Monday, August 3, 2015

Respiratory Syncytial Virus

Chapter 1 – Respiratory Syncytial Virus (RSV)
v History & Physic’ Exam
o  ~ present w/: fever (typic’ low grade); cough; tachypn’; cyanos’; retracti’; wheezi’; rales; & sepsislike presentati’ or apneic episodes (in very young infants).
o  In infant, RSV can cause variety of ill’, presenti’ w/ cold-like ill’, sometimes (+) fever (can also (+) bronchit’, croup, & LRTI s.as (25-40% cases) (+) bronchiolit’ & pneumon').
o  Infant w/ LRTI typic’ (+) runny nose, ↓ed appetite before (+) other sympt’, cough usu’ (+) at 1-3 days later, then ~ (+) sneezi’, fever, & wheezi’. In very young infant, ~ only (+) irritabil’, ↓ed activi’, & apnea.
o  Phys’ exam’ of infant w/ RSV Lower Respiratory Tract Infection (LRTI) (+) evidence of diffus’ small airway ill’. 40% cases in child’, + related otitis media (~ viral & or bacterial). Hydrati’ status assessm’ (eg: via skin turgor, capillary refill, & mucous membran’) is importa’ at infant w/ bronchiolit’.
o  In adults (particular’ (+) at healthcare workers & caretakers of small child’), usu’ lasts < 5 days usu’ w/ Upper RTI (URTI)-consistent sympt’ (can include rhinorrhea, pharyngit’, cough, headache, fatig’, & fever), but at high-risk Px (immunosupressed or (+) certain chronic ill’) ~ (+) more +++ sympt’ (LRTI-consistent) s.as pneumon’.
v Complicati’
o  InPx RSV LRTI infant has higher risk (~ lasts > 10 years) for subseq’ wheezi’ & abnorm’ pulmon’ funct’.
v DDx
o  High risk of for +++ RSV infec’, in:
o  Prematu’ infant in 1st year of life (younger child at RSV season, the higher risk).
o  Infant w/ chronic lung ill’ (eg: bronchopulmon’ dysplas’, or cystic fibrosis) during 1st 2 years of life.
o  Child w/ hemodynamical’ signific’ congeni’ ♥ ill’, espec’ w/ ↑ed pulmon’ blood flow.
o  Immunodefici’ Px.
o  Child’ w/ metabol’ disord’, structur’ airway abnorm’, & neuromuscul’ disord’.
o  Children of multiple births ( ≥ triplets).
o  Adenoviruses
o  Asthma
o  Bronchiolitis
o  Croup
o  Human Metapneumovirus
o  Influenza
o  Neonatal Sepsis
o  Other respiratory viruses
o  Parainfluenza Virus
o  Pediatric Bronchitis
o  Pediatric Pneumonia
v Workup
o  Lab studies
§  General’ Ø indicated @ in infant w/ bronchiolit’ who is comfortab’ in room air, well-hydrated, & feeding adequate’.
§  Øspecific lab studies: CBC (~ (+) normal or mild’ ↑ed WBC count & ↑ed % of band forms); blood culture (frequent’ obtained, rare’ (+) pathogen’ bacter’); Arterial Blood Gas (~ indicated if (+) concerni’ CO2 retenti’); serum electrolyte concentrati’; urinalysis; O2 saturati’ measurem’.
§  Specific lab studies (~ indicated for deciding of Tx (eg: withdrawi’ unnecessary antibiot’) needs of Px isolation, education for parents & staff) to confirm RSV infec’ are readi’ availab’ & performab’ on sample of secretion ((for virus) culture, antigen-reveali’ technic, or PCR) taken by washi’, suctioni’, or swabbi’ the nasopharynx (molecular probes to detect RSV at clinic’ specimen ~ more sensitive).
§  General’, Antigen-detecti’ & culture technic’re reliab’ in young child, less useful in older child & adults.
§  RT-PCR should be considered, espec’ toward older children & adult Pxs because their respirat’ specimens ~’ve low viral loads.
§  Antigen-detecti’ technic ~ (+) Dx w/in hours & obtained reliably w/o sophisticated virolo’ Lab. (Critical) Test performa’ monitoring to maintain appropriate sensitivity & specificity.
o  Chest Radiography
§  Frequent’ obtained at child +++ RSV infec’. Typic’ (+) hyperinflated lung fields w/ diffuse ↑ in interstiti’ markings. 20-25% cases, (+) areas of atelectasis or pulmon’ infiltrates. General’, not specific & not course-predictive except if infant w/ addition’ find’ of atelectasis or pneumon’ (~ (+) +++ course).
o  Histolo’ Find’
§  (In infant whose died of RSV bronchiolit’) (+) MN cell & neutrophil infiltrati’ of peribronchiol’ areas, necrosis of small airway epitheli’, plugging of lumens w/ exudat’ & edema, & atelectasis & hyperinflati’.

Croup

Chapter 1 – Croup
v History
o  Usu’ starts w/ Øspecific respirat’ sympt’: rhinorrhea, sore throat, cough. General’ fever is low grade (38-39OC), can > 40OC. W/in 1-2 days, (oft’ sudden’) (+) characteris’ hoarseness, barking cough, & inspirat’ stridor, along w/ variab’ degree of respirat’ distress. Perception: sympt’ worsen at night. Sympt’ typic’ resolve w/in 3-7 days, but can last for 2 weeks.
o  Spasmod’ (recurr’) croup typic’ presents @ night w/ sudden onset of barking cough & stridor. Child ~’ve had mild upper resiprat’ complaints prior to this, but more oft’ has presented well prior to sympt’ onset. Allergic factors ~ cause recurr’ croup due to respirat’ epithel’ changes from viral infec’.
o  Recurr’ croup child’ report’ sympt’ relief when treated for gastroesophag’ reflux (GER).
v Physic’ Exam’
o  Wide varia’ of physic’ present’. Most child’ only (+) barki’ cough & hoarse cry. Some ~ (+) stridor only @ activi’ or agitation, others’ve audib’ stridor at rest & clinical’ evident respirat’ distress. +++ly affected child’ ~ (+) quiet stridor due to bigger degree of airway obstruction. @ Child’, typic’ Ø appear toxic.
o  Child’s sympt can range from minim’ inspirat’ stridor to +++ respirat’ fail’ due to airway obstruction. If mild, resti’ respirat’ sound is normal; mild expirat’ wheezi’ ~ heard. If more +++, (+) inspirat’ & expirat’ stridor at rest w/ visib’ suprastern’, inter- & sub-cost’ retract’. Air entry ~ poor. Lethargy & agitat’ due to marked respirat’ diffcul’ à hypoxem’ & ↑ed hypercarbia. During episode of +++ cough, ~ (+) sudden respirat’ arrest.
o  Other respirat’ distress’s warni’ signs: tachypn’, tachy♥, out of proportion to fever, & hypotonia. If child’ w/o adequate oral intake, (+) dehydration. Cyanosis, late, ominous sign.
o  Scori’ syst’
· Westley Score (wide use @ research & Tx protocol’s evaluati’, its clinic’ value Ø yet extensive’ studied): Inspirat’ stridor: (-) – 0, at agitat’ – 1, at rest – 2; Retracti’: (-) – 0, mild – 1, moderate – 2, +++ - 3; Air entry: normal – 0, mild ↓ - 1, heavy ↓ - 2; Cyanosis: (-) – 0, at agitat’ – 4, at rest – 5, Conscious’: normal, includi’ sleep – 0, depressed – 5.
< 3: mild ill’. 3-6: moderate ill’. > 6: +++ ill’.
· Mild: (+) occasional barki’ cough, no stridor at rest, mild or no suprastern’ or subcost’ retracti’. Moderate: frequent cough, audib’ stridor at rest, visib’ retracti, little distress or agitat’. +++: frequent cough, +++ inspirat’ (occasional’ + expirat’) stridor, conspicu’ retracti’, ↓ed air entry on auscult’, +++ distress & agitat’. Lethargy, cyanos’, & ↓ing retracti’ presage respirat’ fail’.
· Alberta Clinical Practice Guideline Working Group classifi’:
o  Mild: occasion’ barki’ cough, no audib’ stridor at rest, & no or mild suprastern’ & or intercost’ retracti’.
o  Moderate: frequent barki’ cough, easi’ audib’ stridor at rest, suprastern’ & stern’ wall retracti’ at rest, & no or minim’ agitat’.
o  +++: frequent barki’ cough, +++ inspirat’ (occasion’ + expirat’) stridor, +++ stern’ wall retracti’, & +++ agitat’ & distress.
o  Impendi’ respirat’ fail’: barki’ cough (oft’ Ø +++), audib’ stridor @ rest, stern’ wall retracti’ ~ Ø +++, lethargy & ↓ed conscious’, & oft’ dusky appear’ w/o supplemental O2 support.
· Tx based on algorithm based on Px’s initial symptoms’s severity.
v DDx
o  Spasmodic croup (recurrent croup)
o  Retropharyngeal abscess
o  Subglottic stenosis
o  Angioedema
o  Allergic reaction
o  Tracheomalacia
o  Laryngeal web
o  Laryngeal papillomatosis
o  Laryngeal hemangioma
o  Subglottic hemangioma
o  Vocal cord paralysis
o  Uvulitis
o  Innominate artery compression
o  Right aortic arch vascular ring
o  Double aortic arch
o  Aberrant subclavian artery
o  Pulmonary artery sling
o  Rarer etiologies in the pediatric population - Laryngeal tuberculosis, neoplasm (compressing trachea), sarcoidosis, Wegener granulomatosis
o  Gastroesophageal reflux (diagnostic consideration for recurrent croup)
o  Bacterial Tracheitis
o  Inhalation Injury
o  Laryngeal Fractures
o  Laryngomalacia
o  Measles
o  Pediatric Airway Foreign Body
o  Pediatric Diphtheria
o  Pediatric Epiglottitis
o  Pediatric Mononucleosis and Epstein-Barr Virus Infection
o  Pediatric Peritonsillar Abscess
v Workup
o  Prmari’ a clinic’ Dx. CBC usu’ Øspecific, WBC ~ suggest viral etio’ w/ lymphocytosis. Specific viral etio’ identification (eg: parainfluenza virus serotype, respiratory syncytial virus (RSV)) via nasal washi’ ~ for determini’ isolation needs in hospital setting, or (in influenza A) antiviral Tx initiati’.
o  Pulse O2metry, most’ normal, used to monitor need for supplement’ O2 support or worsen’ respirat’ comprom’ as evident w/ tachypn’ & poor mainten’ of O2 saturation. ABG is standard’ unnecessary & Ø reveal hypoO2 or hypercarbia unless respirat’ fatig’ ensues.
o  If Px presentat’ w/ fever, tachypn’, & history of ↓ed fluid intake à evaluate Px’s hydration status! Compromised oral intake & inabili’ to mainta’ needed fluid volume ~ need IV fluid support to sustain Px’s fluid needs.
o  Laryngoscopy: indicated only in unusu’ setting (eg: atypic’ course of ill’, child (+) sympt’ suggesti’ underly’ congeni’ or anatomi’ disord’, child (+) bacterial tracheit’ (to get culture to guide antibiot’ Tx)); if throat (+) tongue depression, no epiglottit’ (which (+) erythem’ enlarg’ epiglottis (cherry red epiglott’). Thought that vigor’ exam’ of child’s throat cause laryngospasm & respirat’, but never has been documented.
o  ~ be indicated: direct laryngoscopy if child Ø at acute distress; fiberoptic laryngoscopy; bronchoscopy (for recurr’ croup to rule out airway ill’).
o  (+) High risk of moderate to +++ find’ in laryngo & bronchoscopy & need of further surgic’ interventi’ @ child w/: (1) w/o history of intubati’ but (+) inPx consulta’, or (2) w/ history of intubati’ & age < 36 months.
o  Radiography
§ Plain film can verify presump’ Dx or exclude other stridor-causing ill’. Lateral neck radiog’ can help detect clinical Dx s.as aspirated or esophage’ foreign bodi’, congeni’ subglott’ stenos’, epiglottit’, retropharyng’ absce’, or bacterial tracheit’ (thicken’ trach’). Ø needed @ uncomplica’.
§ ~ (-) at 50% cases @ child.
Anteroposterior (AP) radiog’ of neck’s soft tissues classic’ (+) steeple sign (pencil-point sign), signifies subglott’ narrowi’; lateral neck view ~ (+) distended hypopharynx (ballooni’) at inspirati’.
§ Steeple sign ~ also (+) w/o croup @ epiglottit’, therm’ injury, angioedema, or bacterial tracheit’. Monitor during imaging because progress’ of airway obstruction ~ rapid.
(Figure right below) Croup at child. Steeple sign at proximal trachea evident. AP view.


(Figure right below) Steeple sign on radiog’.

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Saturday, August 1, 2015

Acute Kidney Injury

Chapter 1 – Acute Kidney Injury (AKI)
v History
o  AKI can (+) sympt’ of  chronic kidney disease (CKD) but for shorter time: fatig’, ↓ed weight, anorex’, noctur’, sleep disturban’, & pruritus.
o  (Important) (+) history of etio’ factors: Volume restrict’ (eg: low fluid intake, gastroenterit’); Nephrotoxic drugs; Trauma or unaccustomed exertion; Blood loss or transfusions; Toxic agent exposure, eg: ethanol, & ethylene glycol; Exposure to mercury vapors, lead, cadmium, or other heavy metals which are encounterable in welders & miners.
o  Higher risk of AKI if (+): Hypertensi’; Congesti’ ♥ Fail’(CHF); Diabetes; Multiple Myeloma; Chronic Infection; Myeloprolifer’ ill’; Connective tissue ill’; & Autoimmune ill’.
o  Oliguria general’ favors AKI. Abrupt anuria suggests acute urin’ obstruction, acute & +++ GNephrit', or embolic renal artery obstruction. Gradual’ ↓ed urin’ output ~ indica’ urethr’ strict’ or bladd’ outlet obstruct’ due to prostate enlargem’.
o  ↓ed normal nephron à easy (+) AKI due to nephrotoxin @ Px w/ chronic renal insuffici’.
o  Can help classify AKI’s pathophysiol’ (prerenal, intrinsic ren, or postrenal fail’) à ~ suggest specific etio’.
o  Prerenal fail’
§ Common’ present (+) hypovolem’-related sympt’: thirst, ↓ed urine output, dizzi’, & orthostatic hypotens’. Look for volume loss ~ due to: emesis, diarrh’, sweati’, polyur’, hemorrha’. Advanced ♥ fail’ à ↓ ren’ perfus’ à ~ present w/ orthopnea & paroxysm’ nocturnal dyspnea.
§ Elder w/ vague mental status change is common’ (+) prerenal or normotens’ ischem’ AKI. Insensib’ fluid loss can lead to +++ hypovolem’ @ restricted fluid access (should suspect @ elder, sedated, or comatose Px).
o  Intrinsic Ren fail’
§ AKI’s etio’ classes: glomerular (indica’ by: Nephritic syndr’ of hematur’, edema, hypertens’); or tubular (Acute Tubular Necrosis (ATN) suspect’ @ Pxs presenti’ after period of hypotens’ due to: ♥ arrest, hemorrha’, sepsis, overdose, or surgery).
§ Nephrotoxin history: all of current medications, & radiol’ exam’ (radiocontrastant expos’). Pigment-induced AKI suspect @ rhabdomyolysis (myalg’, recent coma, seizu’, intoxic’, overexercise, limb ischem’), or hemolysis (recent blood transfus’). Allergic interstiti’ nephrit’ suspect’ w/ fever, rash, arthralg’, & certain drugs (s.as: NSAID, & antibiot’) expos’.
o   Postrenal fail’
§ Usu’ @ Elder ♂ w/ prostat’ obstruction & sympt’ of urgency, frequency, & hesitan’. ~ present w/ asympt’, high-grade ((oft’ provides clue: history of gynecol’ surgery or abdominopelvic malignancy) urin’ obstruction due to chronic sympt’.
§ Flank pain & hematur’ ↑ concern on renal calculi or papil’ necrosis as etio’ of urin’ obstruction. Acyclovir, methotrexate, triamterene, indinavir, or sulfonamide ~ crystallize to obstruct tubuli.
v Physic’ Exam’
o  Skin
§ ~ (+): Livido reticularis, digit’ ischem’, butterfly rash, palpab’ purpura (sign of System’ vasculit’); maculopapul’ rash (sign of Allergic interstiti’ nephrit’); track marks (IV drug abuse) (sign of Endocardit’).
§ Petech’, purpura, ecchymos’, & livedo reticularis clues for inflammato’ & vascul’ etio’ of AKI. Infectious ill’, thrombotic thrombocytopenic purpura (TTP), DICoagulation, & embolic phenomena can (+) typic’ cutan’ find’.
o  Eyes & Ears
§ Eye ~ (+): keratit’, iritis, uveit’, dry conjunctiva (sign of Autoimmu’ vasculit’); jaundice (sign of Liver ill’); band keratopathy (hypercalcem’) (sign of Multiple myeloma); DMellitus’s signs; hypertension’s signs; atheroemboli (sign of Retinopathy). Find’ suggesti’ of +++ hypertens’, atheroembol’ ill’; endocardit’ ~ (+).
§ Uveitis’s evidence ~ indicate interstiti’ nephrit’ & necrotiz’ vasculit’. Ocul’ palsy ~ indicate ethylene glycol poisoni’ or necrotiz’ vasculit’.
§ Ear ~ (+): hearing loss (sign of Alport disease & aminoglycoside toxicity); mucosal or cartilagin’ ulceration (sign of Wegener granulomatosis).
o  ♥vascul’ syst’
§ Most important: ♥vascul’ syst’ & volume status assessm'. Must include: pulse rate & BPressu' measured while standing & supine; close exam’ of JVein pulse; careful exam’ of ♥ & lung, skin turgor, & mucous membran’; assessi’ peripher’ edema.
§ ~ (+): Irregular rhythm’ (atrial fibrilla’) (sign of Thromboemboli); murmurs (sign of Endocardit’); pericard’ frict’ rub (sign of Urem’ pericardit’); ↑ed JVDistenti’, rales, S3 (sign of ♥ fail’).
§ Important @ inPx: accurate daily record of fluid intake, urine output, & Px weight. If hypovolem’ or +++ ♥ fail’ à hypotens’ (Ø necessari’ sign of hypovolem’).
§ ♥ fail’ ~ (+) hypotens’, volume expans’ is (+) & effective ren perfus’ is poor (~ à AKI).
§ +++ hypertens’ w/ ren fail’ suggest 1 of these: renovascul’ ill; GNephrit’; vascul’; & atheroembol’ ill’.
o  Abdomen
§ ~ (+): pulsatile mass or bruit (sign of Atheroemboli); abdomin’ or costoverteb’ angle tendern’ (sign of Nephrolith’, papillary necrosis, renal artery thrombosis, renal vein thrombosis); pelvic masses, rectal masses, prostat’ hypertrophy, bladd’ distenti’ (sign of Urin’ obstruction); limb ischem’, edema (sign of Rhabdomyolys’).
§ Can detect bladd’ obstruction as etio’ of ren fail’. Epigastric bruit suggests renovascul’ hypertens’ (~ predispose AKI).
o  Pulmon’ syst’
§ ~ (+): rales (sign of Goodpasture Syndr’, Wegener Granulomatosis); Hemoptysis (sign of Wegener Granulomatosis).
v DDx
o  AKI can be (+) @ chronic ren fail’. Find reversibility of AKI by tracking rate of ren function’s deterioration: if the rate is ↑ed à find & treat the etio’ of the ↑ed rate.
o  Changes in urine output general’ correlate poor’ w/ GFR’s changes. ± 50-60% etio’ of AKI are Øoliguric. Urine output w/ in DDx:
§ Anuria (< 100mL/day) – Urin’ tract obstruction, ren artery obstruction, Rapid’ Progress’ GlomeruloNephrit’ (RPGN), diffuse Bilateral Renal Cortical Necrosis (BRCN).
§ Oliguria (100-400mL/day) – Prerenal fail’, hepatorenal syndr’.
§ Øoliguria (> 100mL/day) – Acute Interstiti’ Nephrit’ (AIN), Acute GNephrit’, partial obstructi’ nephropathy; nephrotoxic & ischem’ ATN, radiocontrast-induced AKI, & rhabdomyolysis.
o  Abdominal aneurysm
o  Alcohol toxicity
o  Alcoholic ketoacidosis
o  Chronic renal failure
o  Dehydration
o  Diabetic ketoacidosis
o  Gastrointestinal (GI) bleeding
o  Heart failure (♥ fail’)
o  Metabolic acidosis
o  Obstructive uropathy
o  Protein overloading
o  Renal calculi
o  Sickle cell anemia
o  Steroid use
o  Urinary obstruction
o  Urinary tract infection
o  Acute Tubular Necrosis
o  Azotemia
o  Chronic Kidney Disease
o  Emergent Management of Acute Glomerulonephritis
o  Hemolytic Uremic Syndrome in Emergency Medicine
o  Henoch-Schonlein Purpura (HSP) in Emergency Medicine
o  Hyperkalemia
o  Hypermagnesemia
o  Hypernatremia
o  Hypertensive Emergencies
v Workup
o  Can help assess AKI’s etio’ & aid in proper Tx: CBC; serum biochemistry; Urine analysis w/ microscopy; urine electrolytes.
o  Ren imaging can be useful in some cases, espec’ @ ren fai’ due to obstructi’. American College of Radiology recommends Doppler method of USG as most appropriate imaging method in AKI.
o  Ren Funct’ Studies
§ (Rate of ↑ depends on level of renal insult; BUN’s also affected positively by protein intake) ↑ed BUN & creatinine, hallmarks of ren fail’. BUN ~ ↑ed @ GI or mucosal bleed’, steroid Tx, or protein loading
§ BUN:creatinine can > 20:1 in (+) ↑ reabsorp’ of urea (eg: @ volume restrict’); this suggests prerenal AKI.
§ Assumi’ Px has no renal funct’:
· BUN’s rise in 24 hours is rough-predictab’ by this formula: [[24-hour protein intake in milligrams][0.16]/[Total body water in mg/dL]] added to BUN value.
· Creatinine’s rise is predictab’ by this formula:
o  For ♂: [[weight in kilograms][28 - 0.2(age)]/[Total body water in mg/dL]] added to creatinine value.
o  For ♀: [[weight in kilograms][23.8 - 0.17(age)]/[Total body water in mg/dL]] added to creatinine value.
§ (General rule) if creatinine gets to > 1.5mg/dL/day à rule out rhabdomyolysis!
o  CBC, peripher’ smear, & sero’
§ Peripher’ smear ~ (+) schistocyt’ in conditions s.as Hemolytic Uremic Syndr’ (HUS) or TTP. ↑ed roleaux formation suggests multiple myeloma (should direct workup toward serum & urine’s immunoelectrophoresis).
§ (These + related find’ aid defini’ AKI’s etio’):
· Myoglobin or free Hemoglobin (Hb) ((+) @ eg: pigment nephropathy).
· ed serum uric acid ((+) @ eg: tumor lysis syndr’).
· ↑ed Serum LDH ((+) @ eg: ren infarc’).
§ Serolo’ tests (only if indicated): Complement Levels; Antinuclear antibody (ANA); Antineutrophil cytoplasmic antibody (ANCA); Anti-glomerular basement membrane (anti-GBM) antibody; Hepatitis B and C virus studies; Antistreptolysin (ASO).
o  Urinalysis
§ (+) tubular cells or their casts à supports ATN’s Dx (oft’ + oxalate crystals).
(Figure right below) Sloughing of cells à (+) granular, muddy brown casts à high’ sensitive of tubular necrosis.

§ Reddish or dark brown urine suggests (+) myoglobin or Hb, espec’ @ (+) dipstick for heme & no RBC @ microscopy. On Dispstick, ~ (+) signifi’ proteinur’ due to tubular injury.
§ In urine: eumorphic RBCs suggests collecting system’s bleed’; dysmorphic RBCs or RBC casts indicate glomerulit’; WBCs or WBC casts suggest pyelonephritis or AIN; (+) eosinophil, Ø necessari’ (+) allergic interstiti’ nephrit’, but helps its Dx.
§ On wright stain or Hansel stain, (+) eosinophil (also (+) @ urinary tract infections (UTIs), GN, & atheroembolic ill’) suggests interstiti’ nephrit’.
§ (+) uric acid crystal ~ represent ATN relat’ to uric acid nephropathy. Usu’ (+) calcium oxalate @ ethylene glycol poisoni’.
o  Fractional Exretion of Sodium & Urea (FENa & FEUrea)
§ Sodium
· Interpret’ @ Px w/ Øoligur’ states, GN, or use diuretics can lead to misDx.
· FENa only useful in AKI if (+) oligur’. FENa (%) = [[UNa/PNa]/[UCr/PCr]]. @ Prerenal azotem’, FENa usu’ < 1%. In ATN, FENa > 1% (except: @ ATN due to radiocontrast nephropathy, +++ burns, acute GN, & rhabdomyolysis).
· If (+) liver ill’, FENa can be < 1% @ (+) ATN. Diuretic ~ cause FENa > 1% à FENa can’t be sole predictor of AKI.
§ Urea
· Diuretic Ø affect urea transport, thus also Ø affect FEUrea. FEUrea < 35% is suggests prerenal state. FEUrea (%) = [[UUrea/PUrea]/[UCr/PCr]].
o  Bladd’ Pressu’
§ (Considered normal) Intraabdomin’ pressu’ < 10 mmHg suggest AKI Ø due to abdomen compartment syndr’. (Abnormal) Intraabdomin’ pressu’ > 10 mmHg (if it’s 15-25 mmHg à particular risk for abdomen compartment syndr’). Intraabdomin’ pressu’ > 25 mmHg à suspect AKI due to abdomen compartment syndr’.
o  Emerging Biomarker
· ↑ed creatinine (reflects +++’ ↓ed glomerular filtration rate (GFR)), late marker of renal dysfunct’.
· Urine neutrophil gelatinase-associated lipocalin (NGAL), detects AKI @ Px w/ ♥pulmon’ bypass surgery.
· Plasma B-type natriuretic peptide (BNP) & NGAL, predictors of early AKI in lower respirat’ tract infection (LRTI). BNP > 267 pg/mL or NGAL > 231 ng/mL suggests AKI (94% sensitivity, 61% specificity).
o  Ultrasonography (USG)
· Hydronephrosis’s degree on USG Ø necessari’ correlate w/ obstruction’s degree. Small ren suggests chronic ren fail’.
· Doppler USG
o  For detecting (+) & nature of ren blood flow (↓ed @ prerenal, & intrarenal AKI). Quite useful for Dx of thromboembolic & renovascul’ ill’. ↑ed resistive indices’re observable @ hepatorenal syndr’.
o  Nuclear Scanning
· Radionuclide imaging w/ technetium-99m-mercaptoacetyltriglycine (99m Tc-MAG3), 99m Tc-diethylenetriamine penta-acetic acid (99m Tc-DTPA), or iodine-131 (131 I)-hippurate can be used to assess renal blood flow, tubular funct’. (+) marked delay in tubular excretion of radionuclide in prerenal & intrarenal AKI, limiting nuclear scans’s value.
o  Aortorenal Angiography
· Can help in Dx of renovascul’ ill: renal artery stenosis; renal atheroembol’ ill; atheroscleros’ w/ aortorenal occlusi’; certain cases of necrotizi’ vasculit’ (eg: polyarterit’ nodosa).
o  Renal Biopsy
· Can be used to identify AKI’s intrarenal causes, justifiab’ if results ~ change Tx (eg: initiati’ of immunosupression). Also ~ indicated if (+) prolong’ ren dysfunct’, & prognosis’s needed to develop long-term Tx. Ren biopsy (+) unexpected Dx @ 40% cases.
· Acute cellu’ or humoral rejecti’ in transplanted ren is definitiv’ diagnosab’ by ren biopsy.

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