Tan, Joyce Anne S.

Tanchuling, Ma. Mercedes Victoria M.

1) Define edema
2) Discuss pathophysiology of the symptom
3) Enumerate common differentials based on
history and PE
4) Identify and interpret pertinent labs
5) Give rational diagnosis based on given
information
6) Discuss initial management of final
diagnosis
7) Appropriate CPGs on diagnosis and
management of final diagnosis
I. Introduction
II. General Data and Chief Complaint
III. Pathophysiology of Edema
IV. History, Physical Exam, Laboratory Findings
V. Primary Working Impression
VI. Differentials
VII. Approach and Management
 “clinically apparent increase in the
interstitial fluid volume, which may expand
by several liters before the abnormality is
evident”
 Abnormal swelling of tissues from
accumulation of fluid in extravascular space
 Seen at the extremities or lower back;
eyelids, scrotum, or labia; or in organs or
extremities at the site of tissue damage
 10 years old
 Female
 Dasmarinas, Cavite
 1st consult at PGH

 Chief
complaint:
Edema
Edema: one or more alterations in the Starling forces ergo increased
flow of fluid from the vascular system into the interstitium or
into a body cavity
 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/bacterial
infection
 Sodium and water retention
congestive heart failure, acute
glomerulonephritis , other forms of renal
failure
1) Capillary leak
2) Reduction of effective arterial volume
3) Renal factors and the RAAS
4) Arginine Vasopressin
5) Endothelin
6) Natriuretic peptides
Usual causes, check for:
 Cardiac – pulses, BP, cold/clammy, DOB
 Liver – jaundice, bleeding problems
 Renal – type of edema, BP
 Nutrition - Kwashiorkor, flag sign
 • conscious, irritable, coherent,
NICRD
• BP 150/90 HR 90 RR 24
History

 3 weeks PTC: (+) fever, Wt 49 kg Ht 152 cm BSA 1.4.

cough, colds • HEENT: AS, slightly pale
- Paracetamol& Carbocisteine: conjunctiva, (+) periorbital, facial
relief edema.
3 days PTC: (+) facial • CHEST/LUNGS: ECE, harsh bs

Physical Exam

edema, abdominal • HEART: AP, NRRR, (-) murmurS
distension, decreased UO, • ABDOMEN: NABS, soft, no
tea-colored urine organomegaly, tenderness, or
- consulted private MD, u/r masses.
diagnosis & medications given, no • EXTREMITIES: FEP, grade II
relief of Sx bipedal edema.
 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, dysuria
 Family history of hereditary nephritis?
 Pigmenturia  Hematuria
 Red urine withour  at least 5 RBCs/HPF
RBCs in urine, with
 Hemoglobinuria coarse granular
 Myoglobinuria casts
 Upper UT vs. Lower
 Drugs/food
UT bleed
 Glormerular

 Isolated Renal Disease   
 Non-glomerular
IgA nephropathy (Berger disease)   
Postinfectious GN
 Upper
(poststreptococcal GN)   
Membranoproliferative GN   
Tubulointerstitial
Focal segmental glomerulosclerosis
  
Vascular
 Multisystem Disease    Crystalluria
Systemic lupus erythematosus
nephritis Hemoglobinopathy
Henoch-Schönlein purpura nephritis
   Anatomic
Goodpasture syndrome   
Hemolytic-uremic syndrome     Lower
HIV nephropathy
Inflammation
Urolithiasis
Trauma
Coagulopathy
Heavy exercise
Munchausen syndrome
Edema secondary to a RENAL CAUSE
 But what type?

Nephritic Nephrotic Nephrotic-nephritic

Hematuria Heavy proteinuria Combination
Proteinuria (>40 mg/m2/hr in
Hypertension children)
Uremia Hypoalbuminemia
Variable renal (<2.5 g/dL)
insufficiency, with: Edema
Azotemia Hyperlipidemia
Oliguria (<400
mL/day)
CBC
hgb 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%
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
 KUB ULTRASOUND: Kidneys are enlarged with
increase in parenchymal echogenicity and fair
corticomedullary 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. No
lithiasis seen.
Bilateral enlarged kidneys with
parenchymal disease.
Acute Nephrotic-nephritic Syndrome:
Hypertension, hematuria, proteinuria,
hyperlipidemia edema
 
Possible Nephritic conditions:
1) Post-infectious GN
2) IgA nephropathy
3) Rapidly Progressive (Crescenteric)
Glomerulonephritis
 
 Rule In Rule Out

Post-infectious Hematuria Cannot be ruled out

Glomerulonephritis History of acute
respiratory infection,
Latent phase

IgA Nephropathy Hematuria Presence of latent phase

after JM’s infection
Hematuria not recurrent
PRGN Hematuria Most patients develop acute
renal failure associated with
nephritic and/or nephrotic
syndrome
10 year-old patient with generalized edema
with associated hypertension, hematuria,
proteinuria, hypoalbuminemia, anemia,
hyperlipidemia and bilaterally enlarged
kidneys.
Edema secondary to Post-Infectious
Glomerulonephritis
 Group A beta hemolytic streptococci Enlargement of kidneys
produce proteins 
 Impaired bicarbonate metabolism;
Protein + glomerulus Impaired glomerular filtration;

NaCl and water retention
Activate alternative complement pathway 
OR cause formation of antigen-antibody
complexes Metabolic acidosis;
 Increased BUN and creatinine
Recruitment of inflammatory cells Edema and hypertension
 anemia
Destroy basement membrane

Hematuria and proteinuria

RBCs in the basement membrane causes
hypercellularity

Renal blood flow compromised

 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)
 Urinalysis: to check if Nephrotic or nephritic
 ABG: for acidosis
 CBC: dilutional anemia?
 Symptomatic
1) Edema – Diuretics
2) Hypertension - ACE inhibitors, Calcium Channel
Antagonists

Furosemide? Antibiotics?

Post-infectious GN spontaneously resolves after a

few weeks or months, so if it’s safe for the
patient to go home, the patient is managed
simply by: Salt and Water retention
 Normalization of Laboratory Anomalies
1) Gross hematuria: 3 weeks
2) Proteinuria: 3-6 months
3) Microscopic hematuria: 12 months
4) Serum C3: 2-3 months
 Abassi ZA et al: Control of extracellular fluid volume and the
pathophysiology 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. Harrison’s Principles of Internal Medicine. 17th
edition. USA: 2008.
 Kliegman, Behrger et al. Nelson’s Principles of Pediatrics, 18th edition
 O'Brien JG et al: Treatment of edema. Am Fam Physician 71:2111, 2005
[PMID: 15952439]