What is Edema, causes and formation

Swelling of lower extremity

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Swelling of lower extremity

Total body water is divided between the intracellular and extracellular spaces. The extracellular space, which comprises about one third of total body water, is composed of the intravascular plasma volume (25%) and the extravascular interstitial space (75%).

The lymphatic system collects fluid and filtered proteins from the interstitial space and returns them to the vascular compartment. Major perturbations in this delicate homeostasis that favors net filtration out of the vascular space, or impaired return of fluid by lymphatics from the interstitial space, will result in edema.

Edema is defined as a palpable swelling caused by an increase in interstitial fluid volume. Edema, other than localized edema, does not become clinically apparent until the interstitial volume has increased by 2.5 to 3 liters.

What is Edema, causes and formation

Starling Forces

Increased venous pressures due to central or regional venous obstruction or to an expansion in plasma volume are transmitted to the capillary bed, thereby increasing hydrostatic pressure and predisposing to edema. Conversely, local auto regulation by smooth muscle sphincters on the pre-capillary (or arterial) side protect the capillary bed from increases in systemic arterial pres-sure, which explains why hypertensive patients do not have edema despite elevated blood pressure.

The major contributors to interstitial oncotic pressure are mucopolysaccharides, filtered proteins such as albumin, capillary wall protein permeability, and the rate of lymphatic clearance. Changes in capillary wall permeability are mediated by cytokines such as tumor necrosis factor, interleukin 1, and interleukin 10, as well as by circulating vasodilatory prostaglandins and nitric oxide. Increased vascular permeability is central to edema resulting from local inflammation (e.g., insect bites), allergic reactions, and burns.

Causes of Edema

  • Increase in intravascular pressure
  • Increase in capillary vessel wall permeability
  • Decrease in the intravascular osmotic pressure
  • Excess bodily fluids
  • Lymphatic obstruction
  • Local injury
  • Infection
  • Medication effect

Acute and chronic lower extremity edema

Acute and chronic lower extremity edema present important diagnostic and treatment challenges. Lower extremities can swell in response to increased venous or lymphatic pressures, decreased intravascular oncotic pressure, increased capillary leak, and local injury or infection.

Chronic venous insufficiency is by far the most common cause, affecting up to 2% of the population, and the incidence of venous insufficiency has not changed during the past 25 years. Venous insufficiency is a common complication of DVT; however, only a small number of patients with chronic venous insufficiency report a history of this disorder.

Venous ulceration commonly affects patients with chronic venous insufficiency, and its management is labor-intensive and expensive. Normal lower extremity venous pressure (in the erect position: 80 mm Hg in deep veins, 20–30 mm Hg in superficial veins) and cephalad venous blood flow require competent bicuspid venous valves, effective muscle contractions, normal ankle range of motion, and normal respiration. When one or more of these components fail, venous hypertension may result.

Chronic exposure to elevated venous pressure by the post-capillary venules in the legs leads to leakage of fibrinogen and growth factors into the interstitial space, leukocyte aggregation and activation, and obliteration of the cutaneous lymphatic network.

Unilateral lower extremity edema

Among common causes of unilateral lower extremity swelling, DVT is the most life-threatening. Clues suggesting DVT include a history of cancer, recent limb immobilization, or confinement to bed for at least 3 days following major surgery within the past month. Lower extremity swelling and inflammation in a limb recently affected by DVT could represent anti-coagulation failure and thrombus recurrence but more often are caused by postphlebitic syndrome with valvular incompetence.

Other causes of a painful, swollen calf include cellulitis, musculoskeletal disorders (Baker cyst rupture (“pseudothrombophlebitis”), gastrocnemius tear or rupture, calf strain or trauma, and left common iliac vein compression (May-Thurner syndrome), as well as other sites of non thrombotic venous outflow obstruction, such as the inguinal ligament, iliac bifurcation, and popliteal fossa.

Bilateral lower extremity edema

Bilateral involvement and significant improvement upon awakening favor systemic causes (eg, venous insufficiency) and can be a presenting symptom of volume overload (HF, cirrhosis, kidney disease (eg, nephrotic syndrome). The sensation of “heavy legs” is the most frequent symptom of chronic venous insufficiency, followed by itching. Chronic expo-sure to elevated venous pressure accounts for the brawny, fibrotic skin changes observed in patients with chronic venous insufficiency as well as the predisposition toward skin ulceration, particularly in the medial malleolar area. Pa in, particularly if severe, is uncommon in uncomplicated venous insufficiency.

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Lower extremity swelling is a familiar complication of therapy with calcium channel blockers (particularly felodipine and amlodipine), pioglitazone, gabapentin, and minoxidil. Prolonged airline flights (longer than 10 hours) are associated with edema even in the absence of DVT. Lymphedema and lipoedema are other causes of bilateral lower extremity edema.

Diagnosis

Patients without an obvious cause of acute lower extremity swelling (eg, calf strain) should have an ultrasound per-formed, since DVT is difficult to exclude on clinical grounds. A prediction rule allows a clinician to exclude a lower extremity DVT in patients without an ultrasound if the patient has low pretest probability for DVT and a negative sensitive D-dimer test (the “Wells prediction rule”).

Assessment of the ankle-brachial pressure index (ABPI) is important in the management of chronic venous insufficiency, since peripheral arterial disease may be exacerbated by compression therapy. This can be performed at the same time as ultrasound.

Caution is required in interpreting the results of ABPI in older patients and diabetics due to the decreased compressibility of their arteries. A urine dipstick test that is strongly positive for protein can suggest nephrotic syndrome, and a serum creatinine can help estimate kidney function.

Treatment

Treatment of lower extremity edema should be guided by the underlying cause. Edema resulting from calcium channel blocker therapy responds to concomitant therapy with ACE inhibitors or angiotensin receptor blockers.

In patients with chronic venous insufficiency without a comorbid volume overload state (eg, HF), it is best to avoid diuretic therapy. These patients have relatively decreased intravascular volume, and administration of diuretics may first enhance sodium retention through increased secretion of renin and angiotensin and then result in acute kidney injury and oliguria.

Instead, the most effective treatment involves (1) leg elevation, above the level of the heart, for 30 minutes three to four times daily, and during sleep; (2) compression therapy; and (3) ambulatory exercise to increase venous return through calf muscle contractions. There is no evidence for benefit or harm of valvuloplasty in the treatment of patients with deep venous insufficiency secondary to primary valvular incompetence.

A wide variety of stockings and devices are effective in decreasing swelling and preventing ulcer formation. They should be put on with awakening, before hydrostatic forces result in edema. To control simple edema, 20–30 mm Hg is usually sufficient, whereas 30–40 mm Hg is usually required to control moderate to severe edema associated with ulcer formation.

To maintain improvement, consider switching from an elastic stocking to one made of inelastic grosgrain material. Patients with decreased ABPI should be managed in concert with a vascular surgeon. Compression stockings (12–18 mm Hg at the ankle) are effective in preventing edema and asymptomatic thrombosis associated with long airline flights in low- to medium-risk persons.

Self-management

Positioning in bed

• Lying in bed with your legs elevated is the best position to help reduce swelling.

• It is best to lie on your back.

• Elevate your legs above the level of your heart, while keeping your upper body flat.

• If you have a hospital bed, you can do this by elevating the foot of the bed.

• If you are in a regular bed, use pillows to elevate each leg. Place the pillows lengthwise under each leg. Use as many pillows as needed to elevate your legs above the level of your heart.

Positioning when sitting

• When sitting in a chair, use a stool to elevate your legs. You can place pillows on top of the stool if needed for higher elevation.

Positioning when standing

• Walking activates your muscles and helps get fluid moving.

• Avoid standing still for a long time, as this will increase swelling. Try walking around or marching on the spot. While you are standing, move your toes up and down to keep the fluid moving.

• You may use a compression bandage, stockings or a pressure garment when standing or walking to reduce fluid build-up in your ankles. Talk to your occupational therapist or physiotherapist about which type of compression garment or bandage would be best for you.

• After walking or standing for a period of time, return to a chair or bed and elevate your legs as described above.

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