Reference : Harrison’s Principles of Internal Medicine, 20th Edition

1. APPROACH TO EDEMA
DR. HARISHMA RAMESH
1

2. EDEMA
‣ Soft tissue swelling due to abnormal
expansion of interstitial fluid volume.
‣ clinically apparent increase in the
interstitial fluid volume , which develops
when starling forces are altered so that
there is an increased flow of fluid from
the vascular system into interstitial.
2

3. STARLING FORCES AND FLUID EXCHANGE

4. STARLING FORCES AND FLUID EXCHANGE
4

5. ‣ Persistence of an indentation of the skin after
pressure - PITTING EDEMA
‣ In subtle form - edema is detected after the
stethoscope is removed from chest wall (the rim of the
bell leaves an indentation on the skin)
‣ When the ring on the finger fits more snugly than in the
past
‣ Patients complains of difficulty in putting shoes
(evening)
‣ Puffiness of the face - periorbital area
HOW TO RECOGNIZE EDEMA?
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6. 6
EDEMA
LOCALISED GENERALISED
usually due to venous or
lymphatic obstruction
(e.g., deep venous
thrombosis, tumor
obstruction, primary
lymphedema).
Soft tissue swelling of
most or all regions of
the body.

7. IF LOCALISED
DAMAGE TO
CAPILLARY
ENDOTHELIUM
Increase the permeability
Permits the transfer of proteins into
the interstitial compartment
Injury to the capillary wall can result
from:
Drugs
Viral or bacterial agents
Thermal or mechanical trauma
THE LOCAL PHENOMENON THAT MAY BE RESPONSIBLE SHOULD
BE CONSIDERED
7

8. IF LOCALISED
Damage to the capillary endothelium -
INFLAMMATORY EDEMA
Non pitting
Localised
(+) signs of inflammation - Calor, Rubor,
Tumor, Dolor
8

9. IF GENERALISED
1.CARDIAC
2.RENAL
3.HEPATIC
4.NUTRITIONAL DISORDERS
Responsible for majority of
patients with Generalised
edema
PRINCIPAL CAUSES SHOULD BE FOUND
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10. 10
1. EDEMA IN
CARDIAC DISEASE

11. As in heart failure, the effects of excess intrarenal and
circulating norepinephrine, angiotensin II, and aldosterone
lead to renal Na retention and worsening edema.
1. EDEMA IN
CARDIAC DISEASE

12. The presence of heart disease is manifested by
Cardiac enlargment
Ventricular hypertrophy
Evidence of cardiac failure - dyspnea, basilar rales,
venous distention and hepatomegaly
1. EDEMA IN
CARDIAC DISEASE
12

13. Nephrotic syndrome
Diminished colloid oncotic pressure - due to losses of large quantities of
protein (>3.5g/day)
With sever hypoalbuminemia (<2.5g/dl) + Reduced colloid osmotic pressure
Na and H2O retained
Cannot be restrained within the vascular compartment
Effective arterial blood volume decline
This initiates the Edema forming sequence
2.EDEMA IN
RENAL DISEASE

14. 2. EDEMA IN
RENAL DISEASE
Edema Results from primary retention of Na and
H2O by the kidney owing to the renal insufficiency
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EDEMA - DIFFUSE,
SYMMETRIC, PROMINENT
IN DEPENDENT AREAS,
PERIORBITAL EDEMA
(MORNING)

15. 3. EDEMA IN HEPATIC
CIRRHOSIS
Intrahepatic HTN acts as a stimulus for renal Na retention and
causes reduction of effective arterial blood volume.
These alteration are frequently complicated by
hypoalbuminemia secondary to reduced hepatic synthesis of
albumin, as well as peripheral arterial vasodilation.
These effects reduce the effective arterial blood volume
Leading to the activation of RAAS and renal sympathetic
nerves
Release - AVP, endothelia and Na.
Water retention

16. In later stages, particularly when there is severe
hypoalbuminemia, peripheral edema may develop.
A sizable accumulation of ascitic fluid may increase
intraabdominal pressure and impede venous return
from the lower extremities and contribute to the
accumulation of edema of the lower extremities.
Initially, the excess interstitial fluid is localized to the
congested portal venous system and obstructed
hepatic lymphatics,in the peritoneal cavity
ascites
3. EDEMA IN HEPATIC
CIRRHOSIS

17. 4. Edema of
nutritional origin
A diet grossly deficient in protein over a
prolonged period may produce hypoproteinemia
and edema.
Edema may actually become intensified – when
famished subjects are first provided with an
adequate diet.
The ingestion of more food may increase the
quantity of sodium ingested, which is then
retained along with water. – re-feeding edema
also may be linked to increased release of insulin,
which directly increases tubular sodium
reabsorption.

18. 5. Other causes of edema
‣ hypothyroidism (myxoedema)
‣ hyperthyroidism (pretibial myxedema
secondary to Graves’ disease).
‣ due to lymphocytic infiltration and
inflammation.
‣ pregnancy
‣ administration of estrogens and
vasodilators
‣ idiopathic edema

19. 5. Other causes of edema - Drug induced
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20. DISTRIBUTION OF EDEMA
U/L EDEMA
results of venous/ lymphatic obstruction
‣ U/L paralysis, thrombophlebitis, chronic
lymphangitis, filariasis, resection of regional
lymph node.
ASCITES
Severe Heart failure and hepatic cirrhosis
‣ JVP elevated in Heart failure, Normal in
cirrhosis
HEART FAILURE
‣ more extensive in legs and to be accentuated in the
evening (feature determined by posture)
‣ When heart failure patient are confined to bed, edema -
pre sacral region
KIDNEY
edema resulting from hypoprotenemia
in nephrotic syndrome
‣ generalised but evident in soft tissue
of eyelids and face
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23. Dietary Na restriction (<500 mg/d) may prevent further edema
formation.
Bed rest enhances response to salt restriction in CHF and cirrhosis.
Supportive stockings and elevation of edematous lower extremities
help to mobilise interstitial
fl
uid.
If severe hyponatremia (<132 mmol/L) is present, water intake also
should be reduced (<1500 mL/d).
TREATMENT
Primary management - identify and treat the
underlying cause of edema.
ADVICE
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24. REFERENCE: HARRISON’S PRINCIPLES OF INTERNAL
MEDICINE, 20TH EDITION
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