Thursday, July 30, 2015

Hantavirus Infections

Chapter 1 – Hantavirus Infections
v History:
· Hantavirus Pulmonary Syndrome (HPS)
o  Incubation time: 1-4 weeks.
o  (1) Prodromal Phase, (2) Cardiopulmon’ Phase, (3) Convalesc’ Phase.
o  Prodromal Phase (3-5 days): fever, headache, & myalgia; (Common, Prodromal) Abdomin’ Pain, emesis, & diarrhea; Minimal or absent respirat’ tract-referable sympt’; (Uncommon) Neurolo’ sympt’ except dizzi’.
o  Cardiopulmon’ Phase (24-48 hours): initiated by dyspnea, dry cough, circulato’ collapse; (Uncommon) Oliguric renal fail’ (Acut’ Tubul’ Necros’).
75% Px w/ Pulmonary edema need mechanical ventilat’.
Resolution phase: +++ diuresis.
o  Convalescent Phase: Rapid improv’.
o  Minimal chronic sequel.
· Hantavirus CardioPulmonary Syndrome (HCPS)
() Quick severity progress’.
o  Incubation (± 3 weeks)
o  (+++ Common, Prodrome, usu’ severe) Fever for 3-10 days + chill, myalgia à likely correlate to viral dissemination.
o  (Other Prodrome) Common: nausea, emesis, malaise, dizzi’, Dyspnea, cough (usu’ dry), headache, abdominalgia, diarrhea.
o  If Andes Virus HCPS: Presentat’: facial flush’, fine petechia, & conjunctivit’.
o  (-): rhinorrh’, pharyngit’, otalgia, (except Andes virus) conjunctivit' or coryza.
o  (Common) Dry cough –(common, + immune response)à Cardiopulmonary Phase (2-7 days):
§ Presentat’: sudden repsirat’ distress, usu’ CardioVascul’ collapse @ hours of hospital arrival.
§ Correlat’ w/ massive capillary leak’ into pulmon’ vascul’ bed.
§ (Precipitat): Pulmon’ edema, bronchorrhea, shock, (sometimes) coagulopathy (Andes Virus) & preterminal arrhythm’.
o  Cardiopulmon’ Fail’: ± 5 days since onset.
(Figure right below) Clinical Progress’ of HCPS.

o  (@ Survivor) Recovery time usu’ w/ Diuretic period ≈ Decline time
o  (@ Convalesc’ period) Usu’ Px recover ≤ little residual effect (several months of fatig’ & ↓ed exerc’ toleran’ usu’ the only sequel).
o  (Help Early Diagnosis) is rodent exposure (+)?
· Pediatric Hantavirus Pulmonary Syndrome
o  (+) @ post-incubation (which ± 2 weeks)
o  Peridomestic’ exposure (69% cases)
o  Peridomestic’ & Occupational Exposure (19% cases)
o  Peridomestic’ & Recreational Exposure (9% cases)
o  Occupational Exposure (4% cases)
o  Entering & or Cleaning rodent-infested structure (9% cases)
o  (Prodrome) Fever, +++ myalgia of large muscles (especial’ @ thigh & lumbar)
o  ~ Cough, Abdomin’ discomfort, & GI disturbance.
o  (Frequent) dizzi’.
o  ~ (-) URTInfection signs s.as: rhinorrhe, & pharyngitis.
o  1-10 days later: (+) Respiratory sympt’ usu’: modest cough & dyspnea.
Rapid worsen’ à Hospitaliz’ indicated.
· Hemorrhag’ Fever w/ Renal Fail’ Syndr’ (HFRS)
o  (Characteris’) Triad (Fever, hemorrhage, & renal insuffici’); & (if +++) hypovolem’ shock. Other common sympt’ @ initial phase of ill’: headache, myalg’, abdnominal’ & back pain, nausea, emesis, & diarrhea. Other sympt’: chills, dizzi’, ↑ed thirst, costovertebr’ tenderness, & flank pain. Ill’: mild - +++.
o  Incub period 4-42 days (± 12-16 days). Subclinic’ infec’ common @ child’.
o  Reported: (+) relation to acute pancreatit’ @ adult ♂; HFRS due to Dobrava virus @ 25y.old ♂ Px, w/ orchitis (atypic’ presentat’).
o  5 Progress’ stages: febrile, hypotensive, oliguric, diuretic, & convalsesc’ (Px can completely skip stages). 1/3 cases have typic’ clinical course.
v Physic’ Exam’
() Vary accord’ to ill’ stage @ presentat’.
· Hantavirus Pulmonary Syndrome
o  (80-90% cases) Fever, tachypnea, rales, & tachy♥.
o  (1/3 presentations) Hypotension.
o  (Uncommon) Rash.
· Hantavirus CardioPulmonary Syndrome
o  Most Px: Tachypnea, Fever, & Tachy♥.
Breath sound @ Lung exam’: Crackles, or ↓ed.
o  (10% cases) Abdomin’ tenderness ~ severe.
HCPS recognized post-laparotomy @ 1 patient.
o  Ø Petechia (but Andes Virus HCPS common' (+) petechia)despite thrombocytopenia.
o  Hallmarks include: Hypotens’, & Respirat’ Distress w/ bilat’ alveol’ infiltra’ @ Radiograph.
· Pediatric Hantavirus Pulmonary Syndrome
o  Rapid onset of Pulmon’ Edema, then respirat.shock, & cardiogen.shock.
o  (Early) ~ unreveal’, but:
(General) Fever (+).
~ Tachy♥.
(Common) Tachypnea.
o  (If (+++)): Ill appearan’ + (+++) ventilato.insufficien’.
· HFRS
o  Febrile stage (@ all Px, for 3-7 days). Characteris’: abrupt fever (range: ± 40OC) onset.
§ Px ~ complain: headache, chills, abdominalg’, malaise, blur’ vision, & lumbalg’.
§ ~ (+): Flushing of face, neck, & chest due to probable vascul’ dysregulation; petechia @ axila & soft palate; absolute brady♥.
§ (1/3 cases) Subconjunctiv’ hemorrhag.
§ ~ (+) mild’ ↑ed HCT due to hemoconcentration. Leukocytosis w/ atypic’ lymphocyt’. Characteris’: Thrombocytopen’ (also defines progn’ & severity of renal fail’).
§ Observable onset of proteinuria (transient & usu’ resolves w/in 2 weeks if proteinuria’s due to Hantavirus nephritis) & microhematuria.
o  Hypotens’ Stage (occurs @ 11% cases & coincides w/ defervescen’), for few hours – 2 days. Characteris’: hypotens’ & renal fail’.
§ ~ (+): tachy♥ (~ presages shock); acute abdomen due to paralytic ileus; convulsions or purposeless moves; (coagulation profile) prolong’ of bleed’ time, PTime, aPTT.
o  Oliguric Stage (65% cases), for 3-6 days.
§ Acute Kidney Injury, characteris’: oliguria, hypotens’; bleed’ tendency (due to uremia); & edema. BUN & serum creatinine’re @ peak. Usu’ + thrombocytopenia’s resoluti’.
§ ~ (+) pulmon’ edema.
o  Diuretic Stage, for 2-3 weeks.
§ (+) Diuresis (range: 3-6L/day) after previous’s stage’s sympt’ disappear. ↓ed collecting duct’s responsive’ to vasopressin.
§ If inadequate fluid replacem’: (+) rapid signs of dehydration @ +++ shock. Should monitor Px’s volume status closely.
o  Convalesc’ Stage, ~ for 3-6 months.
§ Clinic’ recovery usu’ starts @ mid' of week 2 + gradual resoluti’ of sympt’ & azotem’.
§ Renal tubules’s concentrating capacity recovers over many months.
§ ~: still (+) fatig’, intention tremor, & complain oft’ of myalgia. (+) weight gain.
v Causes
· Hantavirus Pulmonary Syndrome (HPS)
o  Etio of Most HPS in U.States, thought to be SNVirus.
· Hantavirus CardioPulmonary Syndrome
o  In U.States, HCPS main etio’: Sin Nombre Virus (via inhalat’ of aerosol’ virus from rodent’s dried excreta, vector: Deer Mouse (persistent shedder, no obvious harm)).
o  Incidence’s parallel w/ infected rodent’s epidemio’.
o  Storm à wet and mild condition à ↑ some food sources for deer mice à ↑ deer mice.
o  (Infected) rodent aggressivity à rodent density ↑ horizontal inter-rodent viral transmis’.
· Pediatric Hantavirus Pulmonary Syndrome
o  Human Infection’s thought to involve: inhalat’ of concentrat’, aerosol’ excreta & salive of chronic’ infected rodent; infected rodent bite; Ingest thing that’s contaminated by the agent.
o  (Evidence) (@ U.States) HPS virus Ø spread person-person; but Andes virus (@ South Argentina).
· HFRS
o  Severity of ill’ depends on virus’s type (also affect form of ill’), & geograph’ distribution. Hantaviruses related to HFRS inter alia: Hantaan virus (HNTV), Dobrava/Belgrade Virus (DOBV), Seoul Virus (SEOV), Puumala Virus (PUUV), & Saaremaa Virus (SAAV), while HPS’s etio’ are: SNV & related viruses.
o  Korean Hemorrhagic Fever, severe HFRS @ Asia, etio’: Hantavirus, transmitted by infected A agrarius (striped field mouse).
o  Balkan Hemorrhagic Fever, severe HFRS @ Balkan countries, etio: DOBV, transmitted by infected A flavicollis mouse (yellow-necked field mouse).
o  Mild-moderate HFRS, etio’: SEOV, transmitted by infected Rattus rattus (black rat) or Rattus novergicus (urban rat).
o  Nephropathiepidemica, mild HFRS @ Europe, etio’: PUUV, transmitted by infected Clethrionomys glariolus (Europan bank vole).
o  Virus’s usu’ transmitted via inhalat’ infected animal excreta (ie: urine, feces, saliva); ~ also via rodent bites; (23 May 2014) no reported interhuman transmiss’. Epidemiol’ links viral exposu’ to activiti’ s.as: heavy farm work, low socioeconomic status, military exercises, ground-sleeping, & threshing.
v Differen’ Diagnos’
· Hantavirus Pulmonary Syndrome
o  Drug-Induced Non♥ Pulmon’ Edema.
o  Group 1 (>10 cases):
Ethchlorvynol
Narcotics: Heroin, Propoxyphene, Methadone, Naloxone.
Tocolytics: Bitodrine, Isoxsupnne, Salbutamol, Terbutaline.
Salicylate
Hydrochlorothiazide
Protamine
Recombinant interleukin 2
o  Group 2 (5-10 cases)
Cyclosporine
Tricyclic antidepressants
Amiodarone
Vinca alkaloids and mitomycin
Bleomycin
Cytarabine (cytosine arabinoside)
o  Group 3 (controversial areas)
Amphotericin and granulocyte infusions
Insulin and diabetic ketoacidosis
o  Group 4 (<5 cases)
Streptokinase
Trimethoprim-suffamethoxazole
Flurazepam
Lidocaine
Sclerotherapy
Nitroprusside
Intrathecal methotrexate
() (Ø @ HPS) @ ♥ Pulmon’ Edema: usu’ L.ventricul’ S3 gallop rhythm, & cardiomega’.
o  Acute Respirat’ Distre’ Syndr’
o  (+) @ HPS, (-) @ ARDS: On Radiograph: centr’ infiltrate distributi’, (-) pleural effusion; On, Radiograph, Characteris’: earlier appear’ of interstit’ edema (Kerley B lines), pericard’ haziness, & perihilar cuffing.
o  Pneumonic Plague
o  (-) @ HPS, (+) @ Pneumonic Plague: critical’ ill (@ HPS: less ill), adenopathy suggesting pre- or concomit’ Pneumonic Plague, & hemoptys’.
o  Atypic’ community-acquired Pneumon’
o  (Zoonotic): Legionaires Disease: ~ resemble HPS: @ mild’ ↑ed serum transaminase, ~ GI sympt’, (unusual) +++ renal insuffic’.
o  Differ: @ HPS: frequent’ cardiopulmon’ collapse (seldom @ Legionaires Disease but in terminal stage), (-) relative brady♥.
o   (Non Zoonot’): Tularemia & Q Fever, similari’ w/ HPS: headache, myalgia.
o  @ Q Fever: usu’ antecedent: contact w/ sheep or parturient cat; (-) @ HPS: splenomega’, relative brady♥.
o  @ Tularemia: usu’ antecedent: contact w/ deer, rabbit, or deer flies; (-) @ HPS: Bilateral hilar adenopathy, & bloody pleural effus’.
o  Influenza
o  (+) @ HPS: headache, & myalgia; (-) @ HPS: dry cough & sore throat, usu’ + rhinorrhea.
· Hantavirus CardioPulmonary Syndrome
o  Acute Respiratory Distress Syndrome
o  Anthrax
o  Bacterial Pneumonia
o  CBRNE - Plague
o  Leptospirosis in Humans
o  Phosphine toxicity
o  Pneumonia in Immunocompromised Patients
o  Pneumonia, Mycoplasma
o  Pneumonic plague
o  Q Fever
o  Rapid Testing for HIV
o  Salicylate toxicity with pulmonary edema
o  Septic Shock
o  Severe Dengue Infection
o  Shock, Cardiogenic
o  Toxicity, Phosgene Influenza
o  Tularemia
o  Viral Pneumonia.
· Pediatric Hantavirus Pulmonary Syndrome
o  Leptospirosis
o  Meningococcal Infections
o  Neonatal Sepsis
o  Pediatric Plague
o  Rickettsial Infection
o  Tularemia
· HFRS
o  Spotted fevers
o  Murine typhus
o  Malaria
o  Non-A, non-B hepatitis
o  Colorado tick fever
o  Septicemia
o  Heat stroke
o  Disseminated intravascular coagulation (DIC)
o  Leptospirosis
o  Scrub typhus
o  Hemolytic uremic syndrome
o  Acute kidney injury
o  Acute abdominal diseases
o  Acute Poststreptococcal Glomerulonephritis
v Workup
· Hantavirus Pulmonary Syndrome
o  Lab’ Studies
§ Usu’ (+) left-shift leukocytosis w/ left-shift (if + atypic’ lymphocytosis à very suggesti’ for Hantavirus infec’), thrombocytopenia, & ↑ed Hematocrit due to hemoconcentration.
§ (Common) (+) atypic’ lymphocyt’ @ peripher’ smear.
§ If (+) Immunoblasts à HPS diagn’.
§ Mild’ ↑ed liver transaminases. Marked’ ↑ed serum LDH.
§ (Most Px w/ normal fibrinogen’s level) mild’ ↑ed activated partial thromboplastin time (if fibrinogen concentration begins to fall à sign of DIC).
§ (Uncommon) ↑↑↑ed BUN & serum creatinine. (50% cases) (+) proteinuria (Ø as severe as @ Hemorrhagic Fever with Renal Fail’ Syndr’ (HFRS)).
§ Low serum bicarbonate reflects degree of acidosis.
§ (Most cases) ↓ed serum albumin, representi’ acute phase reactant that ~ observed @ many types of infec’. +++ hypoalbuminemia @ previously healthy Px  + acute onset of respirat’ distress à should suggest HPS.
§ Lactic acidoses + rapid respirat’ deterioration à usu’ indicate death w/in 1-2 days.
§ (50% cases) ↑ed serum creatinine kinase.
§ Tissue culture Hantavirus isolation Ø clinical’ availab’ due to biosafe’ issues @ technical difficulties.
§ Specific diagn’ ~ via serolo’, PCR, & immunohistochemist’ (IHC) studies.
o  PCR can help detect viral RNA in blood & tissues.
o  IHC can help detect viral RNA in formalin-fixed tissues w/ specific antibodies.
o  (Most common) HPS is confirmed by Hantavirus IgM- and IgG-specific sero’ results, usu’ measured by doing ELISA.
(1st 1/3 cases) (+) ↑ed IgM titer @ clinical presentat’; (2nd 1/3 cases) ↑ed titers ofIgM & IgG to Hantavirus @ presentat’; (3rd 1/3 cases) ↑ed IgG titer (Ø IgM’s) @ convalescent.
o  Imaging studies
§ Chest Radiography typic’ (+) non♥ pulmon’ edema’s pattern:
o  sillhouet’ Ø enlarged.
o  (Characteris’) Perihilar haziness (shaggy ♥ sign).
o  (Virtual’) All Px (+) interstiti’ edema due to pulmon’ capillary leak which manifest radiolo’ as peribronchial cuffing or Kerley B lines.
o  Other tests
§ Arterial blood gas evaluati’ ~ reveal respirat’ fail’-relat’ hypoxem’. Px’s concurr’ hypocapn’ confirms that gas exchange (Ø ventilation) probl’ causes respirat’ distress.
§ Normal pulmon’ wedge pressu’; ↓ed ♥ index (CI); ↑ed system’ vascul’ resistan’ (SVR).
o  Histolo’ Find’
§ (Of Lung) (+) capillarit’ & or pulmon’ capillary leak syndr’ w/o hemorrhage.
§ (if (+) +++ & or prolong’ hypotens’) ren ~ (+) ATNecrosis histolo’ find’.
· HCPS
o  Lab’ Studies
§ Results vary w/ phase of ill’.
§ CBCount (most useful) should (+) @ arrival and 24 hours after: ~ normal or slight’ low PC @ prodromal phase.
§ PCount (initial’) ~ normal. (98% cases) present w/ PC < 150 x 109/L. Dramatic fall on PC sometimes heralds HCPS’s ♥pulmon’ phase).
§ On (+) Leukocytosis or (occasional’) leukopenia. Severe clinical course’s predictable by (+) WBC ≥ 90,000/μL & (+) immunoblasts.
(Figure right below) HCPS’s immunoblast.

§ Diagn’ Triad: Low PC; left-shift @ peripher’ smear; & immunoblast count > 10% of total lymphoid series. If there’re relative’ many HCPS w/ (+) Diagn’ Triad à prepare Px for aggresive critical Tx & possibly ECMOxygenation.
§ On HCT: Hemoconcentration due to massive capillary leak & presages bad progn’. (50% cases, sign of severe ill’) HCT > 50% @ ♂, & > 48% @ ♀: ~ (+) @ ♥pulmon’ phase.
§ AST, ALT, & LDH ‘re oft’ ↑ed (can be 2-5x normal values), sometimes as early as prodromal phase.
§ SNVirus rarely (+) ↑ed CPKinase level & (+) renal fail’ (known via serum creatinine); unlike Black Creek Canal, Bayou, & Andes hantaviruses.
§ PTime & activated partial thromboplastin time (aPPT) are usu’ normal in SNV. Few DIC cases’re associat’ w/ HCPS.
§ On arterial blood gases (ABGs): progress’ metabol’ acidos’ & +++ hypoxem’ mark ♥pulmon’ phase.
§ Reported: Lactate as high as 9.5mg/dL @ severe HCPS. Lactate level > 4mg/dL is related to high death rate).
§ Serolo’ tests
§ (@ onset of sympt’) Px has uniform’ (+) antiviral IgM (most’ + IgG). (+) IgM or 4x ↑ in serum IgG disting’ acute infec’ from past expos’.
§ S.as: Western blot assay & (dipstick-type test, 100% sensitivity for SNV antibodies @ clinical phase of ill’) RIBAs (most common), ELISA, indirect immunofluoresc’, CFixation, among others.
§ Viral RNA’s also detectable by RT-PCR. Only @ early stage: possible fulminant infec’-causing Hantavirus RNA detect’ by PCR.
§ Postmorem tests can be via IHC for N-atigens.
o  Imaging Studies
§ Radiography
§ Oft’ normal @ presentat’; (1/3 cases, @ presentat’) (+) evidence of pulmon’ edema. (Virtual’, w/in 48 hours) All Px demonstrate edema & --(2/3 cases)à +++ bilateral airspace disease.
(Figure right below) ♥Pulmon’ phase + characteris’ radiol’ evolution.

§ Mild interstiti’ pulmon’ edema à +++ bilateral alveolar edema in basilar or perihilar pattern.
§ (Common) Pleural effus’.
§ Normal ♥ size (barring concomit’ ♥ ill’).
§ Echo♥graphy
§ (Occasional’) useful to disting’ ♥genic pulmon’ edema from Ø♥genic edema typical’ seen @ HCPS
§ Global ♥ dysfunc’ (+) @ HCPS’s later stages.
o  Procedures
§ Flow-directed pulmon’ artery catheterization (PAC), or Swan-Ganz catheter can be useful tool to aid resuscitative fluid Tx of HCPS (can also offer valuable diagn’ & progn’ info). Low pulmon’ occlusion pressu’ (pulmon’ capillary leak-consistent) & low CI characterize early HCPS.
§ Advanced HCPS: +++ ↓ed CI; & increased SVResistance.
§ CI < 2L/min/m2 (a marker to predict 100% death w/o further intervention) has been successful’ criteria to start rescue ECMO Tx.
· Pediatric HPS
o  Lab’ Studies
§ Needs high suspicion’s index, suspect @ +++ respirat’ sympt’ w/ history of rural/wildern’ travel or rodent expos’.HCPS prodrome: fever, cough, myalg’, chills, & nausea, then a rapid worsen’ respirat’ phase. Presumpt’ diagn’ can be make based on (+) pulmon’ interstiti’ edema on chest radiograph related to leukocytosis, thrombocytopen’, & hemoconcentration.
§ Lab results w/ diagn’ value:
§ Tetrad (sensitive & specific early clue; if + rapid onset of respirat’ insuffici’ à should suggest diagn’):
o  Thrombocytopen’ (notable early in ill’).
o  (+) (oft’ w/ Left-shift Leukocytosis).
o  abnormal lymphocyt’ & immunoblasts (+) @ peripher’ blood smear.
o  (+) ↑ed HCT (due to fluid ultrafiltrat’ into lungs).
§ (+) Prolonged aPTT.
§ ~ (+) mild’ ↑ed AST & LDH.
§ ABGases shows desaturat’.
§ Serolo’ is useful @ Hantavirus diagn’: Most Px (+) IgM & IgG ELISA @ hospital admission.
§ PCR can detect Hantavirus in tissue. IHC stain can reveals Hantaviral antigen in tissue.
o  Imaging Studies
§ (@ Early in ill’) Chest radiograph usu’ shows peribronchial cuffing & Kerley B lines.
§ @ Px w/ full-blown HPS: (+) Rapid progress’ of bilateral interstiti’ & alveol infiltrates.
o  Procedures
§ (General, @ +++ HPS Px) PAC: ↓ed stroke volume index (SVI), & CI ≤ low-normal.
§ ↑ed Pulmonary Vascular Resistan’ Index.
§ ↑ed SVR + failed volume replacement for ↓ed CI’s & SVI’s correction: disting’ HPS from septic shock.
o  Histo’ Find’
§ Unlike ARDS due to other etio’: Ø marked necrosis, PMN WBC infiltrat’, pneumocyt’ II hyperplas’, or dense hyalinization.
§ EMicroscopy of lung tissue: intact & somewhat swollen vascul’ endotheliu; inflammato’ cell infiltrat’ @ capillari’, interstiti’, & alveoli; endotheliocytes’s cystoplasm’s viral inclusions; Ø necrosis or structural cellu’ defect responsible for capillary leak.
§ Other tissue: ~ (+) immunoblasts infiltrat’, s.as @: lymph nodes, spleen, liver, other organs’s blood vessels.
(Figure right below, Light Microscopy) HPS’s histopatho’: (+) interstiti’ & alveol’ edema, alveol' hemorrhag’, & MNuclear interstiti’ pneumonit’ composed of macrophag’ (= MΦ) & T lymphocyt’. Courtesy of the Centers for Disease Control and Prevention. 

· HFRS
o  Lab’ Studies
§ HFRS’s geograph’ distribution, rodent exposu’ history, clinical picture, & lab data suggests the diagn’.
§ ELISA to detect antihantaviral-specific IgM early in ill’.
§ ↑ed Antihantaviral IgG titer ~ prolong’ (as long as 10 years).
§ Blood find’ usu’ show clinical’ signific’ leukocytosis; HCT ≥ normal; & thrombocytopen’.
§ Can be (+) ↑ed liver enzymes, BUN, & serum creatinine.
§ ~ (+) Hyponatremia, hyperphosphatemia & hyperkalemia @ oliguric stage.
§ Complement C3 ~ ↓ed à HFRS is also DDx of hypocomplementic acute nephritic syndr’.
§ Coagulation profile ~ altered w/ prolonga’ of PT, aPTT, or bleed’ time; & ↑ed fibrin-degradation products’s levels.
§ Urinalysis consistent’ shows hematuria, & (~ last for years after attack) proteinuria.
§ ↑ed Nitric Oxide (NO) level @ HFRS’s acute phase is correlated to disease’s activity.
§ If (+) ↑ed serum amylase & lipase + severe abdominalg’ à suggests acute pancreatit’ (confirmab’ by CT scan: (+) edema of pancreas & peripancreatic tissues).
o  Imaging Studies
§ @ Kidney: T1-weight’ MRI of kidney shows well-defined zone of low-signal intensity (blood product’s deposition) @ (33% cases) subcortic’ medul’; MRI T2-weight’ images correlated w/ HFRS’s renal histopathol’ find’.
§ (Characteris’) On T2- & T1-weight’ MRI of ren show (+) corticomedullary differentiation à disting’ HFRS from another etio’ of acute renal injury.
§ @ ØHFRS etio’ of acute renal injury: cortical blood product deposition causes ↓ed corticomedullary differentiation on T1-weighted MRI & enhanced corticomedullary margin on T2-weighted MRI.
§ (< 1% cases) (+) Intracranial hemorrhage. Hemorrhage & necrosis of adenohypophysis (common @ fatal HFRS) –(if survive)à ~ (+) panhypopituitarism.
§ Abdomin’ Radiograph: ~ (+): (74% cases) ascites; (69% cases) paralytic ileus + intestinal wall thicken’; retroperitoneal edema (obscured psoas shadow (68% cases) & obscured renal shadow (53% cases)); & renal enlarg’ (23% cases). @ Px w/ pulmon’ involvem’: Chest Radiograph: interstiti’ edema (14-44% cases); subsegmental atelectasis (38% cases); pleural effus’ (6-32% cases); & ♥mega’ (6-21% cases).
o  Other tests
§ Ren biopsy (Øessenti’ for Dx), indicated if Dx’s unclear & Px’s status of hemodynamic & coagulation’s stable.
o  Histolo’ Find’
§ Features of acute interstiti’ nephrit’, s.as: acute tubular necrosis w/ evident glomerul’ & endothel’ damage. Hemorrhag’ necrosis’s been reported (+) in renal medulla. Hemorrhage (+) @ different organs, espec’: ♥’s R.atrium; adenohypophysis; pancreas; & skin.
§ ~ (+) pulmon’ infiltrat’; & (occasional’) (+) pulmon’ edema. Atypic’ MN cells’s infiltrat’ in spleen, lymph node, & liver portal triad’s been reported.

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