5 Hemorrhagic Fever With Renal Syndrome

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5 Hemorrhagic Fever With Renal Syndrome

  1. 1. Hemorrhagic Fever with Renal Syndrome Department of Infectious Diseases Third Affiliated Hospital of Sun Yat-sen University Lin Yang
  2. 2. <ul><li>■ Definition </li></ul><ul><li>▲ Infectious diseases with natural source </li></ul><ul><li>▲ Caused by Hantan virus </li></ul><ul><li>▲ Characterized by fever, hemorrhage, </li></ul><ul><li>proteinuria, shock and acute renal </li></ul><ul><li>failure. </li></ul><ul><li>▲ Five phases in the typical cases </li></ul>Febrile phase, Hypotensive (shock) phase, Oliguric phase, Diuretic phase, Convalescent phase
  3. 3. Epidemic Hemorrhagic Fever ( EHF) Suggested name by WHO in 1982: Hemorrhagic Fever with Renal Syndrome (HFRS)
  4. 4. Hantan virus ▲ Member of the family of Bunyaviridae ▲ Feature of virus Single-strand negative RNA virus Circular or oval in shape 78~210 nm in diameter Envelope proteins:glycoprotein1(G1) glycoprotein2(G2) Viral genome—RNA : L M S gene ■ Etiology
  5. 5. <ul><li>Viral proteins </li></ul><ul><li>L--- Polymerase </li></ul><ul><li>M---Envelope protein G1 and G2 </li></ul><ul><li>the membrane antigen </li></ul><ul><li>G2: contain neutrolization antigen </li></ul><ul><li>(vaccine antigen) </li></ul><ul><li>S---Nucleocapsid protein: </li></ul><ul><li>strong antigenicity and immunogenicity, and containing complement binding antigen. </li></ul>
  6. 6. ▲ Serologic type of Hantan virus Over twenty serologic types hantaan virus (type I, HTNV) seoul virus(type II, SEOV) puumala virus (type III,PUUV) prospect hill virus(type IV,PHV) dobrava-belgrade virus (DEOV)
  7. 7. Human HFRS : caused by four type of virus: hantaan virus (type I, HTNV) seoul virus(type II, SEOV) puumala virus (type III,PUUV) dobrava-belgrade virus(DEOV) China: Hantaan virus Seoul virus hantaan virus and DEOV show stronger pathogenecity than type II and III virus
  8. 8. ▲ Resistance of virus Low resistance: Inactivated by acid (<pH 5.0), ethanol, ether, chloroform. heat in 56 ºC for 30min or 100ºC for 1min. Be sensitive to alcohol ultraviolet rays
  9. 9. ■ Epidemiology 1. Sources of infection ▶ In our country: Apodemus agrarius Mus norvegicus Apodemus sylvaticus Citellus undulatus ▶ Laboratory Rats ▶ Other animals: cats dogs rabbits Patients:unimportant Infected field rats, house rats
  10. 10. Apodemus agrarius Mus norvegicus
  11. 11. <ul><li>2. Modes of transmission: Five </li></ul><ul><li>1>.Air-borne transmission </li></ul><ul><li>via inhale aerosol contaminated with virus- </li></ul><ul><li>containing excretion or secretion of rats </li></ul><ul><li>2>.Food-borne transmission </li></ul><ul><li>via oral and esophageal mucosa </li></ul><ul><li>(eat food contaminated with virus-containing excretion or secretion of rats) </li></ul>
  12. 12. <ul><li>3>. Infection via contact </li></ul><ul><li>Be bitten by rats or wound is contaminated </li></ul><ul><li>with virus-containing excretions or </li></ul><ul><li>secretions of rats </li></ul><ul><li>4>. Vertical transmission: </li></ul><ul><li>mother to baby, very rare </li></ul><ul><li>5>. Arthropod-borne : </li></ul><ul><li>rats mite, red mite, harvest mite may carry Hantan virus. need to be confirmed </li></ul>
  13. 13. <ul><li>3. Epidemic features </li></ul><ul><li>1>. District localization: mainly in Asia. </li></ul><ul><li>Europe and Africa, America </li></ul><ul><li>In China: higher incidence </li></ul><ul><li>except for Qinghai and Xizhang provinces </li></ul><ul><li>2>.Seasonality </li></ul><ul><li>May occur all the year, however seasonality </li></ul><ul><li>▶ March to May transmitted by house rats </li></ul><ul><li>▶ November to January and May to July </li></ul><ul><li>transmitted by Apodemus agrarius </li></ul>Epidemic peak : three
  14. 14. <ul><li>3>. Epidemic form </li></ul><ul><li>three kinds of epidemic form: </li></ul><ul><li>sporadic, endemic, seldom epidemic </li></ul><ul><li>4>. Occupation and age </li></ul><ul><li>▶ Residents in countryside </li></ul><ul><li>▶ urban and rural worker </li></ul><ul><li>Most victims are young adults . </li></ul>
  15. 15. <ul><li>4. Susceptibility </li></ul><ul><li>▶ Susceptibility is universal </li></ul><ul><li>▶ Low rate of covert infection (3.5.-4.3%). </li></ul><ul><li>▶ Stable immunity obtain from illness </li></ul><ul><li>IgG against type I virus: last for 1-30 years </li></ul><ul><li>IgG aganst type II virus: last less 2 years </li></ul>
  16. 16. ■ Pathogenesis Pathogenesis of HFRS is not so clear. ▲ Virus is the initiator ▲ Immune responses, humoral and cellular immune response,both involves in the pathogenesis
  17. 17. 1.Direct damage by Hantan virus Virus infection---replication in infected cells, especially in endotheliocytes of small blood vessels---damage on cells. 2. Immune-mediated damage Type III,I,II, and IV hypersensitivity reactions; CTL reaction-mediated damage; Cytokine-mediated cells damage
  18. 18. 1>Type III hypersensitivity reaction Hantan virus infection—induce specific antibodies—immune complex-activating complements-accumulation of immune complex in small blood vessels, basement of glomerulus and renal tubule--- damage
  19. 19. 2> Other hypersensitivity reaction Type I--IgE mediated damage. Type II-- linear IgG immune complex–accumulation in platelet and basement membranes of renal tubule Type IV— CD8+ cell mediated immune damage.
  20. 20. 3>.Cellular immune response: Hantan virus infection –activation of CD8 + T cells—CTL response–release lymphokines — damage 4>. Hantan virus—lymphocyte and macrophage—cytokins: such as interleukin1(IL-1), IFNr, tumor necrosis factor(TNF)—damage
  21. 21. <ul><li>■ Pathophysiology </li></ul><ul><li>1.Shock </li></ul><ul><li>Primary shock and secondary shock </li></ul><ul><li>2.Hemorrhage </li></ul><ul><li>3.Acute renal failure </li></ul>
  22. 22. <ul><li>1. shock </li></ul><ul><li>Virus and immune response--- small blood </li></ul><ul><li>vessel damage---permeability of vessel --- </li></ul><ul><li>plasma exudation---blood volume ---blood </li></ul><ul><li>concentrate, viscosity of blood ---DIC---blood </li></ul><ul><li>flow ---blood volume ---hypotension shock </li></ul>
  23. 23. <ul><li>Secondary shock: </li></ul><ul><li>Occur in diuretic phase </li></ul><ul><li>Reasons: </li></ul><ul><li>Severe hemorrhage </li></ul><ul><li>Secondary infection </li></ul><ul><li>Imbalance of fluid, electrolytes </li></ul>
  24. 24. <ul><li>2. Hemorrhage </li></ul><ul><li>Petechia, ecchymosis in skin and mucosas, </li></ul><ul><li>visceral bleeding </li></ul><ul><li>Reasons: </li></ul><ul><li>Capillary damage; </li></ul><ul><li>Platelet decrease and dysfunction; </li></ul><ul><li>DIC; increased Heparin-like substance; anuria </li></ul>
  25. 25. <ul><li>3. Acute renal failure </li></ul><ul><li>Reasons: Six </li></ul><ul><li>1>.Exudation of plasma, blood volume </li></ul><ul><li>blood concentrate---blood flow in kidney </li></ul><ul><li>glomerular filtrate rate (GFR) </li></ul><ul><li>2>.Immune-mediated kidney damage </li></ul><ul><li>small vessel and renal tubule </li></ul><ul><li>3>.Renal interstitial hemorrhage and edema --- </li></ul><ul><li>crush renal tubule </li></ul>
  26. 26. <ul><li>4>. Renal tissue necrosis </li></ul><ul><li>5>. Activation of renin </li></ul><ul><li>angiotensin II—renal arterial </li></ul><ul><li>contract---renal cortex blood flow – </li></ul><ul><li>GFR (glomerular filtrate rate) </li></ul><ul><li>6>. Renal tubule was blocked </li></ul><ul><li>by proteins and casts </li></ul>
  27. 27. <ul><li>■ Pathology </li></ul><ul><li>1. Organ of pathological damage </li></ul><ul><li>▲ Small blood vessel and kidney </li></ul><ul><li>▲ Other organs </li></ul><ul><li>Such as heart, liver and </li></ul><ul><li>brains, so on. </li></ul>
  28. 28. <ul><li>2. Pathological feature </li></ul><ul><li> pathological changes </li></ul><ul><li>Endotheliocytes of small blood vessel </li></ul><ul><li>congestion, edema, </li></ul><ul><li>hemorrhage, necrosis. </li></ul><ul><li>pathognomonic lesion of HFRS in kidneys. </li></ul><ul><li> Similar pathological changes in various organs . </li></ul><ul><li> without significant inflammatory reaction </li></ul>
  29. 29. <ul><li>■ Clinical Manifestations </li></ul><ul><li>▲ Incubation period: 1-2 weeks </li></ul><ul><li>▲ Three major manifestations : </li></ul><ul><li>1> pyrexia, intoxication </li></ul><ul><li>2> hyperemia and hemorrhage </li></ul><ul><li>3> hypotension and renal malfunction </li></ul><ul><li>▲ Five typical phase. Five clinic types </li></ul>
  30. 30. <ul><li>A:Five typical phase </li></ul><ul><li>1.Febrile phase </li></ul><ul><li>2.Hypotensive (shock) phase </li></ul><ul><li>3.Oliguric phase </li></ul><ul><li>4.Diuretic phase </li></ul><ul><li>5.Convalescent phase </li></ul>
  31. 31. <ul><li>1.Febrile phase </li></ul><ul><li>Pyrexia </li></ul><ul><li>Intoxication symptoms </li></ul><ul><li>Capillary damage signs </li></ul><ul><li>Kidney damage signs </li></ul>■ Clinical Manifestations
  32. 32. <ul><li>1.Febrile phase </li></ul><ul><li>1>. Pyrexia </li></ul><ul><li>acute onset, 39 o C- 40 o C, </li></ul><ul><li>lasts 3-7 days </li></ul><ul><li>Feature of pyrexia: </li></ul><ul><li>Sustained fever or remittent fever. </li></ul>For most cases, going to more serious with pyrexia gradually disappeared
  33. 33. <ul><li>2>.Intoxication symptoms </li></ul><ul><li>a. Three ache </li></ul><ul><li>headache </li></ul><ul><li>because of small vessel expansion </li></ul><ul><li>lumbago, orbital pain . </li></ul><ul><li>because of hyperemia and edema in tissue. </li></ul><ul><li>b.Gastrointestinal symptoms </li></ul><ul><li>hiccup vomiting </li></ul><ul><li>abdominal pain and diarrhea </li></ul>
  34. 34. <ul><li>3>. Capillary damage signs </li></ul><ul><li>a . hyperemia </li></ul><ul><li>Flush over face, neck and chest skin </li></ul><ul><li>(three flush) </li></ul><ul><li>drunkenness </li></ul><ul><li>b. Hemorrhage </li></ul><ul><li>For most cases, petechia, ecchymosis, </li></ul><ul><li>or stripe-shaped bleeding in chest and </li></ul><ul><li>back skin, conjunctiva bleeding. </li></ul><ul><li>For a partial cases, hematuria, DIC </li></ul>
  35. 35. <ul><li>c. Exudative edema </li></ul><ul><li>mainly babular conjunctiva edema. </li></ul><ul><li>palpebra edema and face edema </li></ul><ul><li>4>. Kidney damage signs </li></ul><ul><li>Proteinuria, sometimes with casts, blood </li></ul><ul><li>cells and membrane-shaped substance </li></ul><ul><li>consisting of protein, blood cells and </li></ul><ul><li>mucosal epithelia. </li></ul>
  36. 36. <ul><li>Summary in febrile phase </li></ul><ul><li>Pyrexia, three flush, three ache, </li></ul><ul><li>hemorrhage and conjunctiva edema , </li></ul><ul><li>malaise, </li></ul><ul><li>proteinuria , sometimes with casts, blood </li></ul><ul><li>cells and membrane-shaped substance </li></ul>
  37. 38. Patient with HFRS
  38. 39. Patient with HFRS: petechia, ecchymosis
  39. 40. <ul><li>2.Hypotensive(shock) phase </li></ul><ul><li>1> Occur during defeverscence in 4 to 5 days </li></ul><ul><li>of diseases course, lasts 1 to 3 days. </li></ul><ul><li>2>. Main signs: Hypotension or shock </li></ul><ul><li>3>. nausea, vomiting, abdominal pain. </li></ul><ul><li>Platelet , hematocrit value </li></ul><ul><li>proteinuria, leukocytosis, </li></ul><ul><li>atypical lymphocytes >10% </li></ul>■ Clinical Manifestations
  40. 41. <ul><li>3. Oliguric phase </li></ul><ul><li>Oliguria or anuria </li></ul><ul><li>Uremia </li></ul><ul><li>Metabolic acidosis and imbalance of </li></ul><ul><li>fluids and electrolyte </li></ul>■ Clinical Manifestations
  41. 42. <ul><li>3. Oliguric phase </li></ul><ul><li>Occur during or soon after hypotensive </li></ul><ul><li>phase, in 5 to 8 days of diseases course, </li></ul><ul><li>lasts 2-5 days. </li></ul><ul><li>1>. Oliguria or anuria </li></ul><ul><li>Oliguria: urine volume < 500ml/24h </li></ul><ul><li>Anuria: urine volume < 50ml/24h </li></ul>
  42. 43. <ul><li>2>.Uremia </li></ul><ul><li>a. gastrointestinal symptoms </li></ul><ul><li>hiccup, vomiting, abdominal pain, </li></ul><ul><li>diarrhea </li></ul><ul><li>b. Aggravating hemorrhage </li></ul><ul><li>hemoptysis, hematemesis, </li></ul><ul><li>hematuria or melena </li></ul><ul><li>c. Nervous system symptoms </li></ul>
  43. 44. <ul><li>3>. Metabolic acidosis and imbalance of </li></ul><ul><li>fluids and electrolyte </li></ul><ul><li>▲ Metabolic acidosis </li></ul><ul><li>▲ fatal hyperkalemia </li></ul><ul><li>▲ hypervolemic syndrome </li></ul><ul><li>edema and restlessness </li></ul><ul><li>high blood pressure </li></ul><ul><li>engorged neck veins </li></ul><ul><li>. </li></ul>
  44. 45. <ul><li>4 Diuretic phase </li></ul><ul><li>▲ Urine >3000ml/24h </li></ul><ul><li>Occur in 9 to 14 days of diseases course, </li></ul><ul><li>last for 1 day or several months </li></ul><ul><li>▲ Three phase </li></ul><ul><li>according to urine volume and azotemia signs </li></ul><ul><li>► Transition phase </li></ul><ul><li>► Early stage of diuretic phase </li></ul><ul><li>► Late stage of diuretic phase </li></ul>■ Clinical Manifestations
  45. 46. <ul><li>1>. Transition phase </li></ul><ul><li>a.Urine from 500ml to 2000ml/24h </li></ul><ul><li>b. BUN and Cr persistently </li></ul><ul><li>c. State of patient may change to more </li></ul><ul><li>serious. </li></ul>more serious although urine increase high mortality
  46. 47. 2>. Early stage of diuretic phase u rine volume > 2000ml/24h no marked decrease in azotemia 3>. Late stage of diuretic phase a. urine volume > 3000ml/24h in most of cases: 4000 to 8000/24h, 15000ml/24h b. azotemia improving, BUN falling down c. Secondary shock, dehydration hypokalemia, hyponatremia
  47. 48. <ul><li>5. Convalescent phase </li></ul><ul><li>urine return to 1000-2000ml/24h </li></ul><ul><li>normal appetite </li></ul><ul><li>taking 1-3 months for recovering </li></ul>Five phase be not seen in every case. hypotension and /or oliguria phase may be absent in atypical cases ■ Clinical Manifestations
  48. 49. <ul><li>B:Five clinic types </li></ul><ul><li>1. Mild type </li></ul><ul><li>2. Moderate </li></ul><ul><li>3. Severe </li></ul><ul><li>4. Very serious </li></ul><ul><li>5. Atypical type </li></ul>
  49. 50. <ul><li>1. Mild type: </li></ul><ul><li>T< 39 o C ,mild intoxication </li></ul><ul><li>symptoms without oliguria </li></ul><ul><li>and shock </li></ul>
  50. 51. <ul><li>2.Moderate: </li></ul><ul><li>T>39 o C , severe intoxicating </li></ul><ul><li>symptoms, drunkenness, </li></ul><ul><li>conjunctiva edema, </li></ul><ul><li>hemorrhage, hypotension, </li></ul><ul><li>oliguria and marked proteinuria . </li></ul>
  51. 52. <ul><li>3.Severe: </li></ul><ul><li>T>40 °C , more severe intoxicating </li></ul><ul><li>symptoms, shock, bleeding, </li></ul><ul><li>oliguria for less than 5 days or </li></ul><ul><li>anuria for less than 2 days. </li></ul>
  52. 53. <ul><li>4.Very serious: </li></ul><ul><li>The symptoms and signs in </li></ul><ul><li>severe type with one of following </li></ul><ul><li>six signs: </li></ul><ul><li>1>. hard-corrective shock </li></ul><ul><li>2>.bleeding in main organ </li></ul><ul><li>3>. acute renal failure </li></ul><ul><li>4>. Cardiac failure </li></ul><ul><li>pulmonary edema </li></ul><ul><li>5>. Complication in Central </li></ul><ul><li>nervous system </li></ul><ul><li>6>. Serious secondary infection </li></ul>
  53. 54. <ul><li>5. Atypical </li></ul><ul><li>T<38 °C , atypical symptoms </li></ul>
  54. 55. <ul><li>■ Laboratory Finding </li></ul><ul><li>1. Blood routine </li></ul><ul><li>leukocytosis , 15-50x 10 9 /L, </li></ul><ul><li>neutrophils dominated in early stage, </li></ul><ul><li>lymphocytes in late stage. </li></ul><ul><li>Atypical lymphocytes10%~15% </li></ul><ul><li>hematocrit value and hemoglobin rise, </li></ul><ul><li>thrombocytopenia </li></ul>
  55. 56. <ul><li>2.Urine routine </li></ul><ul><li>Proteinuria, sometimes with casts, blood cells </li></ul><ul><li>and membrane-shaped substance , consisting </li></ul><ul><li>of protein, blood cells and mucosal epithelia. </li></ul><ul><li>may be found in 2 days of diseases course </li></ul>
  56. 57. <ul><li>3. Blood biochemical examination </li></ul><ul><li>BUN and Cr increased. </li></ul><ul><li>CO 2 -CP decreased. </li></ul><ul><li>hyperkalemia in oliguric phase. </li></ul><ul><li>hypokalemia in diuretic phase. </li></ul>
  57. 58. <ul><li>4. Blood coagulating function examination </li></ul><ul><li>thrombocytopenia, platelet </li></ul><ul><li>prolongated PT </li></ul><ul><li>Fibrinogen decreased </li></ul><ul><li>secondary fibrin lysis </li></ul>
  58. 59. <ul><li>5. Serological tests </li></ul><ul><li>Hantan virus antigen and specific antibody test </li></ul><ul><li>by IFAT, ELISA, RIA or WB. Antibody against </li></ul><ul><li>nuclear protein is useful for diagnosis. </li></ul><ul><li>1> IgM antibody </li></ul><ul><li>1:20 positive: diagnosis marker </li></ul><ul><li>2> IgG antibody: </li></ul><ul><li>> 4 times/week useful for diagnosis. </li></ul><ul><li>Anti-G2--- estimate prognosis . </li></ul><ul><li>6. Molecular biological tests </li></ul><ul><li>Viral RNA by RT-PCR </li></ul>
  59. 60. <ul><li>■ Complications </li></ul><ul><li>1.Visceral bleeding </li></ul><ul><li>Intracrania hemorrhage </li></ul><ul><li>hemoptysis, hematemesis, </li></ul><ul><li>hematuria, cerebral hemorrhage </li></ul>
  60. 61. 2. Complication in central nervous system Encephalitis and meningitis Intracrania hemorrhage and cerebral edema
  61. 62. <ul><li>3.Pneumon edema </li></ul><ul><li>commonly occur in hypotensive phase and </li></ul><ul><li>oliguric phase. </li></ul><ul><li>ARDS: Mortality ~ 67%) </li></ul><ul><li>(Adult respiratory distress syndrome) </li></ul><ul><li>Reasons: </li></ul><ul><li>increasing permeability of the pulmonary </li></ul><ul><li>capillarries, and decreasing in alveolar surface </li></ul><ul><li>activating substances </li></ul>
  62. 63. <ul><li>4.Others </li></ul><ul><li>Secondary infection with bacterials </li></ul><ul><li>Spontaneous rupture of the kidneys </li></ul><ul><li>Hepatitis, myocarditis, pericarditis </li></ul>
  63. 64. <ul><li>■ Diagnosis </li></ul><ul><li>▲ Epidemiologic data </li></ul><ul><li>▲ Clinical feature </li></ul><ul><li>▲ Laboratory examinations </li></ul>
  64. 65. <ul><li>1. Epidemiologic data </li></ul><ul><li>place, season, </li></ul><ul><li>history of contacting rats or excretion </li></ul><ul><li>and secretions of rats </li></ul>
  65. 66. <ul><li>2. Clinical features </li></ul><ul><li>three manifestations in early stage and the </li></ul><ul><li>course of five phase in typical case </li></ul><ul><li>► Pyrexia, “three aches”, intoxicating symptoms </li></ul><ul><li>► “ Three flush”: face, neck and chest skin. </li></ul><ul><li>conjunctiva congestion and edema. </li></ul><ul><li>hemorrhage </li></ul><ul><li>► Oliguria, renal region pain on percussion </li></ul><ul><li>► Five phase in typical case </li></ul>Five phase is not observed in every case. hypotension and /or oliguria phase may be absent in atypical cases
  66. 67. <ul><li>3.Laboratory data </li></ul><ul><li>1>. Blood </li></ul><ul><li>Leukocytosis </li></ul><ul><li>atypical lymphocytes>10% </li></ul><ul><li>thrombocytopenia. </li></ul><ul><li>2>. Urine : </li></ul><ul><li>proteinuria . </li></ul><ul><li>membrane- shaped substance in urine. </li></ul><ul><li>3>. Virus antigen and antibody </li></ul><ul><li>Viral RNA by RT-PCR </li></ul>
  67. 68. ■ Differential diagnosis 1. In febrile phase with common cold, influenza, Septicemia . 2. In Hypotensive phase with other infection shock 3. P yrexia, intracrania hemorrhage and cerebral edema with meningococcal meningitis     
  68. 69. 4.Oliguria and renal failure with acute nephritis 5.Pyrexia and hemorrhage with Leptospirosis 6. Marked hemorrhage with: thrombocytopenic purpura, gastrointestinal bleeding caused by gastric ulcer .
  69. 70. <ul><li>■ Prognosis </li></ul><ul><li>Fatality is related to clinical type, whether being </li></ul><ul><li>treated earlier. </li></ul><ul><li>mortality 1%~5%. </li></ul><ul><li>major reasons for death : </li></ul><ul><li>renal failure, cerebrohernia </li></ul><ul><li>secondary septicemia </li></ul><ul><li>massive bleeding. </li></ul><ul><li>mortality higher in infection with type I virus. </li></ul>
  70. 71. <ul><li>■ Treatment </li></ul><ul><li>▲ Principle of treatment </li></ul><ul><li>● Diagnosis, rest and treatment in early </li></ul><ul><li>● Treatment in near hospital </li></ul>
  71. 72. ▲ Treatment  Supportive treatment  Anti-viral therapy  Symptomatic treatment
  72. 73. <ul><li>1. Supportive treatment </li></ul><ul><li>bed rest </li></ul><ul><li>easy digestive food </li></ul><ul><li>vitamins </li></ul><ul><li>Intravenous fluids containing </li></ul><ul><li>suitable glucose, electrolytes </li></ul>
  73. 74. 2. Treatment in febrile phase Principle of treatment a>.Anti-virus therapy b>.Reduce exudation of plasma c>.Reduce intoxicating symptoms d>.Preventing from DIC
  74. 75. 1 >.Anti-viral therapy: important giving anti-virus drug in early stage. (Ribavirin(virazole) 1.0g iv drip with 10%GS qd for 3-5 days 2>.Reduce permeability of small vessel and exudation Lutin and Vitamin C
  75. 76. <ul><li>3>.Reduce intoxicating symptoms </li></ul><ul><li>a> For hyperpyrexia </li></ul><ul><li>Physical measures to decrease temperature. </li></ul><ul><li>For example: putting ice-bag on head, neck or </li></ul><ul><li>big vessel location. </li></ul><ul><li>Avoiding using heavy antipyretics </li></ul><ul><li>b>.Corticosteroids for hyperpyrexia and heavy </li></ul><ul><li>intoxicating symptoms </li></ul><ul><li>Dexamethasone 5-10mg iv. Drip </li></ul><ul><li>c> c>.Anti-vomiting: </li></ul><ul><li>20mg of Paspertin im p.r.n </li></ul>
  76. 77. 4>.Prevention from DIC a>. Reduce the blood viscosity Danshen solution, Dextran 40 b>. anti-coagulation therapy Heparin should be given once the CT is less than 3 min or APTT less than 34 seconds.
  77. 78. 3.Treatment in Hypotensive phase Principle of treatment: ► Supplement blood volume ► Correct acidosis 1>.Supplement blood volume A.Principle: early rapidly adequate
  78. 79. 1>.Supplement blood volume A.Principle: early rapidly adequate B:kinds of fluids: Crystalloid fluids and Colloid fluids containing suitable glucose, electrolytes and vitamins: Ringer’s Solution Normal saline solution Dextran, 20% Mannitol Plasma, albumin, Artificial plasma.
  79. 80. 2>Correct metabolic acidosis 5% sodium bicarbonate solution. The amount calculated according to CO 2 CP value. 3>.Blood vessel activating drugs for hypotension and shock: aramine, dopamine, 654-2
  80. 81. 4>.Corticosteroids Reduce severe toxemia, Reduce permeation of small vessel Improving microcirculation of tissue. 10~20mg of Dexamethason is given by intravenous drip.
  81. 82. 4.Treatment in oliguric phase Principle of treatment : ► Balance intra-environment ► Diuretic therapy ► Catharsis therapy for preventing from hypervolemia ► Dialysis therapy
  82. 83. 1>.Balance intra-environment a>.Correct imbalance of fluid electrolytes, acid- base Closely observe and record urine volume. Examine blood biochemical parameter and renal function adjusting amount of fluid and electrolytes
  83. 84. b>. Reducing protein degradation and control of azotemia. Food containing high vitamins high carbohydrate, low protein. For the serious patient : Supplement glucose 200~300g every day by intravenous drip 20-25% GS with insulin.
  84. 85. 2>.Diuretic for oliguria 20%Mannitol solution. lasix (furosemide) 3>Catharsis therapy for hypervolemia inducing diarrhea to take out fluids by intestinal. 50% Magnesium Sulfate solution 20%Mannitol solution
  85. 86. Reducing blood volume therapy For hypervolemia with cardiac failure and pulmonary edema, taking out 300ml ~400ml blood may be useful. used rare now
  86. 87. <ul><li>4>.Dialysis therapy </li></ul><ul><li>for serious azotemia </li></ul><ul><li>▲ very important, save life </li></ul><ul><li>▲ Hemodialysis or Peritoneal dialysis </li></ul>
  87. 88. <ul><li>▲ Marker of giving Dialysis therapy : </li></ul><ul><li>Oliguria lasts for 4 days or anuria lasts </li></ul><ul><li>for 24 hours with one of following five signs : </li></ul><ul><li>a>.Seral BUN >28.56mmol/L; </li></ul><ul><li>b>.BUN increasing more than 7.14mmol/L </li></ul><ul><li>every day; </li></ul><ul><li>C>.Blood potassium > 6mmol/L; </li></ul><ul><li>d>.hypervolemia or/and pulmonary edema; </li></ul><ul><li>e>.being terrible fretful or cerebral edema. </li></ul>
  88. 89. 5 . Treatment in Diuretic phase a. Keeping balance of fluid and electrolytes. b.Preventing and treatment secondary infection: antibiotics
  89. 90. 6.Convalescent phase a:Supplement nutrition food. b:Examination renal function, blood pressure, pituitary function at regular interval.
  90. 91. 7.Complications treatment 1>. Hemostatics therapy for heavy bleeding such as gastrointestinal hemorrhage treatment of DIC: according to different phase of DIC, giving EACA, protamine ,respectively.
  91. 92. 2>.Treatment ARDS a: Control of amount of intravenous infusion. b: Giving oxygen, or mechanical ventilation: positive end expiratory pressure. c.Corticosteroids: 20 to 30mg of dexamethasone d. Cedilanid for cardiac failure.
  92. 93. 3>.Treatment of central nervous system complications a> Diazepam for tics b>.Cerebral edema and high intracranial pressure: 20% of mannitol or/and lasix dripped intravenously.
  93. 94. 4>. Prevention and treatment of secondary infections: Antibiotics 5>. Spontaneous rupture of the kidneys Surgery therapy
  94. 95. <ul><li>■ Prophylaxis </li></ul><ul><li>1. Exterminate field rats, house rats. </li></ul><ul><li>2.Wipe out mites: </li></ul><ul><li>Drugs: </li></ul><ul><li>Derivatives of pyrethrin </li></ul><ul><li>Organic phosphoric compounds </li></ul><ul><li>Preventing from biting . </li></ul>
  95. 96. <ul><li>3.Vaccine </li></ul><ul><li>Two Kinds of vaccines can be available: </li></ul><ul><li>► Against Hantan virus type I </li></ul><ul><li>► Against Hantan virus type II </li></ul><ul><li>A ntibody production: </li></ul><ul><li>88%-94%, and last for 3~6 months </li></ul><ul><li>Inoculation of the vaccine is carried out one </li></ul><ul><li>month earlier than epidemic , and a bloost </li></ul><ul><li>injection should be given one year later. </li></ul>
  96. 97. THANKS!!!
  97. 98. <ul><li>SUMMARY </li></ul><ul><li>1.HFRS:Infectious diseases caused by Hantan virus </li></ul><ul><li>2. Major sources of infection: </li></ul><ul><li>Infected field rats, house rats, </li></ul><ul><li>3. Epidemic features: </li></ul><ul><li>three epidemic peaks: </li></ul><ul><li>March to May: by house rats </li></ul><ul><li>November to January, May to July: by Apodemus agrarius </li></ul>
  98. 99. <ul><li>4. Pathogenesis </li></ul><ul><li>  ▶ V iral direct damage of Hantanvirus. </li></ul><ul><li>▶ Immune-mediated damage </li></ul><ul><li>5. Pathological damage and feature </li></ul><ul><li>major in small blood vessel and kidney. </li></ul><ul><li>congestion, edema, hemorrhage, necrosis. </li></ul><ul><li>6. Pathophysiology: </li></ul><ul><li>Shock Hemorrhage Acute renal failure </li></ul>Without significant inflammatory reaction
  99. 100. <ul><li>7.Clinical feature </li></ul><ul><li>Fever, three flush, three ache, exudative edema, hemorrhage, proteinuria, shock and acute renal failure. Five phase in typical cases. </li></ul><ul><li>8. Diagnosis </li></ul><ul><li>Combination of epidemiologic data, clinical feature and laboratory examinations data. </li></ul>9.Principle of treatment: diagnosis, rest and treatment early Treatment in near hospital 10. Principle of treatment for each phase ??
  100. 101. <ul><li>11. Treatment </li></ul><ul><li>1>. Supportive treatment </li></ul><ul><li>2>. Anti-viral therapy </li></ul><ul><li>3>.Symptomatic treatment </li></ul>12. Prevention 1>. Exterminate field rats, house rats 2>. vaccines ► Against Hantan virus type I ► Against Hantan virus type II
  101. 102. THANKS!!!

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