The document discusses the pathophysiology of edema, describing how fluid accumulation occurs in tissues due to imbalances in hydrostatic and oncotic pressures across capillaries. It classifies edema as inflammatory, non-inflammatory, generalized, or localized; and discusses specific causes of edema like heart failure, nephrotic syndrome, cirrhosis, and lymphatic or venous obstruction. Investigations and physical exam findings for evaluating different types of edema are also outlined.

1. PATHOPHYSIOLOGY OF
EDEMA
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2. 3rd MBBS
Morning Group A1 (Roll No. 1-10)
Kay Zin Soe Kaung Htet Kyaw
K Thari Swe Kaung Htet Lin
Kaung Sett Lwin Kaung Naing Maw
Kaung Zaw Htet Kaung Myat Kyawe
Kaung Htet Kyaw Kaung Myat Phyoe
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3. DEFINITION
• Oedema results from the accumulation of excess
fluid in the interstitial spaces or serous cavities.
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4. Classification
Depending on nature of fluid
• Inflammatory edema ( due to increased vascular permeability)
• Non-inflammatory edema ( due to osmotic or hydrostatic pressure
imbalance)
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5. 5
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6. • Depending on site of collection
Generalized edema
due to transudation of salt and water, as in
e.g- hypoproteinemic syndrome
congestive cardiac failure
acute glomerular nephritis
nephrotic syndrome
cirrhosis
Localized edema due to
• increased permeability of small blood vessels, e.g, infection, trauma, burns,
allergy
• lymphatic obstruction, e.g – malignancy, filariasis, chronic infection.
• venous obstruction, e.g – thrombosis, malignant infiltration 6
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7. THE LEAK OF VEINS
Tumor
Heart failure
Enteropathy (protein-losing)
Liver failure
Endocrine (hypothyroidism, aldosterones,diabetes)
Altitude sickness
Kidney disease (renal failure, nephrotic syndrome)
Obstruction of lymphatics
Filariasis
Venous thrombosis
Eclampsia / pregnancy
Iatrogenic
Nutritional deficiency
Sepsis / capillary leakage 7
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(from Davidson Differential Diagnosis Mnemonics)
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8.  About 24 litres of fluid are filtered through the capillaries per day.
85% - reabsorbed into the capillaries.
15% - returned to the circulation via lymphatics
 The formation of ISF is regulated according to the Starling hypothesis,
which incorporates 5 factors –
capillary hydrostatic pressure,
interstitial tissue pressure,
plasma oncotic pressure,
endothelial permeability and
lymphatic function.
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10.  The arterial hydrostatic pressure, in excess of tissue pressure, tends
to cause transudation of salt and water out of the capillaries
 The oncotic pressure of plasma proteins tends to draw fluid back
in.
 There is thus on overall loss of fluid from the capillary at its
arterial end, reabsorption at the venous end.
 About 15% of fluid accumulating in the interstitial space passes
into lymphatic vessels. From here, it passes into the general
circulation via the main lymphatic channels.
.
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11. • A low plasma oncotic pressure or increased hydrostatic pressure
at the venous end of capillary will tend to cause edema.
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12. Generalized Edema
• Na+ is the most important osmotically active constituent of the
ECF.
• The control of EFC volume ( & the formation of edema)
mainly control by the factors that regulate the accumulation of
Na+ in the body and excretion of Na+ by the kidneys.
• About 85% of filtered Na+ is reabsorbed in proximal
convoluted tubules.
• The remaining 15% is variably reabsorbed in the distal tubule,
partly with Cl- ions and partly in exchange for K + and H+ ions.
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13.  The regulation of sodium excretion is probably mainly
through adjustment of this 15%.
 'Aldosterone ' effects on distal renal tubule, causing Na+
reabsorption and K+ excretion.
 This effect is blocked by spironolactone.
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14. An important stimulus to aldosterone release comes from Renin-Angiotensin-Aldosterone
System.
Any fall in ECF volume (e.g- hypotension, hemorrhage or dehydration)
Simulate Juxtaglomerular Apparatus of Kidney
Renin secretion
ACE
Angiotensinogen Angiotensin I Angiotensin II
. (Liver) (Lung) 14
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15. Angiotensin II Stimulate "aldosterone" secretion from adrenal cortex
Vasoconstriction
Secretion of ADH by acting on hypothalamus
Final result is salt & water retentions.
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16. Generalized Edema
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17. Hypoproteinemic State
 The major part of plasma oncotic pressure can be attributed to its
albumin content.
 Hypoalbuminemia may be due to -
 failure of synthesis
 protein malnutrition (Kwashiorkor)
 cirrhosis
 long lasting ill-health from many causes
 increased loss as in nrephrotic syndrome.
 When serum albumin falls below 25 g/l, there is transudation of
solutes (mainly salt and water) out of the capillaries into intercellular
space.
 When this comportment is expanded by about 10%, clinically evident
edema appears.
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18. ↓ Plasma protein level
(esp. albumin)
↓oncotic pressure
• .
transudation of solutes
Edema
.
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19. Heart Failure Left Heart Failure
↓Cardiac output ↓Effective arterial blood volume
Accumulation of fluid in LV ↓Renal perfusion
Congestion of blood in LA RAA System activation
↑ADH
Congestion of blood in pulmonary veins ↑aldosterone
↑ Capillary hydrostatic pressure Salt & water retentions
Pulmonary edema Fluid overload
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20. Right Heart Failure
↓ Contraction of RV ↓Cardiac output from LV
Congestion of RA ↓Arterial Blood Volume
Congestion of SVC & IVC RAA System activation ↑ADH
↑Congestion in venules & capillaries Salt & Water retentions
Generalized Edema
.
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21. Passive congestion of "Liver“
Liver function
↓ Plasma protein synthesis
↓ Plasma oncotic pressure
Generalized Edema
 In Heart failure, unless the cardiac output is restored or renal sodium and
water retention is reduced (e.g.- diuretics, or aldosterone antagonists),
fluid retentions occurs and edema worsens. 21
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22. 22
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23. Nephrotic Syndrome
Heavy Proteinuria
Hypoalbuminuria
Leaky glomerular
capillary wall ↓Plasma oncotic pressure
Generalized edema
Fluid retention Hypervolemia
Salt & Water RAA system
Retention
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24. 24
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25. Cirrhosis
Cirrhosis
Nodule & fibrosis plasma protein synthesis
Sinusoidal hypertension ↓ oncotic pressure
Portal Hypertension Generalize Edema
Ascities
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26. 26
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27. Investigations of Generalized edema
 Chest X-ray - sign of heart failure, cardiomegaly
 Plasma albumin - low in nephrotic syndrome, cirrhosis,
malnutrition
 Blood urea and electrolytes - diminished GFR in renal
disease or in severe cardiac failure
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28. Localized edema
1. Oedema due to increased Permeability of
small Blood vessels
 Increased permeability is due to local release of
inflammatory mediators, e.g.-histamine, bradykinin , and
cytokines ,which cause vasodilation and increase
capillary permeability.
e.g. Acute inflammatory edema(e.g.-infection)
Allergic edema
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29. 29
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30.  Angio-edema is a specific form of allergic edema,
affecting face, lip & mouth.
 Swelling may develop rapidly and may be life-
threatening if upper airway is involved.
.
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31. (2)Lymphatic Obstruction
• Impaired lymphatic drainage result in edema (lymphedema).
• Lymph vessels have a large collateral circulation, so that , with
any block, edema extend over a wide area.
• Secondary cancer in lymph nodes may cause edema , but
usually the block is more extensive by dissection of nodes and
radiography, e.g.-in the treatment of breast cancer.
• In filariasis, lymphatic obstruction occurs due to the
widespread fibrosis in lymphatic channels caused by the adult
filarial worms.
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32. 32
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33. (3)Venous obstruction
Major cause - deep vein thrombosis, external pressure
from a tumor or pregnancy, or valvular incompitance.
 SVCO is caused by a tumor in superior mediastinum,
commonly lung cancer.
.
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34. 34
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35. Investigations of Localized edema
• Chest X-ray – SVCO
• Pelvic ultrasound or CT scan – pelvic tumor or lymphatic
enlargement
• Lymphangiography – abnormal lymphatic architecture,
lymph nodes replaced by tumor
• Doppler ultrasound or venography – to confirm diagnosis
of venous obstruction
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36. Examination of Edema
 Apply firm pressure with your thumb for at least 15 sec on
antero-medial aspect of shin. (Macleod’s)
 Finger pressure leaves temporary indentions in the skin
Pitting Edema
 Lymphoedema and myxoedema do not pit on pressure.
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37. References
• Macleod's Clinical Examination, 12th Edition
• Robbins and Cotran Pathologic Basis of Disease,8th Edition
• Davidson's Principles & Practice of Medicine, 21st Edition
• Tutorials in Differential Diagnosis, 4th Edition
• Dr. Daw Myint Myint Khin's Symptom Analysis
• Internet Websites.
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38. Case Discussion
Presented By Ma Kay Zin Soe

39. Patient’s History
Particulars of the patient
• A 64 year old, gentleman, U Hla Win, a bank manager,
was admitted to MU (II), MGH on 23.2.2013 with the
chief complaint of -
 Breathlessness for 3 months
 Swelling of the leg for 2 weeks
 Cough for 2 weeks

40. History of Present Illness
 Breathlessness- The patient complained of breathlessness for 3
months which worsen in cold weather and at night. He was not able
to lie flat (orthopnoea) and woke up at night due to difficulty in
breathing (PND). He was dyspnoeic at rest and couldn’t do light
works. (Dyspnoea on exertion) NYHA- grade IV
 Cough- The patient complained of dry cough sometimes with
sputum (white color). He became dyspnoeic after coughing and also
complained of wheezing.
 Swelling of the leg- He had swelling of the leg for 2 weeks. It started
from foot and progressed to the knee. There is swelling of the
abdomen.
 Associated symptoms- He has palpitation when hungry but no chest
pain.

41. System Review
• On reviewing respiratory system, he has cough sometimes with
sputum, dyspnoea, wheezing but no haemoptysis and chest pain.
• On reviewing gastrointestinal system, he has loss of appetite,
abdominal distension but no vomiting, nausea, indigestion,
heartburn, abdominal pain and change in bowel habit.
• On reviewing genito-urinary system, he has reduced urine output
but no dysuria and haematuria.
• There are no cardinal symptoms of central nervous system such as
headache, dizziness, faints, fits, altered sensation, weakness, visual
disturbance, hearing problems.
• On reviewing endocrine system, he has palpitation but neither fine
finger tremor nor eye signs.

42. Past Medical and Surgical History
• The patient has a history of tuberculosis in 1994 and
took proper medication. He has no history of
hospitalization, blood transfusion, rheumatic fever,
hepatitis, heart disease, diabetes mellitus and
hypertension.

43. Family History
• He is married and has 9 children. All are healthy. There is
no sign of similar illness in his family.

44. Drug History
• He has no regular taking drugs and no known drug
allergy.

45. Social History
• He had been smoking for about 30 years and betel
chewing for about 20years. He has a habit of alcohol
drinking.

46. Physical Examination
General Survey
• A 64 year old gentleman with average height and weight
is lying in his bed. He is well conscious and well
cooperated. He is rather dyspnoeic but not restless. (He is
given oxygen). A canular is inserted in the right hand. No
gynaecomastia and no spider naevi.

47. General Examination
• Forehead- febrile
• Eye-pallor (-), jaundice (+), subconjunctival hemorrhage
(-), xanthelesma (-), corneal arcus (+), features of
Horner’s syndrome
• Nose- nasal flaring (-), nasal polyp (-)
• Ear and nose discharge- discharge (-)
• Mouth- angular stomatitis (-)
• Lips- tobacco staining (-), pursed lip breathing (-)

48. • Tongue- central cyanosis (-), oral thrush (-)
• Teeth and gums- dental caries (+)
• Tonsillar enlargement (-)
• Neck- dilated veins (+), visible neck gland enlargement (-),
accessory muscles of respiration are working,
supraclavicular excavatum (+)
• Upper extremities- clubbing (+), peripheral cyanosis (-), pallor
(-), flapping tremor (-), features of CO2 retention (-), Osler’s
node (-), Janeway’s leision (-)
• Lower extremities- peripheral cyanosis (-), clubbing (+),
dependent oedema (+)

49. Systemic Examination
Cardiovascular System
Pulse
• Rate-68 beats/min
• Rhythm- regular
• Volume- moderate
• Character- no special character
• Condition of the vessel wall- not thickened
• Equality on both sides-equal on both sides
• Radio-femoral delay- no radio-femoral delay
• All peripheral pulses are intact
Blood pressure-100/ 70 mmHg
JVP-5.5cm above the sternal angle(raised)

50. Examination of the Precordium
• Inspection-shape of the chest is symmetrical on both side
and there is no precordial bulging. Diffuse precordial
pulsation is not seen. Apex beat not visible. There is no
epigastric pulsation. There is no scar, skin lesion, dilated
veins over the Precordium.

51. • Palpation- apex beat is palpable at left 5th ICS within the midclavicular line
with normal character and no thrill. There is no left parasternal heave. There is
no epigastric pulsation. There is palpable P2 but no palpable A2.
• Percussion- is omitted. (not pericardial effusion)
• Auscultation-
- At the MITRAL AREA-normal first and second heart sounds. No
added sound and no murmur.
- At the TRICUSPID AREA- normal first and second heart sounds. No
added sound and no murmur.
- At the PULMONARY AREA-normal first heart sound and loud
second heart sound. No added sound and no murmur.
- At the AORTIC AREA- normal first and second heart sounds. No
added sound and no murmur.

52. Signs of Congested Heart Failure
• Raised JVP(+)
• Bilateral fine basal crepitation (+)
• Dependent bilateral oedema (+)
• Enlarge tender liver (-)

53. Respiratory System
Lying position
• Inspection
-Shape of the chest is symmetrical on both sides.
Respiratory rate is 15 times/min.
-Chest wall movement is symmetrical on both sides.
-Apex beat is not visible.
-There is no scar, skin lesion, dilated veins. There is no
supraclavicular, suprasternal, intercostal, sub costal
muscles indrawing.

54. • Palpation- trachea is slightly deviated to right. Chest wall
movement is symmetrical on both sides. Vocal fremitus is
reduced on left lower zone. Palpable accompaniments are
absent.
• Percussion- normal resonance (+). Liver dullness starts at 5th
ICS. Cardiac dullness is from 2nd to 5th ICS.
• Auscultation- vesicular breath sound with ronchi is heard all
over the lungs' field. Vocal resonance is reduced on the left
lower zone.

55. Sitting position
• Inspection-shape of the chest wall is symmetrical on
both sides. Chest wall movements are equal on both
sides. There is a cyst on the right upper part of the back.
• Palpation-chest wall movements are symmetrical on both
sides. Vocal fremitus is reduced on the left lower zone.
• Percussion- normal resonance ispressent all over the
lungs' field.
• Auscultation- vesicular breath sound with bilateral
basal crepitation is heard. Vocal resonance is reduced
on the left lower zone.

56. Abdominal Examination
• Inspection- Contour is normal, flanks are full, abdomen
moves with respiration, no visible mass, no visible
peristalsis, no scar, skin lesions and dilated veins.
• Palpation- There is no tenderness and no palpable mass.
Liver and spleen are not palpable. Kidneys are not
blottable.
• Percussion-shifting dullness (+)
• Auscultation- Normal bowel sounds are present.

57. Differential diagnosis
 Generalize oedema and ascities are present, so this may be due
to
• Congested cardiac failure
• Acute glomerulonephritis
• Nephrotic syndrome
• Cirrhosis of liver
 The patients has clubbed fingers and ascites which are the
characteristics of cirrhosis of liver but no palmar erythema,no
spider naevi, no gynaecomastia, no splenomegaly,no
haematamesis, no malena. Therefore cirrhosis of liver is
excluded.

58.  The patient has no smoky urine(no proteinuria), no
haematuria. So, Nephrotic syndrome and acute
glomerulonephritis are excluded.
 And there is no weight loss, no diarrhea, and no steatorrhoea.
Therefore nutritional disorder is excluded.
 Signs of heart failure such as dyspnoea, orthopnoea, PND,
cough, ascites, ankle oedema are present.

59. Provisional Diagnosis
• Congested cardiac failure

60. Investigation
• ECG, Chest X-ray, Echocardiography,
• Blood for complete picture,
• Ultrasound abdomen,
• Urine REME,
• Serum electrolytes
• LFTs