorrhagic Fever with Renal Syndrome Zhang Dazhi, M.D Department of Infectious Disease The second hospital of CMU Overview Pathogen: Hantaviruses Clinical features: fever;renal failure;shock; hemorrhagic manifestations Hemorrhagic fever with renal syndrome(HFRS) includes a group of clinically similar illnesses nEpidemic hemorrhagic fever(China) nKorean hemorrhagic fever(Korean) nNephropathis epidemica(Puumala Virology of Hantaviruse Belong to the family Bun-yaviridae Spherical enveloped viruses about 80-120 nm in diameter Genome consists of three single-stranded, negative sense RNA segments-S, M, L n S (small): encodes neucleocapsid protein n M (medium): encodes envelope glycoprotein n L(large): encodes polymerase The viruses that cause hemorrhagic fever with renal syndrome include: nHantaan nDobrava-Belgrade nSeoul n Puumala Sin Nombre virus can cause hantavirus pulmonary syndrome (America) Virology of Hantaviruse Epidemiology Sources of transmission: rodent reservoirs Virus species ReservoirEpidemic stabilization of the azotemia nLate polyuric stage: Daily urine volume 3000ml; recover of the azotemia Fluid replacement is inadequate secondary shock Clinical Manifestations: Convalescent stage last for as long as 1-3 months Daily urine volume returns to normal Clinical Manifestations What are five progressive stages of HFRS? Febrile stage; Hypotensive stage; Oliguric stage; Polyuric stage; Convalescent stage Laboratory findings Blood routine test nLeukocytosis with a left shift nElevated hematocrit lever nThrombocytopenia nAtypical lymphocytes Q:Viral infections causing leukocytosis uHFRS uInfectious mononucleosis uJapanese encephalitis uRabies Laboratory findings Urine routine test nHeavy proteinuria nHematuria nCast uMassive protein and shedded epithelial cells in urine form Membrane-like substance Laboratory findings Biochemical tests nElevated levels of liver enzymes, BUN, and serum creatinine n Electrolyte disturbances n Altered coagulation profile Laboratory findings Etiological diagnosis nEnzyme-linked immunosorbent assay (ELISA) Antihantaviral-specific IgM1:20(+) Early diagnostic value Antihantaviral-specific IgG1:40(+) Fourfold or greater rise in IgG titer can also confirm suspected cases nIsolation of virus nRT-PCR: identify viral RNA Summary of the clinical features A triad of fever, hemorrhage, and renal insufficiency 5 progressive stages: Febrile stage Hypotensive stage Oliguric stage Polyuric stage Convalescent stage Laboratory finding: n Leukocytosis and thrombocytopenia n Proteinuria n Elevated levels of BUN, and serum creatinine Complication Digestive tract bleeding Intracranial hemorrhages Myocardial damage Pulmonary edema :ARDS, heart failure Secondary Infections Spontaneous kidney rupture Treatment: overview Early recognition and hospitalization, bed rest Treatment is supportive Prevent for secondary infection Prevent the GI bleeding Treatment: Febrile stage Anti-viral therapy: IV ribavirin Preferably begun within the first 4 days of illness Reduce exudate: Rutosids and vitamin C Management of the fever and toxic symptoms nPhysical cooling nShort course dexamethasone Prevent DIC Treatment: Hypotensive stage Supplement of blood volume nModest crystalloid infusion nHuman serum albumin nPlasma Vasoactive agents nDopamine, norepinephrine Correction of acidosis n 5% Sodium Bicarbonate Injection Treatment: Oliguric stage Maintenance of internal environment homeostasis nRestrict the volume of infusion Daily urine volume + 500-700ml nControl the azotemia Supply sufficient carbohydrate to reduce the protein degradation nMaintaining electrolyte balance Treatment of Hyperkalemia nCorrection of acidosis 5% Sodium Bicarbonate Injection Treatment of hyperkalemia Stop further potassium accumulation Protect the cardiac membrane Calcium gluconate 10% Shift the potassium from the blood into the cell Insulin Removal of potassium from the body Haemodialysis, Furosemide Treatment: Oliguric stage Diuretics: furosemide Catharsis :rheum officinale Consider Dialysis in following conditions nSevere azotemia nFluid overload that cannot be managed with diuretics nHyperkalemia refractory to medical therapy nSevere acid-base disturbances Treatment Polyuric stage Maintain fluid and electrolyte balance Prevent secondary infection Antibiotics with nephrotoxic potential should be avoided Convalescent stage Monitored in rest home Prognosis Fatality rate ranges from 5 to 15% with Hantaan virus to less than 1% for Puumala virus infection For survivors, convalescence can take several months but recovery is often complete Prevention Rodent control Avoid contact with rodent urine, droppings, saliva, and nesting materials Vaccination Home work 1 .Hantaan virus is mainly transmitted by A. Patients B. Carriers C. Swine D. Mosquitoes E. Rodents (E) Home work 2 .The most cardinal reason of bleeding in febrile period of EHF is A. DIC B. Heparin-like substance increasing C. Thrombocytopenia and vascular injury D. Azotemia E. Coagulation factor decreasing (C) Home work 3.The main reason for early shock in EHF is A. Infection. B. Blood plasma-losing C. Hypervolemia D. Hemorrhage E. Vomiting . (B) Home work 4.The patient had fever, lumbago, headache for three days. Physical examination: drunken face, petechiae in axillary folds, chemosis. Blood routine test: WBC 19109,N 83%, PLT 20109. Urine protein (+), RBC 3-5/HP .The diagnosis may be
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