EDEMA

CONTENTS• EDEMA - Pathophysiology - How to approach • Acute poststreptococcal glomerulonephritis• Nephrotic syndrome• Renal failure

EDEMA• Defined as a palpable swelling produced

by expansion of the interstitial fluid volume• Localized or Generalized• Severe generalized edema is known as

anasarca

PATHOPHYSIOLOGY OF EDEMA

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.

STARLING FORCES

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

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

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)

LOCALIZED EDEMA

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

LOCALIZED EDEMA• Increased permeability of capillary wall - infection - burn - trauma• Allergic reaction : angioedema

HOW TO APPROACHEDEMA

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

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

RENAL CAUSES

RENAL CAUSES• Acute post streptococcal glomerulonephritis• Nephrotic syndrome• Acute renal failure• Chronic renal failure

Acute PoststreptococcalAcute PoststreptococcalGlomerulonephritisGlomerulonephritis

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

• epidemic usually from skin infection • different attack rate in difference family due to genetic factor

EpidemiologyEpidemiology

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

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)

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

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

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

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

glomerulus may produce the following dysmorphic RBC's

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

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

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

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

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

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

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

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

Other Other AGN in childrenAGN in children

Less common

- MPGN (Membranoproliferative glomerulonephritis)

- IgA nephropathy - lupus nephritis - Familial nephritis - Infective endocarditis-related nephritis

Nephrotic syndrome

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

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

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

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

Clinical features• Edema

Distribution : - periorbital areas

- dependent areas : lower legs - genitalia - pleural effusion and ascites Often preceded by Hx of URI

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)

Physical Examination

• Height & Weight• Blood pressure• Pulse, capillary refill time• Pleural effusion, ascites, edema• Acute complication : Hypovolemia,

Infection, Thrombosis

Atypical features

1. Age <1yr or > 12 yrs2. Persistent HT3. Gross hematuria4. Renal impairment (without

hypovolemia)5. Decreased C3

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

InvestigationInvestigation• IgG, IgA decrease • BUN, Cr, electrolyte • electrolyte: hyponatremia, hyperkalemia (early

creatinine rising)

fat fatcastscasts

ComplicationsComplications

• Hypovolemia• Protein malnutrition & malabsorption • Infection• Acute renal failure• Thrombosis• Hypocalcemia

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.

ARFCauses

- Hypovolemia ATN - Intratubular obstruction from protein cast - Renal vein thrombosis - Acute interstitial nephritis (diuretics)

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

Hypocalcemia• Decreased total calcium & ionized calcium

- Hypoalbuminemia - Loss vitamin D binding protein in urine - Decreased GI absorption

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

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

5. Edema - salt restriction - Diuretics mild case : thiazide + K sparing diuretics severe case : loop diuretics

Approach to management in children with NS

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

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

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

Corticosteroid• Tuberculin test• Chest X ray• Stool concentration for parasite * 3 days

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

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

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

Indication for alternative immunomodulartory Rx

• Frequent relapse• Steroid dependent

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

Second line drugs : Alkylating agents

• Cyclosporin 3-5 mg/kg/day

side effects : effectively maintains remission but relapse after discontinuation

renal toxicity

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

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%

ACUTE RENAL FAILURE

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)

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

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

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

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

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

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

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

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

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

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

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

RBCRBC DysmorphicDysmorphic RBCRBC RBCRBC cast cast

HyalineHyaline castcast Granular castGranular cast

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)

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

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

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

Postrenal failure

Removal of obstruction Rx postobstructive uropathy Rx voiding dysfunction and UTI Stabilization of electrolyte abnormalities

Treatment

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

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

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

- 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

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

Hyperkalemia

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)

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

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

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

Chronic renal failure

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

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

อาการทางคลินิกเมื�อเขา้สูไ่ตวายระยะสดุท้าย

– ปัสสาวะลดน้อยลงมาก– ซดีมาก– บวม เหนื�อยง่าย– อ่อนเพลีย– pulmonary edema – hypertensive encephalopathy

↓ GFR

Phosphorus clearance ↓ การขบักรดลดลง ซดี

Hyperphosphatemia, hypocalcemia,

hyperparathyroidismActive vitamin D deficiencyChronic metabolic acidosis

Anemia, renal osteodystrophy

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

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

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

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

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

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

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

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

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

ARF & CRFARF & CRF

TESTThe following features are observed in thenephrotic syndrome A. hypoalbuminuriaB. HyperlipidemiaC. HypocalcemiaD. Increased intravascular volumeE. Minimal changes disease

• B• C• E

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

• B• E

TESTThe following are complications of CRFA. osteomalaciaB. HTC. HypokalemiaD. UremiaE. anemia

• A• B• D• E