This document summarizes leg swelling (edema) and its various causes. It begins by defining edema and mechanisms that can cause it like increased capillary permeability or pressure. It then categorizes causes of edema as either central (bilateral) or local (unilateral). Specific conditions that can lead to edema like cardiac failure, nephrotic syndrome, filariasis, and deep vein thrombosis are described. The document provides details on clinical presentations and risk factors for different types of edema.

1. Moderator:
Dr P P Dhar
Asstt. Prof
Deptt of surgery, smch
Seminar on
Leg swelling & it’s causes
Presenter
Biswajit Deka
2nd year PGT
Deptt of surgery

5. Edema
• Collection of fluid in the interstitial spaces or serous cavities.
• Becomes evident only when 5-6 litres of fluid has
accumulated in the water depots
• Pitting on pressure occurs when the circumference of the
limb is increased by 10%

6. Mechanism
• Increased capillary permeability when it is damaged.
(Acute inflammation)
• Increased capillary pressure, (Cardiac failure)
• Decreased osmotic pressure of blood (hypoproteinemia)
• Damaged lymphatic drainage (filariasis)

7. Causes
CENTRAL (Bilateral)
A. Cardiac : CCF , pericarditis
B. Renal : acute nephritis , nephrotic syndrome
C. Hepatic : cirrhosis, portal HTN
D. Venous : IVC obstruction

8. Contiue…
E. Endocrine : Myxedema
F. Allergic : angioneurotic edema
G. Nutritional : anemia , hypoproteinemia , beri beri
H. Toxic : epidemic dropsy

9. I . Drugs : corticosteroids, estrogen, progesterone,
MAO inhibitor, phenylbutazone , methyl-dopa ,
hydralazine, nifedipine
J . . Retroperitoneal fibrosis
K . Obesity : lipodystrophy , lipoidosis
L . Hemarthrosis , calf mascle hematoma , myositis ossificans

10. LOCAL (Unilateral)
A. Lymphatic
I. Filariasis
II. Pressure from growth / tumour
III. Radiation
B. Traumatic : bruises, fractures , sprains ,achilles tendon rupture
C. Infections : cellulitis
D. Metabolic : gout

11. E . Venous : DVT
Post thrombotic syndrome
varicose veins
Klippel trenaunay syndrome
external venous compression
ischemia reperfusion
F . Arterial : AV malformation
aneurysm
G . Hereditary : Milroy’s disease

12. UNILATERAL EDEMA
Painless Painful
Onset
From birth Late onset
Mllroy‘s
Disease
Filariasis
Involve only
Big toe with
Tophi
Gout
Part of the
limb afected
and painful
Cellulitis
Filariasis Venous
Thombosis
Absentpresent
Linear and
streaks
Involves the
whole limb

13. BILATERAL EDEMA
With
lossof
weight,
Cachexia
Starvation
Edema feetWith Ascites
Hypertension
Hematuria
Proteinuria
With puffy face
Malnutrition,
PEM,
Kwarshiorkor
Nephritic
syndrome
Dialated veins
over chest and
abdomen Idiopathic
JVP raised
Ascites
Hepatomegaly
Polyarthritis
LVF Diuratic
induced
Constipation
Rough skin
Hoarsevoice
Pitting
Sudden onset
Wheezing
Itching
Generalise
d without
any cause
Angio-
neurotic
Edema
Myxedem
Hypoproteinemia,
Hyperlipidemia,
Proteinuria,
Lipiduria
Nephritic
syndrome
JVP raised
Chest signs
Massive
edema feet
Splenomegaly
Pericardial
Effusion
Portal
Hypertension
Inferior Vena
Cave
Obstruction
Present AbsentPresent
only left
limb
H/O
Diureti
c intake
Cariac
Failure
Nutritional
Onset
DRUGS CAUSING EDEMA
Calcium Channel blockers
Estrogens
Steroids
Carbenoxolone

14. Clinical Spectrum of Venous thromboembolism
• Deep venous thrombosis (uncomplicated)
• Phlegmasia alba dolens
• Phlegmasia cerulea dolens
• Venous gangrene
• Pulmonary embolism
• Isolated distal deep venous thrombosis
Only 40% of ambulatory ED patients with PE have concomitant DVT

15. Phlegmasia alba dolens
§ AKA ”Milk/White Leg"
§ Massive iliofemoral occlusion
§ spares collateral veins
§ lack of venous congestion

16. Phlegmasia cerulea dolens
§Painful Blue Leg"
§Massive iliofemoral occlusion
§Extensive vascular congestion and venous ischemia
§

17. Risk factors
• Age 50-60s
• Malignancy (20-40%)
• Idiopathic (10%)
• Inherited thrombophilia
• Pregnancy
• Trauma/surgery
• IVC filter

18. Filariasis
§ Nematodes – Wuchereria bancrofti (90%)
Brugia mayayi
Brugia timori
§ Infection occurs in lymphatic systems, connective tissues & serous cavities
§ Adults seen in lymphatic vessels
§ Off springs seen in peripheral blood during night
§ Larva & microfilaria : not pathogenic

19. Stages of pathogenesis
• Dilatation of lymphatic vessels
• Infection of lymphatics (lymphangitis)- due to mechanical
irritation & toxins from matabolisim & dead larva
• Obstruction of the nodes and lymphatics

20. Causes of lymphatic obstruction
• Machanical blocking by dead worms
• Obliterative endolymphangitis : endothelial proliferation &
inflammatory thickening of walls of lymphatic vessles
• Excessive fibrosis of lymphatic vessles
• Fibrosis of afferent lymph nodes

21. Cellulitis
• An acute , diffuse, spreading infection of the skin,
involving deeper layers of the skin and
the subcutaneous tissue
• Causes : staph ,
streptococcus group A,B
pseudomonas
klebsiella

22. Varicose veins
• Subcutaneous dilated veins 3mm in diameter or larger
• Dilated ,Elongated and tortuous with intermittent blowouts

23. Baker’s cyst (ruptured)
• It is a distended bursa or herniation of synovial membrane through the
posterior part of capsule of the knee or escape of fluid through normal
communication of bursa with the knee.
• MC : 4-7yrs and 35-70 yrs
• Adults > children

24. Lymphedema
• It is abnormal limb swelling caused by the accumulation of increased amounts of
high protein ISF secondary to defective lymphatic drainage in the presence of
(near) normal net capillary filtration.
• Incidence : 1/6000 live birth
• Overall prevalence : 0.13-2%
• Primary : cause unknown
(congenital lymphatic dysplasia)
• Seconadary : clear underlying cause

25. Radiation
• Fibrosis of lymphatics

26. DVT
the classical signs of pain & redness may be absent

27. Myxedema ,Hypothyroidism , Hyperthyroidism

28. • Myxedema is a specific form of cutaneous and dermal edema secondary to
increased deposition of connective tissue components.
• The connective fibres are separated by an increased amount of protein and
mucopolysaccharides.
• These can include glycosaminoglycans, hyaluronic acid, chondroitin sulfate
and other mucopolysaccharides.
• This protein-mucopolysaccharide complex binds water, producing non-
pitting boggy edema,

29. Mechanism for deposition of GAGs
A . Fibroblast stimulation : It is thought that fibroblast stimulation by
the TSH receptor increases the deposition of glycosaminoglycan,
which results in an osmotic edema and fluid retention.
• It is thought that many cells responsible for forming connective tissue
react to increases in TSH levels.[

30. B. Lymphocyte stimulation: In Graves' thyroid disease, lymphocytes react
against the TSH receptor by inappropriately producing thyroid-
stimulating immunoglobulin (IgG; type II hypersensitivity).
• Lymphocytes react not only against thyroid receptors, but also any
tissue with cells expressing the receptor.
• This can lead to tissue damage and scar tissue formation, explaining the
deposition of glycosaminoglycans

31. Klippel-Trenaunay’s syndrome
• Rare , AGGF1 mutation
• Present at birth or develops in early childhood
• Comprises an abnormal lateral venous complex, capillary naevus,
bony abnormalities, hypo/aplasia of deep veins & limb lengthening
• Lymphatic abnormalities often coexist

33. Milroy's disease
• Autosomal dominant (gene FLT 4 –codes VEGFR 3)
• characterized by lymphedema(legs) caused by congenital abnormalities
in the lymphatic system.
• Disruption of the normal drainage of lymph leads to fluid accumulation
and hypertrophy of soft tissues.
• It is also known as Milroy disease, Nonne-Milroy-Meige
syndrome and hereditary lymphedema.

34. Milroy’s disease

35. Post thrombotic syndrome
• Swelling, usually of the whole leg, d/t iliofemoral venous
obstruction
• Comprises of skin changes , secondary varicose veins on the leg
and collateral veins on the lower abdominal wall
• Venous claudication may be present