final cc edema

8/8/2019 final CC edema

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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]

final cc edema

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