Venous Ulcer



Fig. 10.1
(a) In a limb with normal venous pump, effects of exercise on calf volume and venous pressure measured on the dorsum of the foot. (b) Effects of exercise on calf volume and venous pressure measured on the dorsum of the foot in a patient with post-thrombotic syndrome and venous hypertension



Multiple hypotheses have been proposed for venous ulceration. Fibrin cuff theory states that there is leakage of fibrinogen in extravascular space, and over time pericapillary fibrin cuff is formed which causes ischemia of dermis making it prone for ulceration [8]. In another “leukocyte entrapment” theory, extravasation and activation of leucocytes has been given utmost importance, which further sets in a chronic inflammatory reaction [9].

Venous hypertension leads to extravasation of macromolecules and red blood cells, which further set in a secondary inflammatory reaction. Activated endothelial cells release vasoactive agents, inflammatory mediators, chemokines, express adhesion molecules, and prothrombotic precursors. Increased expression of ICAM-1, recruitment of leukocytes, and their endothelial transmigration leads to initiation of inflammatory cascades that have been regularly demonstrated in patients’ venous ulcers. There is increased production of cytokines (TGF-β1, TNF-α, IL-1) and increased MMPs that have been shown to be a key component of development, chronicity, and the delay of healing of venous ulcers [810].



10.3 Clinical Assessment (Figs. 10.2 and 10.3)




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Fig.10.2
Varicose veins in popliteal region


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Fig. 10.3
Varicose ulcer

Clinical assessment of patient with varicose veins should be carried out as outlined in Table 10.1. Additionally detailed examination of ulcer and surrounding is very important [11]. It is recommended to keep a photographic record of ulcers on every visit.


Table 10.1
Clinical evaluation










































































































































































































































































































































History

1. Basic details

 (a) Age:

  Younger, otherwise asymptomatic patients with family history: primary varicose veins

 (b) Female gender: hormonal factors

  (i) Primary: progesterone

  (ii) Induced: oral contraceptive pills, postmenopausal hormone replacement therapy

 (c) Occupation: disease of occupations involving prolonged standing

2. Chief complaints and history of present illness

Record symptoms and signs for each leg separately

 (a) Prominent veins:

  (i) Describe distribution of veins in patient’s language, i.e., inner side of thigh, outer side thigh, inner /outer/aspect of leg/behind knee

  (ii) Duration

  (iii) Unilateral/bilateral

  (iv) Associated symptoms: pure cosmetic or associated symptoms

  (v) Any history of bleeding from veins

 (b) Leg swelling:

  (i) Unilateral/bilateral

  (ii) In ankle region or in thighs as well

  (iii) Relation to long-standing posture

  (iv) Diurnal variation

 (c) Leg pain:

  (i) Anatomical distribution of pain

Most of patients with varicose veins have neurological claudication or knee joint disorder with associated asymptomatic varicose veins

  (ii) Pain score (0–10): document to compare with posttreatment pain scores

  (iii) Duration

  (iv) Ask leading question:

   Pain is in joints or in between joints (thigh/calf/leg)

   Lower back pain

   Multiple joint pains

Venous claudication

Venous claudication is defined as “bursting” thigh pain and “tightness” that develops during exercise in patients with iliofemoral venous thrombosis. Peripheral arterial disease is not a factor. The pathophysiology of venous claudication is related to the high outflow resistance associated with venous collaterals. Venous volume increases but proximal venous flow is unable to increase because of the fixed resistance of the collaterals, which results in the clinical syndrome

 (d) Itching:

  (i) Rule out localized itching due to skin disorder

  (ii) Check for ongoing skin disorder treatment

 (e) Night cramps:

  (i) Frequency

  (ii) Variation

 (f) Pigmentation:

  (i) Pattern

  (ii) Progression

 (g) Healed/active/recurrent ulcer

  (i) Total number of ulcers

  (ii) Mode of onset of ulcer: spontaneous/traumatic

  (iii) Duration of ulcer; if healed, how long it took

  (iv) In recurrent ulcers: total number of events

  (v) If active soakage present: how many times dressing has to be changed

3. Past history:

 (h) Previous DVT:

  (i) Direct evidence

   1. History of warf/acitrom intake

   2. Documented history of DVT

   3. History of regular INR monitoring

  (ii) Indirect evidence: especially if current symptoms started after the inciting event only

   1. History of acute onset painful swelling of lower limb in the past

   2. History of major orthopedic trauma/immobilization

   3. Major abdominal/neuro/ortho surgery

   4. Malignancy

 (i) History of breathlessness

  (i) Acute onset shortness of breath might be associated with episode of pulmonary embolism

  (ii) Chronic PE may result in pulmonary hypertension with secondary right heart failure

4. Treatment history

 (i) Oral contraceptive use

 (ii) Hormone replacement therapy

 (iii) Oral anticoagulants

5. Family history

6. Personal history

 (a) Smoking

7. Comorbidities

Always to be recorded in all vascular cases
 
(✓?⁄✘)

If yes: duration (years)

Diabetes
   

Hypertension
   

IHD
   

Smoking
   

Obesity
   

Chronic renal failure
   

Examination

Standing position in good light

(In presence of nurse when examining a female)

Inspection

1. Distribution of varicosities: GSV territory/SSV territory/other

 (a) Saphena varix: blow out at saphenofemoral junction—look for visible cough impulse (Morrissey’s sign)

 (b) Lateral vein in thigh associated with limb hypertrophy and port-wine stain: KT syndrome

 (c) Refluxing vein connecting GSV-SSV territory: Giacomini vein

 (d) Abdominal veins: rule out IVC obstruction

2. Obvious limb swelling

 (a) Differentiate from lymphedema (foot involvement)

 (b) Differentiate from lipedema

3. Skin changes:

 (a) Redness: local thrombophlebitis

 (b) Pigmentation: distribution in leg

 (c) Lipodermatosclerosis (LDS): localized chronic inflammation and fibrosis of skin and subcutaneous tissues of lower leg, sometimes associated with scarring or contracture of the Achilles tendon. LDS is sometimes preceded by diffuse inflammatory edema of the skin, which may be painful and which often is referred to as lipodermitis. LDS must be differentiated from lymphangitis, erysipelas, or cellulitis by their characteristically different local signs and systemic features

Try to pinch skin: in pigmentation it can be pinched easily whereas not in lipodermatosclerosis

 (d) Itching marks

 (e) Atrophie blanche (white atrophy)

  Localized, often circular whitish, and atrophic skin areas surrounded by dilated capillaries and sometimes hyperpigmentation. Sign of severe CVD, and not to be confused with healed ulcer scars. Scars of healed ulceration may also exhibit atrophic skin with pigmentary changes but are distinguishable by history of ulceration and appearance from atrophie blanche and are excluded from this definition

 (f) Corona phlebectasiae

  Fan-shaped pattern of numerous small intradermal veins on medial or lateral aspect of ankle and foot. Commonly thought to be an early sign of advanced venous disease. Synonyms include malleolar flare and ankle flare

 (g) Eczema: erythematous dermatitis, which may progress to blistering, weeping, or scaling eruption of skin of leg. Most often located near varicose veins but may be located anywhere in the leg. Usually seen in uncontrolled CVD but may reflect sensitization to local therapy

4. Characteristics of venous ulcer

 (a) Site: premalleolar and malleolar region of ankle

 (b) Superficial

 (c) Sloping edges

 (d) Healthy granulation tissue in base—if no infection

 (e) Exudative, weepy

 (f) Surrounding +/− skin maceration

 (g) Pigmentation and lipedermatosclerosis in surrounding skin

Also inspect

Scrotum for any obvious swelling

Groin for any lymph nodes

Abdomen for any previous abdominal surgery

Lateral aspect of thigh/knee for orthopedic procedures scar mark

Scar marks of any previous varicose vein surgery

Palpation

Feel the patient’s legs from ankle to the groin in standing position

 1. SF junction reflux:

  Place middle and index finger tips over cribriform fossa. Ask patient to externally rotate the examined limb and flex at the knee 5–10°. Ask patient to cough with face turned to opposite side. Feel for an impulse on your fingertips

 2. Schwartz test:

  In the above test, place the other hand’s index and middle finger at any point distal to SF junction in the anatomical course of GSV and feel the vibration transmitted by tapping at SF Junction. This indicates the level of serial valve incompetence in GSV starting from SF junction

 3. Trendelenburg test:

  Repeat the above in supine position and compress the SF junction and ask patient to rise into standing position and observe pattern of filling of distal veins

  Note: Trendelenburg test can be performed by tourniquet application at different levels to check reflux from SF junction, mid-thigh perforator, above-knee perforators, and below-knee perforators following the same principle as the above

 4. SP junction reflux:

  Place middle and index finger tips over popliteal fossa just above the knee crease. Ask patient to extend the knee. Ask patient to cough. Feel for an impulse on your fingertips

 5. Perforator “blowouts”(Fegan’s sign):

Feel along the course of GSV and SSV and palpate any prominent defect in fascia with prominent varicose bulge, which may signify perforator incompetence at that level

 6. Modified Perthes test:

  With patient in supine position, limb is elevated and a tourniquet is tied below the saphenofemoral junction. Patient is then asked to walk for 50 m. Deep venous outflow obstruction is suspected if there is GSV or SSV

  Varicosities or calf pain increase on walking

 7. Warning: please remember all this may be possible in thin patients, and may not be visible or palpable in obese patients

 8. Feel for thrill to rule out AV fistula

 9. Check for pedal edema

  (a) Pitting

  (b) Nonpitting

  (c) Brawny

 10. Palpate all peripheral arterial pulses and record ankle-brachial index

 11. Measurements

  (a) Height

  (b) Weight

  (c) Limb length

  (d) Limb circumference

   (i) Calf level: 10 cm below tibial tuberosity

   (ii) Thigh level: 15 cm above medial condyle of femur

 12. Pes equinus:

  Palpate and assess ankle movements: fixed flexion deformity is generally a contraindication for venous intervention

  Also palpate

   1. Groin for lymph nodes

   2. Abdominal/pelvic/testicular mass

   3. Direction of flow in abdominal veins, if present

Auscultation:

SF junction

SP junction

Bruit

C E A P classification (Fig. 10.4 )

Clinical classification

 C0: no visible or palpable signs of venous disease

 C1: telangiectasies or reticular v

 C2: varicose veins

 C3: edema

 C4a: pigmentation or eczema

 C4b: lipodermatosclerosis or atrophie blanche

 C5: healed venous ulcer

 C6: active venous ulcer

S: symptomatic, including ache, pain, tightness, skin irritation, heaviness, and muscle cramps, and other complaints attributable to venous dysfunction

A: asymptomatic

Etiologic classification

 Ec: congenital

 Ep: primary

 Es: secondary (post-thrombotic)

 En: no venous cause identified

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May 13, 2017 | Posted by in GENERAL SURGERY | Comments Off on Venous Ulcer
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