EDEMA 08-2014
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EDEMA
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CONTENTS• EDEMA - Pathophysiology - How to approach • Acute poststreptococcal glomerulonephritis• Nephrotic syndrome• Renal failure
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EDEMA• Defined as a palpable swelling produced
by expansion of the interstitial fluid volume• Localized or Generalized• Severe generalized edema is known as
anasarca
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PATHOPHYSIOLOGY OF EDEMA
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GENERALIZED EDEMA1) An alteration in capillary hemodynamics that
favors the movement of fluid from the vascular space into the interstitium.– increased capillary hydrostatic pressure– decreased capillary oncotic pressure– increased capillary permeability
2) The retention of dietary or intravenously administered sodium and water by the kidneys.
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STARLING FORCES
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Capillary hydrostatic pressure gradient
• Arterial pressure (minor)– precapillary vasoconstriction
• Venous pressure (major)– Causes of increased venous pressure
• Intravascular volume expansion• Venous outflow obstruction
• Interstitial pressure– Low compliance compartment
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Capillary oncotic pressure gradient
• Serum albumin concentration : hypoproteinemia (malnutrition, cirrhosis, nephrotic syndrome)– Interstitial oncotic pressure changes in
parallel with capillary oncotic pressure– ∆π (i.e., πc –πi) is constant if changes πc are
gradual• Acute decreases in πc (e.g., rapid saline infusion)
lead to abrupt declines in ∆π and edema formation
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Capillary hydrostatic permeability
• Burns– Reactive oxygen species, histamine
• Cytokine/interleukin mediation– Immunotherapy (IL-2)– Sepsis (IL-2, TNF)– Diabetes mellitus – Kwarshiorkor (leukotrienes)– Ovarian hyperstimulation syndrome – Idiopathic capillary leak ( IL-2, kinins)
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LOCALIZED EDEMA
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LOCALIZED EDEMA• Disease of lymphatic system - Filariasis - Cellulitis - Neoplasm - Surgical excision • Disease of venous obstruction - Thrombophlebitis - Thrombosis - Neoplasm - Varicosity (Varicose veins) - Arteriovenous fistula - Lymph node mass
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LOCALIZED EDEMA• Increased permeability of capillary wall - infection - burn - trauma• Allergic reaction : angioedema
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HOW TO APPROACHEDEMA
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EDEMAHx & PE
Localized edema Generalized edema
1. Nephrotic syndrome2. Acute glomerulonephritis3. Chronic glomerulonephritis : Hereditary nephritis, interstitial nephritis, polycystic kidney, IgA nephropathy, secondary glomerulonephritis (Henoch Schoenlein purpura) 4. Acute and chronic renal failure
1. Cardiac problems 2. Drugs, hormones3. Hypoalbuminemia4. Liver causes5. Nutritional causes6. Collagen vascular disease7. Others : severe anemia,Idiopathic edema, myxedema To be continue !!!!
Non renal causes Renal causes
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Non renal causes1. Cardiac problems• Congestive heart failure• Pericardial effusion• Constrictive pericarditis2. Drugs, hormones• Minoxidil, NSAIDs, estrogen, steroid, calcium channel blockers3. Hypoalbuminemia• Malnitrition : Kwarshiorkor, protein losing enteropathy4. liver causes• Biliary atresia• Cirrhosis• Hepatic failure (increased hydrostatic pressure due to portal
hypertension, decreased oncotic pressure)5. nutritional causes• Vitamin C deficiency, beri beri6. Collagen vascular disease : Scleroderma
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RENAL CAUSES
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RENAL CAUSES• Acute post streptococcal glomerulonephritis• Nephrotic syndrome• Acute renal failure• Chronic renal failure
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Acute PoststreptococcalAcute PoststreptococcalGlomerulonephritisGlomerulonephritis
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EpidemiologyEpidemiology
• most common form of AGN• peak incidence 2- 15 yr• male : female 2: 1• sporadic > epidemic• attack rate in family member of affected patient 20 - 40%• sporadic usually from pharyngitis
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• epidemic usually from skin infection • different attack rate in difference family due to genetic factor
EpidemiologyEpidemiology
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OOrganismrganism• Beta streptococcal gr.A • nephritogenic strain : M type - pharyngitis 1,3,4,12,18,25,49 - skin infection 2,49,55,57,60• may be Streptococcal gr. C & G
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Pathogenesis
• remain incompletely understood• more 1 streptococcal Ag & mechanism
may involve 1. circulating immune complex2. in situ immune complex : Ag-Ab in renal3. molecular mimicry: Ag(renal)-Ab4. direct complement activation : alternative
pathway (C3)
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Clinical features• variable from asymptomatic to oliguric ARF latent period • post pharyngitis 7-14 days• post skin infection 14-21 days• 38% latent period < 7 days • 9% latent period > 3 weeks)
• If latent period < 7 days suggest exacerbation of
underlying
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Clinical features• EdemaEdema usually abrupt onset at periorbital area
• Hematuria (100%) > 80% microscopic ( may resolve in 1 yr )
~ 30 % gross ( resolved in 1-2 wks )
• Oligulia (50%) commonly transient , if anuria indicates crescentic GN
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Clinical features
• Hypertension > 75% pathogenesis unknow : multifactorial partly by ECF expansion & cytokines• CHF 20%• Encephalopathy uncommon 5-10% more frequent in children, may be from severe HT, CNS vasculitis • Others N/V, anorexia, lethargy, back pain, abdominal pain
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Lab findingsLab findings• U/A - proteinuria nephrotic range 10-20% (frequent in adult) - dysmorphic rbc, rbc cast, hyaline cast - wbc in early phase may be predominate (2-3 days ) - decrease Na & Ca excretion
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glomerulus may produce the following dysmorphic RBC's
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Lab findings• CBC CBC - mild dilution of Hb concentration
- wbc & platelet usually normal - occasionly thrombocytopenia • renal functionrenal function - rising BUN & Cr ( due to decreased GFR & R
BF ) - normal serum Na, may be mild hyponatremia
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Lab findings
SerologySerology
• ASO titer in pharyngitis 80% has 4 folds rising in skin infection may not rising 50%
• Anti DNaseB rising in > 90%• complement decreased C3 but C4
normal
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Typical poststreptococcal glomerulonephritis
1. Typical presentation with no finding other systemic disease
2. Evidence of prior streptococcal infection - throat or skin lesion +ve - Elevated Ab titer (acute & convalescent titer )3. Complement abnormalities typical - Decreased CH50 & C3 during acute phase - levels rise toward normal by 6-8 wks - C4 usually normal
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Typical poststreptococcal glomerulonephritis
4. Beginning recovery in 1 wk ( ควรลงมาปกติภายใน 2 wk)
- diuresis - BP normalized- BUN, Cr begin to fall5. Normalization of urine sediment- resolution of gross hematuria by 2-3 wks- resolution of proteinuria by 3-6 months- resolution of microscopic hematuria by 1 yr
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Treatment
• admit if obvious edema, HT, rising BUN & Cr
• Bed rest as necessary• Fluid & salt restriction• Specific intervention for the following - HT, volume overload, encephalopathy - Hyperkalemia & acidosis
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Treatment• Confirm likelihood of poststreptococcal
infection• Pen V oral * 10 days• Observe for onset of recovery within 7
days• Keep high index of suspicion for other
disease
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Treatment of HT assoc Treatment of HT assoc iated with AGN iated with AGN
- Mild moderate - Mild moderate Severe Severe
Diuretics Diuretics Furosemide iv/oral Furosemide iv
Vasodilator Vasodilator Hydralaz ine
Hydralazine Na nitr
oprusside iv Ca channel blocker Ca channel blocker Nifedipine
or al Nifedipine ACEI ACEI Captopril oral
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Indication for renal biopsyIndication for renal biopsy1. Atypical presentation2. ประวติัโรคไตในอดีต หรอืมปีระวติัครอบครวัเป็นโรคไต3. anuria, nephrotic range proteinuria4. Complement ไมต่่ำ�า5. Creatinine raising6. การหายของโรคชา้ - Oliguria, azotemia > 2 weeks - Hypertension > 3 week - Gross hematuria > 2 week - C3 decrease > 3 mo - Proteinuria > 6 mo
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Other Other AGN in childrenAGN in children
Less common
- MPGN (Membranoproliferative glomerulonephritis)
- IgA nephropathy - lupus nephritis - Familial nephritis - Infective endocarditis-related nephritis
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Nephrotic syndrome
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Nephrotic syndrome
Generalized edema
Heavy proteinuria 50 mg/kg/day or 40mg/m2/hr Hypoalbuminemia albumin < 2.5 g/dl Hyperlipidemia cholesterol >250 mg/dl
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Primary glomerular diseasePrimary glomerular disease
• Minimal change nephrotic syndrome (MCNS) m/c in Europe• Mesangial proliferative glomerulonephritis(MesPGN) m/c in Thailand• Focal segmental glomerulosclerosis (FSGS)• Membranoproliferative glomerulonephritis (MPGN) associated LE• Membranous glomerulonephropathy (MGN)
Cause of nephrotic syndrome in children
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Secondary nephrotic syndrome
- Associate with systemic disease : SLE, HSP- Postinfectious : syphilis, malaria, hepatitis B/C, CMV, HIV, schistosomiasis- malignancy : lymphoma- Associate with drugs : NSAID, penicillamine,
gold, Heroin- Associate with toxins or allergens : bee sting,
food allergy
Cause of nephrotic syndrome in children
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Epidemiology• Incidence 2-7 new cases /100,000 children• 80% age of onset < 6 yrs• peak age of onset occurs at 2-3 yrs (preschool)• male : female = 3:2• genetic predisposition : 3.4% positive family Hx
HLA B8, DR-3, DR-7
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Clinical features• Edema
Distribution : - periorbital areas
- dependent areas : lower legs - genitalia - pleural effusion and ascites Often preceded by Hx of URI
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Clinical features• GI : Abdominal pain (due to bowel ischemia,
peritonitis) Diarrhea (due to bowel wall swelling) Umbilical & inguinal hernia
• HT : 20%, usually transient May be present in hypovolemic children (due to compensatory systemic vasoconstriction)
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Physical Examination
• Height & Weight• Blood pressure• Pulse, capillary refill time• Pleural effusion, ascites, edema• Acute complication : Hypovolemia,
Infection, Thrombosis
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Atypical features
1. Age <1yr or > 12 yrs2. Persistent HT3. Gross hematuria4. Renal impairment (without
hypovolemia)5. Decreased C3
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Investigation• UA : proteinuria > 2+
oval fat body, hyaline cast microscopic hematuria 20-25%
• urine protein 24 hr• Serum albumin• Serum cholesteral• CBC : increased Hct• Complement : C3, C4 normal
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InvestigationInvestigation• IgG, IgA decrease • BUN, Cr, electrolyte • electrolyte: hyponatremia, hyperkalemia (early
creatinine rising)
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fat fatcastscasts
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ComplicationsComplications
• Hypovolemia• Protein malnutrition & malabsorption • Infection• Acute renal failure• Thrombosis• Hypocalcemia
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Infection• : Due to
- Decreased IgG, IgA - Decreased factor B defective opsonization
• : Peritonitis, cellulitis, asymptomatic UTI, pulmonary & menigeal infection
• : Organism – Streptococcus, Pneumococcus,E. coli Hemophilus, Klebsiella spp.
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ARFCauses
- Hypovolemia ATN - Intratubular obstruction from protein cast - Renal vein thrombosis - Acute interstitial nephritis (diuretics)
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Thrombosis1. Hypercoagulability from
- Loss antithrombin III, protein C & S in urine - Hemoconcentration - Increased coagulation factors : F I, VII, VIII, X - Increased platelet aggregation
2. Deep vein thrombosis, renal vein thrombosis, cerebral cortical vein thrombosis
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Hypocalcemia• Decreased total calcium & ionized calcium
- Hypoalbuminemia - Loss vitamin D binding protein in urine - Decreased GI absorption
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Definition Remission : urine protein dipstick 0-trace for 3 consecutive days
Relapse : urine protein > 2+ for 3 consecutive days, having previously been in remission
Frequent relapser : > 2 in 6 months of initial remission or > 4 within any 12 month period
Steroid-dependent : 2 consecutive relapses occuring during tapering of steroid Rx or within 14 days after
its cessation
Steroid-resistant : failure to achieve remission despite full dose Rx for 8 wks
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Approach to management in children with NS
1. Activity : encourage to mobilized as normal2. Diet : no added salt protein 1 g/kg/day (130-140% normal requirement )3. Fluid intake : restrict during edema4. Immunization : no immunization during Rx with steroid pneumococcal vaccine, varicellar
and influenza vaccine
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5. Edema - salt restriction - Diuretics mild case : thiazide + K sparing diuretics severe case : loop diuretics
Approach to management in children with NS
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Approach to management in children with NS
6. Intravenous 20% albumin - in symptomatic case (respiratory distress due to ascites & pleural effusion), genital swelling, cellulitis, hypovolemia - iv 0.5-1 g/kg in 1-2 hr + furosemide 1-2 mg/kg
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Corticosteroid
First episode
• Prednisolone 60 mg/m2/day(max 80 mg) x 4-6 wks then 40 mg/m2/alt day (max 80 mg) x 4-6 wks then tapering in 3-5 months Higher dose & longer duration decrease relapse
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Adverse effect of Adverse effect of corticosteroidscorticosteroids - susceptibility to infection - mood and behavior disturbance - increased appetite, wt gain, obesity - cushinoid appearance - acne - hirsutism - striae - posterior subcapsular cataract, glaucoma - HT - growth suppression, puberty delay - adrenal suppression , impaired glucose metabolism - dyspepsia , peptic ulcer, pancreatitis - Osteoporosis, avascular osteonecrosis, proximal myopathy
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Corticosteroid• Tuberculin test• Chest X ray• Stool concentration for parasite * 3 days
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Frequent relapsing nephrotic syndrome
Rx : Prednisolone 60 mg/m2/day (max 80 mg) until
urine protein negative x 3 days then
40 mg/m2/ alternate day (max 80 mg) then tapering
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Steroid dependent nephrotic syndrome
Rx : Prednisolone 60 mg/m2/day (max 80 mg) until urine protein negative x 3 days then
40 mg/m2/alt day (max 80 mg) then tapering and maintain at low dose for 3-12 months
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Indication for alternative immunomodulartory Rx
1. Relapse while taking prednisolone > 1 mg/kg on alternate day
2. Relapse while taking prednisolone > 0.5 mg/kg on alternate day, plus > 1 the following :
- Unacceptable adverse effects of steroids - High risk of adverse effects of steroids approaching puberty, DM - Unusually severe relapses hypovolemia, thrombosis, sepsis, ARF
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Indication for alternative immunomodulartory Rx
• Frequent relapse• Steroid dependent
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Second line drugs : Alkylating agents
• Cyclophosphamide 2 mg/kg/day x 12 wks 3 mg/kg/day x 8 wks side effects : leukopenia, hemorrhagic cystitis, gonadal toxicity, pulmonary
fibrosis CBC• Chlorambucil 0.2 mg/kg/day x 8-12 wks
side effects : convulsion, 2nd malignancy, gonadal toxicity
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Second line drugs : Alkylating agents
• Cyclosporin 3-5 mg/kg/day
side effects : effectively maintains remission but relapse after discontinuation
renal toxicity
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Indication for kidney biopsy Pretreatment
Onset < 6 months( 1 yr) or > 8 yr Macroscopic hematuria Microscopic hematuria +persistent HT Low C3 Renal failure not attribute to hypovolemia
Posttreatment Steroid resistance (Rx > 8 week) Early or late non-responder, Frequent relapses
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Outcomes• Mortality 2.5-7.2%
due to hypovolemia, thrombosis, sepsis• Relapse – MCNS 25% single relapse
If remission > 6 months …less likely relapse• MCNS < 5% ESRD• not response to steroid in 8 wks – ESRD 21%• not response in 6 months – ESRD 35%
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ACUTE RENAL FAILURE
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ACUTE RENAL FAILURE
Definition • sudden deterioration in renal function • inability to maintain fluid and electrolyte homeostasis• accumulation of nitrogenous waste products (urea nitrogen and creatinine)
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ACUTE RENAL FAILURE
• Oliguria : urine < 500 ml/1.73m2/day < 1 ml/kg/hr in infants or < 0.5 ml/kg/hr in children
• Anuria : absence of urine production• ~ 50% non oliguric
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Heterogeneous Response Heterogeneous Response ofof Individual NephronsIndividual Nephrons
Variable Damage toVariable Damage toTubular EpitheliumTubular Epithelium
Anatomical DamageAnatomical Damage Functional DamageFunctional Damage
Primary & SecondaryPrimary & SecondaryReduction in GFRReduction in GFR
Decrease in FractionalDecrease in FractionalReabsorptionReabsorption
Decreased tubularDecreased tubularFluid FlowFluid Flow
Increased TubularIncreased TubularFluid FlowFluid Flow
No Contribution to No Contribution to Urine FormationUrine Formation
Responsible forResponsible forUrine FormationUrine Formation
OliguriaOliguria PolyuriaPolyuria
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ARF
Renal Renal 10-30%10-30%
Postrenal Postrenal 5-15%5-15%
PrerenalPrerenal40-80%40-80%
Volume lossVolume losssequestrationsequestration
Hypotension Hypotension
Impaired COImpaired CO
Intra-renalIntra-renal -crystal-crystal
Extra-renal Extra-renal -pelvis/ureter-pelvis/ureter -bladder/-bladder/ urethraurethra**post urethral post urethral Valve**Valve***neurogenic *neurogenic Bladder**Bladder**
Vascular Vascular -small vv-small vv -large vv-large vv
GlomerulusGlomerulus
Tubular Tubular - ischemic- ischemic - toxin- toxin -pigment-pigment
Interstitial Interstitial -inflammation-inflammation -space occupying-space occupying
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BUN/Cr ratioBUN/Cr ratio
>20 <20
Increased ureaformation
Decreased ureaelimination
Decreased ureaformation
False elevationof Cr
Increased Crformation
Decreased Crelimination
High protein intake
Catabolic state
- fever
- tissue necrosis
- corticosteroids
- tetracyclines
- sepsis
Volume depletion
Impaired CO
Obstructive uropathy
Starvation
Advanced liver dis.
Defect of urea cycle enzyme
Rhabdomyolysis
Cimetidine
Trimethoprim
pyrimethamine
Cefoxitin
Ascorbic acid
Levodopa
Methyldopa
Flucytocine Barbiturates
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PathophysiologyClinical phase Pathophysiologic correlatesInitial phase Tubular epithelial cell injury
vasoconstrictionMaintenance phase Tubular obstruction
Passive backflow of filtrateSecondary vasoconstrictionMedullary congestionChanges in glomerular capillary ultrafiltration coefficient
Early recovery phase Restoration of tubular epithelial cell integrity
Phase of functional recovery
VasodilationNephron recruitment
azotemia
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3 phases in the course of ARF3 phases in the course of ARF
• Oliguric phase : usually lasts a few days to 2 weeks• Diuretic phase :
• Recovery phase : vary from a few weeks to several months
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History and physical examination in ARF
1. Hx of any prodomal illness- dehydration- acute pharyngitis / skin infection- fever, other infection, rash, arthropathy
2. Presence or absence of urinary symptoms- hematuria, dysuria, frequency, poor urinary stream
drugs, toxin exposure, antenatal3. Urine output, fluid intake, fluid loss4. Recent BW5. Previous illness: cardiac, liver disease6. Family Hx of renal disease
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History and physical examination in ARF
Physical examination
- BW, Ht, Temp - State of dehydration : dehydration, edema - Respiratory status : tachypnea, fluid overload - Abdomen : renal mass, palpable bladder, CVA tenderness - Neurologic exam : confusion, drowsiness, focal neurological abnormality - Exam for causes or sign of renal failure
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Lab investigationBlood - Electrolyte, BUN, Cr degree of renal impairment , electrolyte imbalance- Ca, PO4 degree of hypo Ca, hyper PO4 - Albumin hypoproteinemia due to proteinuria - PTH evidence of longstanding RF
- Immunologic : C3,C4 immunologic causes CH50, ANA, Anti dsDNA- CBC hemolysis, bleeding, anemia
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Urine
- Protein / Cr ratio- Microscopy cast suggest glomerular dz.- Osmolality evidence of concn defect- Na, Cr, urea to assist distinguishing renal from pre renal cause- myoglobin rhabdomyolysis
Lab investigation
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Urine sediment in ARFCondition Proteinuria Hematuria Microscopy
Prerenal - - Normal
Vascular occlusion
- - Normal
Glomerulo-nephritis
+++ +++ Dysmorphic rbc, granular casts
AIN ++ + wbc (eosinophils) ± wbc cast
ATN - - Muddy brown granular cast, tubular epithelial cell casts
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RBCRBC DysmorphicDysmorphic RBCRBC RBCRBC cast cast
HyalineHyaline castcast Granular castGranular cast
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Prerenal ARF ATN AIN AGN Obstruction early
lateUrine sp.gr >1.020 1.010 1.010 >1.020 variable <1.015 (newborn) (>1.015) (<1.015)Uosm 500 <350 <350 500 >500 <350U/P osm >2 <1 <1U/P cr >40 <20 <20 >15 <15 UNa (mEq/L) <10 >40 >40 <10 <20 >40 (newborn) (<20) (>60)
FENa (%) 1 >2 >2 1 <1 >1 (newborn) ( 2.5) (>2.5)RFI <1 >1 >1 <1 (newborn) (<3) (>3)
BUN/Cr ratio >20 10 10 >20 FE urea <35 >50
FENa (fractional excretion of sodium) = (UNa/PNa) / (UCr/PCr) x 100RFI (renal failure index) = UNa/ (UCr/PCr)
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Complications of ARFComplications of ARF
- Metabolic : acidosis, hypo Ca, hyper PO4,
hyperkalemia,uremia, hyperuricemia ,hyper Mg- CVS : arrythmias, hypervolemia/ hypovolemia, CHF, uremic pericarditis, HT - Respiratory : pulmonary edema- Neurological : mental status changes, seizure- Hematologic : anemia, coagulopathy- Infectious : catheter-related infection, septicemia
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Treatment Provide supportive Rx- Stabilize - Monitor closely : I/O, BW, electrolyte- Prevent sepsis : limit IV line, remove urinary
catheter- Adjust drug according to renal function
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Prerenal failureAdminister fluid challenge
- Use isotonic solution or 5%D/N/2- 5% albumin 10-20 cc/kg
- observe urine output 1-3 cc/kg/hr
Treatment
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Postrenal failure
Removal of obstruction Rx postobstructive uropathy Rx voiding dysfunction and UTI Stabilization of electrolyte abnormalities
Treatment
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Intrinsic renal failure
- Restrict fluids insensible loss + urine output- Insensible loss
300 - 400 ml/m2 as 5-10%D/W- Urine output
ml for ml as 0.45% NaCl- Rx hyponatremia
maintain serum Na 130-135 mEq/L restrict free water
Treatment
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Treatment
Furosemide• Increase urine flow rate• Decrease intratubular obstruction• use in 1st 24-48 hrs • Dose : IV 1- 5 mg/kg/dose continuous drip max 0.5 -1 mg/kg/hr• No evidence of change in renal recovery, need
for dialysis, decreased mortality
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Dopamine
- Synergistic effect with furosemide Dose 0.5-4 µg/kg/min (vasodilation effect)- Side effect : tachycardia, arrhythmia, myocardial ischemia, intestinal ischemia (due to precapillary vasoconstriction)- Evidence controversy
Treatment
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- Rx metabolic acidosis- Replace base deficit if pH < 7.2 or HCO3
< 12 mEq/L up to 16 mEq/L base deficit = 0.6 x BW x (HCO3 desired - HCO3 observed)
2 - ½ over 2-3 hrs, rest over next 24 hrs
- Rx hyper PO4- Calcium carbonate
Treatment
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Treatment hyperkalemia Agent Mechanism Dose Onset of
effectComplications
NaHCO3 Shifts K into cells 1 mEq/kg IV over 10-30 min
15-30 min Hyper NaChange in Ca
10% Ca gluconate
Stabilizes membrane potential (heart)
0.5-1.0 mL/kg IV over 5-15 min (max 10 ml)
Immediate BradycardiaArrhythmiasHypercalcemia
Glucose and insulin
Stimulates cellular uptake of K
Glucose 0.5 g/kgInsulin 0.1 U/kg IV over 30 min
30-120 min Hypoglycemia
-Agonists (albuterol)
Stimulates cellular uptake of K
5-10 mg nebulizer 30 min TachycardiaHypertension
Na polystyrene sulfonate (kayexalate)Kalimate(calcium)
Exchanges Na for K across colonic mucosa
1 g/kg PO or PR q 2-6 hr
Enema:60 minOral :2 hr
HypernatremiaConstipation
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Hyperkalemia
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Treatment HT
Sodium nitroprusside
0.5 to 10 mcg/kg/min IV drip
Labetatol 0.25 to 1 mg/kg IV bolus or0.5 to 3 mg/kg/hr drip
Diazoxide 1 to 5 mg/kg IV push (max 150 mg/dose)
Enalapril 5 to 10 mcg/kg/dayNicardipine 1 to 3 mcg/kg/minNifedipine 0.25 to 1 mg/kg/dose PO, SLQ (max
10 mg/dose)Hydralazine 1 mg/kg IV as first dose then 0.1 to
0.3 mg/kg (max 3.5 mg/kg/day)
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Supplemental nutrition- Goal : to provide sufficient nutrients and adequate caloric intake - Decreased 0.5-1% BW per day over the initial few days- Enteral route
oral/NG feedParenteral
- Calories : 45-50 kcal/kg/day CHO ≥ 70%, Fat ≤ 20%
protein 1-2 g/kg/day low phosphate, potassium
Treatment
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Renal replacement therapyIndication
1. CHF and fluid overload2. Uremic symptoms: N/V, coma, seizure,
uremic pericarditis 3. Metabolic derangement refractory to Rx
(severe metabolic acidosis, severe hyper K, hypo/hyper Na, hyperuricemia, hyper PO4) 4. BUN >150 mg/dl or Cr > 10 mg/dl 5. Toxin : methanol, salicylate, oxalateoptions : HD, PD, CRRT
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Summary of Therapy and Goals in the Initial Phase of Acute Renal Failure
Therapy GoalVolume expansion/hydration Increase in renal blood flow
Prevention of tubular epithelial cell injury
DiureticsOsmotic diureticsLoop diuretics
Restoration of urine flow
Vasoactive agentsDopamineAtrial natriuretic peptide
Restoration of renal perfusion
Cytoprotective agentsFree radical scavengersXanthine oxidase inhibitorsCalcium channel blocking agentsProstaglandins
Preservation of cell integrity
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Chronic renal failure
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สาเหตขุองไตวายเรื้อรงัในเด็กไทย
Causes %
•Obstructive uropathy •Chronic glomerulonephritis •Hypoplastic / dysplastic kidneys
20.68.45
•SLE nephritis •Familial nephritis•Polycystic kidney disease
1.81.70.8
Sumboonnanonda A. J Med Assoc Thai 2000;83: 894-901
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อาการทางคลินิก• ตัวเล็ก เล้ียงไมโ่ต ( failure to thrive ) • เบื�ออาหาร อ่อนเพลีย เหนื�อยง่าย• คันตามตัว • ซดี• ความดันโลหติสงู• สาเหตจุาก glomerular disease :
ปัสสาวะน้อย ปัสสาวะสนี่ำ้าล้างเน้ือ อาจได้ประวติับวมเป็นๆ หายๆ
• สาเหตจุาก tubulo-interstitial disease : จะมอีาการซดีได้เรว็
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อาการทางคลินิกเมื�อเขา้สูไ่ตวายระยะสดุท้าย
– ปัสสาวะลดน้อยลงมาก– ซดีมาก– บวม เหนื�อยง่าย– อ่อนเพลีย– pulmonary edema – hypertensive encephalopathy
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↓ GFR
Phosphorus clearance ↓ การขบักรดลดลง ซดี
Hyperphosphatemia, hypocalcemia,
hyperparathyroidismActive vitamin D deficiencyChronic metabolic acidosis
Anemia, renal osteodystrophy
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ปัจจยัท่ีมผีลต่อเพิม่อัตราเสีย่งของโรคไตเรื้อรงั
• Small birth weight infants• Renal dysplasia or hypoplasia• Urologic disorders esp. obstructive uropathies • DM• SLE• Prior history of HT eg. From renal artery or renal
vein thrombosis in neonatal period • FH of polycystic kidney disease, other genetic
kidney dis• Prior history of ARF, acute nephritis, nephrotic
syndrome, hemolytic uremic,Henoch–SchÖnlein Purpura
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NKF-K/DOQI classification of the stages of CKD
Stage GFR ( ml/min/1.73m2)
description
1 > 90 Kidney damage with normal or increased GFR
2 60-89 Kidney damage with mild reduction of GFR
3 30-59 Moderate reduction of GFR
4 15-29 Severe reduction of GFR
5 < 15 or dialysis Kidney failure
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ประเมนิ GFR สตูรของ schwartz
• Ccr = k x L / Scr (ml /minute /1.73 m2) • K คือ ค่า proportionality
constant ส่ำาหรบัเด็กอายุต่างๆดังนี้
• L = length ( cm)• Scr = serum creatinine
level ( mg/dl)• Ccr = creatinine
clearance
Age group K( mean values)
Low birth weight < 1 yr
0.33
Term infant < 1 yr
0.45
2-12 yr 0.55
Female 13-21 yr
0.55
male 13-21 yr
0.7
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แนวทางการดแูลผู้ป่วย Chronic Kidney Dz.
Stage GFR ( ml/min/1.73m2)
Action plan
1 > 90 Treat primary and comorbid conditions
2 60-89 Esstimate rate of progression of CKD
3 30-59 Evaluate and treat complications
4 15-29 Prepare for kidney replacement therapy
5 < 15 or dialysis
Kidney replacement therapy
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Investigation
Cardiovascular system
BP, chest x-ray , ECG, echocardiogram
Fluid and electrolytes
Serum electrolytes
Growth and development
Wt, height, secondary sex characteristics
Hematological system
CBC, reticulocyte count, bleeding time, iron study
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Investigation
Musculoskeletal system
Calcium, phophorus, alkaline phosphatase, long bone x-ray, bone age, iPTH
Respiration system CXR
Urinary system U/S, VCUG, renal biopsy
Others ( as needed) Uric acid, lipid profiles
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การดแูลรกัษาเด็กไตวายเรื้อรงัCalories RDA ตามอายุ
CHO : protein : fat = 50:10:40Sodium and water
ขึ้นกับอาการ ชนิดของโรคไต และระยะของโรคไต• จ่ำากัดน่ำ้าและโซเดียมใน end stage renal disease และ glomerular disease •ให ้loop diuretics เพื�อลดอาการบวม•ปรบัตามปัสสาวะใน tubulo-interstitial disease
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การดแูลรกัษาเด็กไตวายเรื้อรงัpotassium Potassium exchange resin ใน
chronic hyperkalemia Acidosis Alkaline therapy และ เฝ้า
ระวงัsymptomatic hypocalcemia เมื�อเริ�มรกัษา
ความดันโลหติสงู
ควบคมุน่ำ้าหนัก, ยา
Aluminium toxicity
หลีกเลี�ยงยาและอาหารที�ม ีaluminium
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การดแูลรกัษาเด็กไตวายเรื้อรงั
anemia ป้องกันและรกัษา GI bleeding, malnutrition, uremia
การรกัษาด้วย erythropoietin
ควรเสรมิธาตเุหล็กและ folic
Delayed sexual development
Anabolic or sex steroid
Renal bone disease
จำากัดอาหารท่ีมฟีอสเฟตสงู ให้ phosphate binder และ active vitamin D
Growth retardation
Adequate nutrition, treatment of renal bone disease, dialysis, growth hormone, renal transplantation
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ARF & CRFARF & CRF
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TESTThe following features are observed in thenephrotic syndrome A. hypoalbuminuriaB. HyperlipidemiaC. HypocalcemiaD. Increased intravascular volumeE. Minimal changes disease
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• B• C• E
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TESTThe following are associated with a good prognosis for renal failureA. Nephrotic syndrome caused by
glomerulosclerosisB. NS with minimal change diseaseC. Rapidly progressive GND. SLE relatedE. Poststreptococcal GN
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• B• E
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TESTThe following are complications of CRFA. osteomalaciaB. HTC. HypokalemiaD. UremiaE. anemia
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• A• B• D• E