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Tan, Joyce Anne S.
Tanchuling, Ma. Mercedes Victoria M.
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1) Define edema
2) Discuss pathophysiology of the symptom
3) Enumerate common differentials based on
history and PE4) Identify and interpret pertinent labs
5) Give rational diagnosis based on giveninformation
6) Discuss initial management of finaldiagnosis
7) Appropriate CPGs on diagnosis andmanagement of final diagnosis
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I. Introduction
II. General Data and Chief Complaint
III. Pathophysiology of Edema
IV. History, Physical Exam, Laboratory FindingsV. Primary Working Impression
VI. Differentials
VII. Approach and Management
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clinically apparent increase in theinterstitial fluid volume, which may expandby several liters before the abnormality isevident
Abnormal swelling of tissues fromaccumulation of fluid in extravascular space
Seen at the extremities or lower back;
eyelids, scrotum, or labia; or in organs orextremities at the site of tissue damage
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10 years old
Female
Dasmarinas, Cavite
1st consult at PGH
Chief complaint:
Edema
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Edema: one or more alterations in the Starling forces ergo increasedflow of fluid from the vascular system into the interstitium or
into a body cavity
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Increased (capillary) hydrostatic pressure
hypoalbuminemia in nephrotic syndrome;venous and lymphatic obstruction
Decreased (capillary) oncotic pressure
proteinuria in nephrotic syndrome Increased capillary permeability
drug induced, inflammation, viral/bacterialinfection
Sodium and water retentioncongestive heart failure, acuteglomerulonephritis , other forms of renalfailure
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1) Capillary leak
2) Reduction of effective arterial volume
3) Renal factors and the RAAS
4) Arginine Vasopressin5) Endothelin
6) Natriuretic peptides
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Usual causes, check for:
Cardiac pulses, BP, cold/clammy, DOB
Liver jaundice, bleeding problems
Renal type of edema, BPNutrition - Kwashiorkor, flag sign
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conscious, irritable, coherent,
NICRD
BP 150/90 HR 90 RR 24
Wt 49 kg Ht 152 cm BSA 1.4.
HEENT: AS, slightly pale
conjunctiva, (+) periorbital, facial
edema. CHEST/LUNGS: ECE, harsh bs
HEART: AP, NRRR, (-) murmurS
ABDOMEN: NABS, soft, no
organomegaly, tenderness, or
masses.
EXTREMITIES: FEP, grade II
bipedal edema.
Histo
ry
PhysicalE
xam
3 weeks PTC: (+) fever,cough, colds
- Paracetamol& Carbocisteine:
relief
3 days PTC: (+) facialedema, abdominal
distension, decreased UO,
tea-colored urine
- consulted private MD, u/rdiagnosis & medications given, no
relief of Sx
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Elaborate on URTI
Chronology of edema development
Dyspnea upon exertion, orthopnea, PND
Abdominal pain, flank pain?Decreased appetite, altered taste, altered
sleeping pattern, difficulty concentrating,restless legs or myoclonus?
Frequency, dysuriaFamily history of hereditary nephritis?
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PigmenturiaRed urine withour
RBCs
HemoglobinuriaMyoglobinuria
Drugs/food
Hematuriaat least 5 RBCs/HPF
in urine, withcoarse granularcasts
Upper UT vs. LowerUT bleed
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Glormerular Isolated Renal Disease
IgA nephropathy (Berger disease)Postinfectious GN(poststreptococcal GN)Membranoproliferative GNFocal segmental glomerulosclerosis
Multisystem Disease
Systemic lupus erythematosusnephritisHenoch-Schnlein purpura nephritis
Goodpasture syndromeHemolytic-uremic syndromeHIV nephropathy
Non-glomerular Upper
TubulointerstitialVascularCrystalluriaHemoglobinopathyAnatomic
LowerInflammationUrolithiasis
TraumaCoagulopathyHeavy exerciseMunchausen syndrome
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Edema secondary to a RENAL CAUSE
But what type?
Nephritic Nephrotic Nephrotic-nephritic
HematuriaProteinuriaHypertensionUremiaVariable renalinsufficiency, with:
AzotemiaOliguria (40 mg/m2/hr inchildren)Hypoalbuminemia(
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CBChgb 83 hct .24 plt 388
Seg 0.80 lymph 0.18
ELECTROLYTES
Na 136 mmol/L (140-148 mmol/L)
K 3.7 mmol/L (3.6 5.2 mmol/L)
Alb 19 g/L (34 50 g/L)
phosphorus 1.65 mmol/L (0.81 1.58 mmol/L)
BUN 28.43 mmol/L (2.60 6.40 mmol/L)
Crea 893 mmol/L (53 115 umol/L)
Cholestrol 9.78 mmol/L (4.20 5.20 mmol/L)
ABG
pH 7.28 pCO2 30 pO2 135
HCO3 12.4 BE 12 sats 98.8%
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24-HOUR URINE COLLECTION:
total volume 800 ml/24 hr (500 2000 ml/24 hr)
urine creatinine 0.70 g/24 hr (0.60 2.50 g/24 hr)
urine total protein 3.55 g/24 hr (0.00 1.100 g/24 hr)
URINALYSIS:
yellow /hazy Sp.gr. 1.010 (1.007-1.012)
sugar negative pH 8.5
protein 4+
RBC innumerable cast negative WBC 1-4.HPF
Crystals negative
epithelial cells rare
Bacteria rare mucus threads negative
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KUB ULTRASOUND: Kidneys are enlarged withincrease in parenchymal echogenicity and faircorticomedullary differentiation.
R: 13.2 cm x 6.6 cm x 4.6 cm.
L: 14.4 cm x 7.3 cm x 8.7 cm
The central echo complexes are intact. Nolithiasis seen.
Bilateral enlarged kidneys withparenchymal disease.
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Acute Nephrotic-nephritic Syndrome:Hypertension, hematuria, proteinuria,hyperlipidemia edema
Possible Nephritic conditions:
1) Post-infectious GN
2) IgA nephropathy
3) Rapidly Progressive (Crescenteric)Glomerulonephritis
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Rule In Rule Out
Post-infectiousGlomerulonephritis
HematuriaHistory of acuterespiratory infection,Latent phase
Cannot be ruled out
IgA Nephropathy Hematuria Presence of latent phaseafter JMs infectionHematuria not recurrent
PRGN Hematuria Most patients develop acute
renal failure associated withnephritic and/or nephroticsyndrome
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10 year-old patient with generalized edemawith associated hypertension, hematuria,proteinuria, hypoalbuminemia, anemia,hyperlipidemia and bilaterally enlargedkidneys.
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Group A beta hemolytic streptococciproduce proteins
Protein + glomerulus
Activate alternative complement pathwayOR cause formation of antigen-antibody
complexes
Recruitment of inflammatory cells
Destroy basement membrane
Hematuria and proteinuria
RBCs in the basement membrane causeshypercellularity
Renal blood flow compromised
Enlargement of kidneys
Impaired bicarbonate metabolism;
Impaired glomerular filtration;
NaCl and water retention
Metabolic acidosis;
Increased BUN and creatinine
Edema and hypertension
anemia
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DANGER, DANGER!1) Hypertensive Encephalopathy
2) Congestive Heart Failure w/ Pulmonary Edema
3) Acute Renal Failure with Nephrotic feature of
anasarca
AKI CHUA
AKI: Acute Kidney Injury/ ARF (urine monitoring)
C: Congestions (x-ray)H: Hyperkalemia (peak T-waves in ECG)
U: Uremia (Neuro: drowsy)
A: Metabolic Acidosis (ABG)
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Urinalysis: to check if Nephrotic or nephriticABG: for acidosis
CBC: dilutional anemia?
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Symptomatic1) Edema Diuretics
2) Hypertension - ACE inhibitors, Calcium ChannelAntagonists
Furosemide? Antibiotics?
Post-infectious GN spontaneously resolves after a
few weeks or months, so if its safe for thepatient to go home, the patient is managedsimply by: Salt and Water retention
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Normalization of Laboratory Anomalies
1) Gross hematuria: 3 weeks
2) Proteinuria: 3-6 months
3) Microscopic hematuria: 12 months4) Serum C3: 2-3 months
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Abassi ZA et al: Control of extracellular fluid volume and thepathophysiology of edema formation, in The Kidney, 7th ed, BM Brenner(ed). Philadelphia, Saunders, 2004.
Anacleto, FE. Bedside Pediatric Nephrology. Philippines: Hopemed, 2007.
Fauci, Braunwald et al. Harrisons Principles of Internal Medicine. 17thedition. USA: 2008.
Kliegman, Behrger et al. Nelsons Principles of Pediatrics, 18th edition
O'Brien JG et al: Treatment of edema. Am Fam Physician 71:2111, 2005[PMID: 15952439]