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.
Reference: