Oedema

Table of Contents

Definition of edema

edema may be defined as abnormal and excessive accumulation of “free fluid” in
the interstitial tissue spaces and serous cavities.

Types of edema

The edema may be of 2 main types on the basis of location:

  • Localised when limited to organ or limb e.g. lymphatic edema, inflammatory edema, allergic edema.
  • Generalised (anasarca or dropsy) when it is systemic i distribution, particularly noticeable in the subcutaneous tissues e.g. renal edema, cardiac edema, nutritional edema.

There are 2 types of edema on the basis of fluid filled edema 

  1. pitting edema 
  2. non – pitting edema

There are a few special forms of edema .Depending upon fluid composition, edema fluid may
be:

  • Transudate which is more often case, such as in edema of cardiac and renal disease; or
  • Exudate such as in inflammatory edema.
Types of oedema

Pathogenesis of Oedema

Oedema is caused by mechanisms that interfere with normal fluid balance of plasma, interstitial fluid and lymph flows. The following mechanisms may be operating singly or in combination to produces  oedema:

  • Decreased plasma oncotic pressure
  • Increased capillary hydrostatic pressure
  • Lymphatic obstruction
  • Tissue factors (increased oncotic pressure of interstitial
    fluid, and decreased tissue tension)
  • Increased capillary permeability
  • Sodium and water retention.

Causes of oedema 

  • Allergic reaction, urticaria, and angioedema
  • Cardiac disease
  • Hepatic disease
  • Renal disease
  • Malabsorption/protein-calorie malnutrition
  • Obstructive sleep apnea
  • Pregnancy and premenstrual oedema
  • Cellulitis
  • Chronic venous insufficiency
  • Compartment syndrome
  • Complex regional pain syndrome type 1 (reflex sympathetic dystrophy)
  • Deep venous thrombosis
  • Iliac vein obstruction
  • Lipedema
  • Lymphedema(lymphedema Primary: congenital lymphedema,
    lymphedema praecox, lymphedema tarda )
  • Secondary: from axillary lymph node dissection, surgery (e.g., coronary artery bypass graft, inguinal lymphadenectomy) trauma, tumor, radiation, filariasis
  • May-Thurner syndrome (compression of left iliac vein by right iliac artery)

Pathogenesis and Morphology of important types of edema

Renal Oedema

    • edema in nephrotic syndrome

The nephrotic edema is classically more severe and marked and is present in the subcutaneous tissues as well as in the visceral organs. The affected organs is enlarged and heavy with tense capsule.

Microscopically

The oedema fluid separates the connective tissue fibres of subcutaneous tissues. Depending upon protein content, the oedema fluid may appear homogeneous, pale, eosinophilic, or may be deeply eosinophilic and granular.

    • Oedema in nephritic syndrome

Oedema occurs in condition with diffuse glomerular disease such as in acute diffuse glomerulonephritis and rapidly progressive glomerulonephritis (nephritic oedema). The nephritic oedema is usually mild as compared to nephrotic oedema and begins in  loose tissues such as on
the face around eyes, ankles and genitalia. edema in these conditions is usually not affected by gravity.

    • Oedema in acute tubular injury

Acute tubular injury following shock or toxic chemical results in gross edema of  body.

Cerebral Oedema

Cerebral oedema or swelling of brain is most threatening
example of edema. Cerebral oedema can be of 3 types:

VASOGENIC OEDEMA

Vasogenic edema is prominent around cerebral contusions, infarcts, brain abscess and some tumors.

Grossly, the white matter is soft, swollen,  with flattened gyri and narrowed sulci.

Microscopically, there is separation of tissue elements by oedema fluid and swelling of astrocytes. The perivascular (Virchow-Robin) space is widened and clear halos are seen around small blood vessels.

CYTOTOXIC OEDEMA

In this type, the blood-brain barrier is intact and the fluid accumulation is intracellular, occurs in some metabolic derangements, acute hypoxia and with some toxic chemicals.

Microscopically, the cells are swollen and vacuolated. In  situations, both vasogenic as well as cytotoxic cerebral oedema results e.g. in purulent meningitis.

INTERSTITIAL OEDEMA

This type of cerebral oedema occurs when excessive fluid crosses the ependymal lining of  ventricles and accumulates in periventricular white matter.

Hepatic Oedema

Oedema of legs and ascites in cirrhosis of liver is as under:

  • There is hypoproteinemia due to impaired synthesis of proteins by the diseased liver
  • Due to portal hypertension, there is increased venous pressure in abdomen, and hence raised hydrostatic pressure.
  • Failure of inactivation of aldosterone in diseased liver and hence hyperaldosteronism
  • Secondary stimulation of renin-angiotensin mechanism promoting sodium and water retention.

Nutritional Oedema

Oedema due to nutritional deficiency of proteins ( prolonged starvation, famine, fasting), vitamins (beri-beri due to vitamin B1 deficiency) and chronic alcoholism occurs on
legs but sometimes may be more generalised.

Myxedema

Myxedema from hypothyroidism is a form of non-pitting oedema occurring on skin of face and other parts of the body as also in the internal organs due to excessive deposition of glycosaminoglycans in the interstitium.

Pitting edema, bilateral, as observed in a patient with congestive heart failure.
Pitting edema, bilateral, as observed in a patient with congestive heart failure.

Diagnosis  of Common Causes of Localized oedema


Unilateral predominance( means in one side of body) 

Bilateral predominance (means both side of body )

Onset and locationExamination findings
Chronic venous
insufficiency
Onset: chronic; begins in
middle to older age
Location: lower
extremities; bilateral
distribution in later
stages
Soft, pitting oedema
with reddish-hued
skin; predilection for
medial ankle/calf.
Associated findings:
venous ulcerations
over medial malleolus;
weeping erosions
Complex regional
pain syndrome
type 1 (reflex
sympathetic
dystrophy)
Onset: chronic; following
trauma or other inciting
event
Location: upper or lower
extremities; contralateral
limb at risk regardless of
trauma
Soft tissue oedema distal
to affected limb
Associated findings:
(early) warm, tender
skin with diaphoresis;
(late) thin, shiny skin
with atrophic changes
DVTOnset: acute
Location: upper or lower
extremities
Pitting oedema with
tenderness, with or
without erythema;
positive Homans sign
LymphedemaOnset: chronic; insidious;
often following
lymphatic obstruction
from trauma or surgery
Location: upper or lower
extremities; bilateral in
30% of patients
Early: dough-like skin;
pitting
Late: thickened,
verrucous, fibrotic,
hyperkeratotic skin
Associated findings:
inability to tent skin
over second digit,
swelling of dorsum
of foot with squared
off digits, painless
heaviness in extremity
LipedemaOnset: chronic; begins
around or after puberty
Location: predominantly
lower extremities;
involves thighs, legs,
buttocks; spares feet,
ankles, and upper torso
Nonpitting oedema;
increased distribution
of soft, adipose tissue
Associated findings:
medial thigh and
tibial tenderness; fat
pad anterior to lateral
malleoli
Medicationinduced oedemaOnset: weeks after
initiation of medication;
resolves within days
of stopping offending
medication
Location: lower
extremities
Soft, pitting oedema
Obstructive sleep
apnea
Onset: chronic
Location: lower
extremities
Mild, pitting oedema
Associated findings:
daytime fatigue,
snoring, obesity

Diagnostic testing

  • Ultrasonography
  • lymphoscintigraphy
  • MRI

Management of oedema

Management of oedema should be on the basis of etiology .

Chronic venous insufficiency

1. Mechanical therapies, including leg elevation and compression stockings with 20 to 30 mm Hg for mild edema and 30 to 40 mm Hg for severe edema
complicated by ulceration, are recommended.

2.Compression therapy is contraindicated in patients with peripheral arterial disease. A study of 120 patients with venous ulcers showed that 6% had mixed arterial-venous ulcers.

3. Treatment includes daily hydration with emollients and short courses of topical steroid creams for severely inflamed skin.

lymphedema

1. Treatment includes compression stockings at 30 to 40 mm Hg.

2.Pneumatic compression devices have been shown to augment standard therapies. Women with breast cancer– related lymphedema showed statistically significant improvement in lymphatic function following one hour of pneumatic compression therapy.In a study of 155
patients with cancer- and non–cancer-related lymphedema, 95% of patients noted reduction in limb oedema
after using pneumatic compression devices at home.

3.Diuretics do not have a role in the treatment of lymphedema.

DVT(Deep venous thrombosis ) 

Anticoagulation therapy (unfractionated or low-molecular-weight heparin or warfarin [Coumadin]).Anticoagulation, compression stockings should be used after a DVT to prevent post thrombotic syndrome. 

Acute deep venous thrombosis with overlying cellulitis.
Acute deep venous thrombosis with overlying cellulitis.
Medication-induced oedema

 In patients taking calcium channel blockers to treat hypertension, use of angiotensin-converting enzyme inhibitor may be more beneficial than angiotensin receptor blocker therapy in reducing calcium channel blocker–induced peripheral oedema.

Other causes

1.There is no treatment for lipedema. Weight loss does not affect this condition.

2. Complex regional pain syndrome is treated with physical therapy in combination with medications such as systemic steroids and tricyclic
antidepressants.

3.Obstructive sleep apnea is treated with positive pressure ventilation.

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