Varicose Veins (Chronic Venous Insufficiency)

Chronic venous insufficiency (CVI) is failure of the leg veins to return blood to the heart efficiently, most often because the one-way valves within the superficial, deep, or perforating venous system become incompetent and allow retrograde flow (reflux). Under normal conditions, walking activates the calf-muscle pump — sometimes called the "second heart" — which drops ambulatory venous pressure from roughly 80-100 mmHg at rest (standing) to about 30 mmHg with each step. When valves fail, this normal pressure drop does not happen: pressure stays elevated throughout activity, and this sustained ambulatory venous hypertension is the single mechanism underlying every downstream manifestation covered in this chapter, from a visible varicosity to a venous ulcer.^[1]

Three distinct hemodynamic abnormalities can each produce this picture, alone or in combination: valvular reflux (the dominant mechanism, associated with obesity, multiple pregnancies, prolonged standing or sitting, and a history of prior varicose-vein stripping), obstruction (most often a history of deep vein thrombosis, or an anatomic variant such as May-Thurner syndrome), and failure of the calf-muscle pump itself (reduced ankle range of motion from arthritis or prior joint injury, or a shuffling gait from a condition such as Parkinson disease).^[1] Leg changes associated with venous disease are present in an estimated 10-35% of adults; this can progress to venous leg ulceration, which affects roughly 1% of the general population and rises to about 4% of adults over 65.^[1]

This chapter treats compression therapy as its genuine centerpiece — it is the single intervention that most directly reduces ambulatory venous hypertension, and correct compression-class selection, fit, and counselling is one of the most common, practical, and consequential encounters a community pharmacist has with this condition. It is paired with an equally central safety point that is easy to overlook in a busy retail encounter: peripheral arterial disease (PAD) must be screened for — typically via ankle-brachial pressure index (ABI) — before standard high compression is recommended, since applying strong compression over a limb with inadequate arterial inflow can precipitate genuine tissue ischemia. The CEAP classification (Clinical-Etiology-Anatomy-Pathophysiology), detailed in Recognize the Condition, provides the staging framework used throughout the rest of this chapter to match compression class, drug adjuncts, and procedural escalation to disease severity.^[2][1]

Prominent varicose veins on the lower leg — the visible, palpable, tortuous superficial veins that define CEAP class C2. (Jackerhack, CC BY-SA 2.5, Wikimedia Commons)

Symptom spectrum

Symptoms are related to venous congestion and skin changes, and classically worsen through the day, with prolonged standing, and in heat, improving with rest and leg elevation: heaviness, fatigue, throbbing, cramping, burning or aching, itchiness of the skin, and a restless-legs-like discomfort.^[1] Many patients with visible varicosities are entirely asymptomatic and present purely for cosmetic reasons; others with only mild-appearing veins report disproportionate symptom burden — the CEAP clinical class (below) and the symptom burden do not always move together.

The CEAP Clinical Classification — a genuine, usable staging framework

CEAP is the international consensus system for describing chronic venous disorders, and while it has not been correlated with treatment outcomes directly, its clinical (C) component is genuinely useful in practice as the framework this chapter uses throughout to match compression class and treatment intensity to disease severity.^[2][1]

Physical findings across the spectrum

Stasis dermatitis versus cellulitis — a genuinely important distinction

Contact dermatitis (irritant in about 80% of cases, allergic in about 20%) is common in patients using multiple topical products on already-compromised skin; common allergens include lanolin, neomycin, latex, and preservatives in creams and dressing adhesives.^[1]

Venous versus arterial ulcer — feeds directly into the PAD-screening safety point below

Mixed arterial-venous disease is genuinely common — approximately 15-25% of patients with venous disease also have some degree of arterial insufficiency — which is exactly why every patient needs an objective ABI rather than relying on this table (or a palpated pulse) alone.^[1]

Risk factors map onto the three hemodynamic mechanisms described in Clinical Snapshot.^[1]

Valvular reflux

• Obesity
• Multiple pregnancies (mechanical compression of pelvic veins plus hormonally mediated venous wall relaxation)
• Prolonged standing or sitting, whether occupational or recreational
• A prior history of varicose-vein stripping — recurrence is common
• Older age (prevalence and severity both rise with age, particularly past 55) and female sex
• Family history and, rarely, genetic connective-tissue conditions (e.g., Ehlers-Danlos syndrome, Klippel-Trénaunay syndrome)

Obstruction

• A history of deep vein thrombosis (post-thrombotic syndrome)
• May-Thurner syndrome (anatomic compression of the left common iliac vein) — consider in a young woman with unexplained left-leg-predominant chronic swelling

Calf-muscle pump failure

• Reduced ankle range of motion from arthritis, prior joint surgery, or trauma — normal calf-pump function needs a mobile ankle and at least about 10 degrees of dorsiflexion
• An abnormal gait pattern, particularly a shuffling gait, as seen in Parkinson disease and other neurologic conditions affecting mobility
• General immobility or a sedentary lifestyle

Additional considerations

• Smoking — not itself a direct CVI risk factor, but a major driver of concurrent peripheral arterial disease, which is exactly what makes the ABI-screening step in Choose Initial Treatment non-negotiable rather than a formality.
• Diabetes — both a PAD risk factor and, independently, a cause of falsely elevated (non-compressible) ABI readings that can mask true arterial disease (see Assessment & Diagnosis).

History

Cover the risk factors above, any personal history of DVT or venous surgery/procedures, current medications, and comorbidities most relevant to safe compression use — diabetes, peripheral arterial disease, heart failure, and any prior arterial intervention.

Physical examination

Examine both limbs for the physical findings described in Recognize the Condition, palpate femoral, popliteal, dorsalis pedis, and posterior tibial pulses, and assess gait and ankle range of motion (calf-muscle-pump screening). A skilled clinician should not rely on pulse palpation alone: the dorsalis pedis pulse is absent as a normal anatomic variant in roughly 8% of healthy adults, so an impalpable pulse alone neither confirms nor excludes arterial disease — an objective ABI is what actually answers the question.^[1]

Ankle-brachial pressure index (ABI) — the gate before any compression recommendation

ABI measurement is recommended in every patient being considered for compression, and is the single most important safety test in this entire chapter.^[1][3]

Duplex ultrasound

Duplex is the reference-standard investigation for confirming venous reflux and/or obstruction, and is used both to complete the anatomic (A) and pathophysiologic (P) components of CEAP staging and to plan any procedural intervention. A reflux duration of 1 second or more in the deep veins, or 0.5 seconds or more in the superficial or perforator veins, is diagnostic of venous insufficiency at that site.^[1][4] Duplex also reliably distinguishes acute venous thrombosis from chronic venous changes and evaluates arterial flow-limiting lesions where relevant.

Calf-muscle-pump screening

Because calf-pump failure is one of the three core hemodynamic mechanisms, screening for it is a genuine part of the assessment, not an afterthought: assess ankle dorsiflexion range of motion (at least about 10 degrees is needed to fully activate the pump), calf-muscle strength, and gait pattern, watching specifically for a shuffling gait. A patient with deficits in any of these should be referred to physiotherapy, since a treatment program addressing range of motion, strength, and gait can meaningfully improve calf-muscle-pump function and, with it, response to compression.^[1]

Wound assessment (if an ulcer is present)

The MEASURE mnemonic structures a systematic venous ulcer assessment: Measure (length, width, depth), Exudate (amount and character), Appearance of the wound bed, Suffering (pain), Undermining, Re-evaluate at each dressing change, and Edge condition.^[1]

• Reduce ambulatory venous hypertension — the mechanism underlying every manifestation of this disease — primarily through correctly selected and correctly worn compression.
• Screen for peripheral arterial disease (ABI) before recommending or dispensing standard compression, every time — this is a genuine, recurring safety gate, not a one-time check.
• Prevent progression from mild, cosmetic disease to skin changes, edema, or ulceration.
• Heal an existing venous ulcer, with compression as the treatment cornerstone.
• Prevent ulcer recurrence once healed, primarily through sustained garment adherence.
• Manage symptom burden — aching, heaviness, cramping, itching — even when disease is not severe by CEAP stage.
• Recognize when conservative management has reached its limit and escalate to sclerotherapy, endovenous ablation, or surgical ligation/stripping for significant or persistently symptomatic disease, or for recurrent ulceration.
• Set realistic expectations: even with genuinely optimized care, a meaningful proportion of venous ulcers remain unhealed at 24 weeks — this reflects disease severity, not necessarily a treatment failure at any single step.

Compression class selection by CEAP stage / indication

The table below follows the compression-class framework used in the Wounds Canada best-practice document itself.^[1] Prescribing garments above 20 mmHg should be done with, or under the direction of, a trained fitter or clinician.

Bandages/devices versus garments — a genuinely important distinction, not interchangeable terms

Bandaging systems and compression devices are generally used for active venous ulcers and to reduce established lower-leg edema; compression garments (stockings, or wrap-style hook-and-loop systems) are generally reserved for maintenance once edema has already been reduced.^[1] A genuine, common error is measuring and fitting a stocking on a still-edematous limb — as edema resolves the limb shrinks and the garment becomes loose and ineffective. Compression garments should be fitted only after edema has been reduced through bandaging, wraps, or pumps.^[1]

Multi-component bandage systems are more effective than single-component systems, and multi-component systems that include an elastic component outperform those composed mainly of inelastic materials; two-component systems perform comparably to four-layer bandaging.^[5][1] Compression, in whatever form, genuinely increases ulcer-healing rates compared with no compression — this is well-established, high-confidence evidence, not a marginal effect.^[5]

Escalation to procedural treatment

Situational, specialist-directed when varicose veins are significant, persistently symptomatic despite adequate compression, or when ulceration recurs despite genuinely adherent conservative management, escalation to a procedure is appropriate: sclerotherapy (chemical ablation, typically for telangiectasia, reticular veins, and smaller varicosities), endovenous thermal (laser or radiofrequency) ablation, and surgical ligation and stripping of the incompetent superficial vein all aim to remove the source of reflux and reduce the impact of venous hypertension on already-damaged skin.^[4][6][1] The largest and most influential trial on this question, the ESCHAR study (500 patients with isolated superficial or mixed superficial/deep reflux), found similar healing rates whether patients received compression alone or compression plus superficial venous surgery, but significantly lower ulcer recurrence in the surgery group — meaning surgical correction of superficial reflux is genuinely worthwhile primarily for reducing recurrence, not for accelerating the initial healing itself.^[1] A genuinely Canadian practical detail worth knowing when counselling patients: provincial public insurance plans typically cover saphenous vein ligation and stripping, but do not typically cover endovenous laser, radiofrequency, or chemical ablation technologies, which are usually only available through private payment.^[1]

Venoactive drugs — an honest evidence-quality framing, not a substitute for compression

Evidence quality genuinely differs by agent. Pentoxifylline and micronized purified flavonoid fraction (MPFF; diosmin/hesperidin) both have randomized-trial evidence supporting improved venous ulcer healing specifically when added to compression, and are the two agents current multi-society guidance recommends considering for longstanding venous ulcers.^[1][6] Phlebotonics as a broader class — which includes horse chestnut seed extract, rutosides, and other botanical agents — have a materially weaker evidence base: Cochrane-level evidence finds they probably reduce oedema slightly, make little or no difference to quality of life, do not demonstrably improve ulcer healing, and carry a higher risk of adverse events than placebo.^[7] Set patient expectations accordingly — these are, at best, a modest adjunct to compression, never a substitute for it.

Compression stocking counselling — the centerpiece of this chapter

Measurement and fit

Accurate measurement is what separates a therapeutic garment from a decorative one: measure the ankle circumference at its narrowest point just above the malleoli, the calf at its widest point, and the appropriate length. Garments must be re-measured and re-fitted after edema has meaningfully changed — a stocking fitted to a still-swollen limb will be loose and ineffective once the swelling resolves (see Choose Initial Treatment).^[1]

"Put it on before you get out of bed"

This is a genuinely practical, high-value counselling point that is easy to skip in a rushed dispensing conversation: compression stockings should be applied first thing in the morning, while still lying down, before rising — before gravity and a day of standing or sitting allow edema to accumulate. Applying a stocking over a leg that has already swollen during the day is both harder and less effective.

Application technique and donning aids

Many patients — particularly older adults, those with reduced hand strength or dexterity, or those with a large or irregularly shaped limb — genuinely struggle to don a compression garment unassisted. Commercially available donning aids ("donners") make a real, practical difference and should be actively offered, not left for the patient to discover on their own; patients should also be shown how to remove a garment ("doffing") without damaging the garment or the skin. Newer self-adjustable hook-and-loop wrap systems are a genuine alternative for a patient who cannot manage a pull-on stocking, and are increasingly recognized in funding discussions as a legitimate option specifically for this reason.^[1]

Choosing garment length

Knee-high garments are adequate for most CVI, since the relevant venous pathology is predominantly below the knee, and they are generally easier to don and better tolerated for daily long-term wear than a thigh-high or waist-high garment — real-world adherence is itself a genuine clinical variable, and a garment that goes unworn provides no benefit regardless of its labelled pressure.

Skin care around compression

Wash the leg with a pH-appropriate, non-alkaline, allergen-free cleanser, and apply a non-sensitizing moisturizer in a downward motion to maintain skin integrity; confirm with the product information that any cream or emollient used is compatible with the compression garment's material (some products degrade elastic fibres).^[1] Watch for both irritant and allergic contact dermatitis to the garment fabric itself, not only to topical products.

Replacement schedule

Compression garments lose elasticity and therefore therapeutic pressure with regular wear and laundering — a garment worn daily typically needs replacement roughly every 3-6 months to maintain its labelled compression class; reassess this at every follow-up rather than assuming an old, stretched-out garment is still providing therapeutic pressure.

Leg elevation

Elevate the affected limb above heart level for about 30 minutes, three times per day, to assist venous return passively.^[1]

Exercise and calf-muscle-pump activation

Because calf-pump failure is itself a core mechanism (see Risk Factors), exercise is treatment, not just general advice: ankle dorsiflexion/plantarflexion ("ankle pumps"), calf raises, and walking with a proper heel-to-toe gait all directly activate the pump. A structured, supervised exercise program in addition to compression has been associated with meaningfully faster ulcer healing than compression alone in the literature reviewed by Wounds Canada's evidence synthesis — exercise is a genuine adjunct, not an optional extra.^[1]

Other general measures

• Weight management where relevant, as part of the overall care plan rather than a prerequisite for other treatment.
• Avoid prolonged static standing or sitting; take movement breaks.
• Avoid restrictive clothing and habitual leg-crossing, which can further impede venous return.
• Smoking cessation — chiefly relevant to reducing concurrent peripheral arterial disease risk, given how directly that risk shapes what compression can safely be recommended.
• Referral to physiotherapy for a shuffling gait, reduced ankle range of motion, or other calf-muscle-pump deficits identified on assessment.

Pregnancy

Progesterone-mediated venodilation combined with mechanical compression of pelvic veins from the gravid uterus commonly causes new or worsened varicosities during pregnancy. Compression stockings are safe and are first-line management. Most pregnancy-related varicosities regress substantially after delivery, so elective procedural treatment (sclerotherapy, ablation, surgery) is generally deferred until the postpartum period rather than pursued during pregnancy. The hypercoagulable state of pregnancy also raises the stakes of any new superficial thrombophlebitis — assess promptly rather than assuming it is routine venous congestion.

Diabetes

Two separate reasons make ABI interpretation more difficult, and more important, in diabetes: peripheral neuropathy can blunt the pain that would otherwise warn of developing ischemia, and medial arterial calcification commonly produces a falsely elevated (non-compressible) ABI reading above 1.4 — a result that must prompt further arterial testing (e.g., toe-brachial index), not reassurance (see Assessment & Diagnosis).^[1] Infection risk is also higher; monitor any wound more vigilantly.

Older adults and frailty

Thinner, more fragile skin raises the risk of compression-related skin tears or pressure injury from a poorly fitted or incorrectly applied garment. Reduced hand strength and dexterity genuinely complicate donning — proactively offer donning aids, caregiver training, or a lower-force hook-and-loop wrap alternative rather than assuming non-adherence reflects a lack of motivation.

Heart failure

Uncontrolled or decompensated heart failure is an absolute contraindication to standard high compression, since mobilizing peripheral edema fluid into the central circulation can precipitate volume overload.^[3] Any compression use in a patient with a heart failure history needs cardiology coordination and typically a reduced-pressure, closely monitored approach rather than the standard compression ladder applied unmodified.

Obesity

Standard-sized garments may not fit reliably; custom-fit or extra-wide compression products are often needed, and accurate measurement of an irregularly shaped limb is genuinely more difficult and may require padding to protect bony prominences and narrow areas from excessive localized pressure.^[1] Obesity is independently a risk factor for both CVI and DVT, reinforcing the value of the broader weight-management conversation as part of the overall plan.

Phlebolymphedema (venous disease with coexisting lymphedema)

Combined venous and lymphatic disease typically needs higher compression classes (III-IV) and different bandaging/garment considerations than CVI alone. This chapter does not duplicate dedicated lymphedema management — refer to the Canadian Lymphedema Framework (canadalymph.ca) for lymphedema-specific guidance.^[1]

Reduced mobility and neurologic gait disorders

Parkinson disease, arthritis, and other conditions producing a shuffling gait or reduced ankle range of motion directly impair calf-muscle-pump function (see Risk Factors and Assessment & Diagnosis) — refer to physiotherapy for targeted range-of-motion work, strengthening, and gait retraining rather than treating this purely as a compression-garment problem.

• Reassess CEAP clinical stage and symptom burden periodically, and confirm the prescribed compression class still matches current status as edema and skin findings change.
• For an active ulcer, reassess using the MEASURE parameters at each dressing change, and set realistic expectations: even with genuinely optimized care, an estimated 30% of venous leg ulcers remain unhealed at 24 weeks — this is a known feature of the disease's healing trajectory, not automatically a sign that something has gone wrong.^[1]
• Reassess ABI periodically, and specifically whenever pain develops or worsens with compression, when new arterial symptoms appear, or when diabetes is progressing — do not treat a single normal ABI as permanently reassuring.
• Check garment condition at follow-up and reassess the replacement schedule — a visibly stretched-out or long-worn garment may no longer be delivering its labelled pressure even if it still looks intact.
• Reinforce adherence at every visit. Recurrence after a healed ulcer or resolved edema is disproportionately linked to patients discontinuing maintenance compression once the visible problem has resolved — this is one of the most common, and most preventable, causes of relapse.^[1]
• Follow post-procedural patients (sclerotherapy, ablation, surgery) per the proceduralist's specific protocol, typically including a defined period of continued compression afterward.

1. Before assuming a therapy has failed, confirm it was actually implemented correctly: garment class, correct fit and measurement, correct application timing ("before you get out of bed"), and genuine daily wear duration are all common, under-recognized sources of apparent treatment failure.
2. Re-screen ABI if healing stalls or pain worsens with compression — evolving arterial disease is a real and sometimes overlooked explanation, not only "the ulcer being stubborn."
3. Consider repeat duplex ultrasound if a missed source of reflux, a new obstruction, or recurrence after a prior procedure is suspected.
4. Add pentoxifylline (or MPFF, where the specific product is available and appropriate) if not already part of the regimen — alongside compression, not instead of it.
5. Reassess for infection, biofilm, and adequacy of debridement in a stalled ulcer rather than only adjusting the compression or the drug regimen.
6. Refer for procedural evaluation (sclerotherapy, endovenous ablation, or surgical ligation/stripping) if genuinely optimized conservative therapy has not achieved adequate symptom control, or has not achieved healing, over an adequate trial period.
7. Escalate to a specialized wound-care or vascular clinic for a refractory ulcer — recognizing, as above, that a meaningful proportion of venous ulcers remain unhealed at 24 weeks despite care that has genuinely been optimized at every step.

• Recommending or dispensing standard high-compression hosiery without first confirming arterial status by ABI — the single most important safety step in this entire chapter.
• Assuming a palpable pedal pulse rules out arterial disease — it does not, and the dorsalis pedis pulse is absent as a normal variant in about 8% of healthy adults.
• Treating an ABI above 1.4 as reassuring — it commonly reflects calcified, non-compressible vessels (especially in diabetes) rather than genuinely adequate arterial flow, and needs further testing, not reassurance.
• Fitting a compression garment before edema has been adequately reduced with bandaging, wraps, or a pump — the garment will be loose and ineffective once the limb shrinks further.
• Confusing stasis dermatitis for cellulitis and prescribing an unnecessary antibiotic course — or, in the other direction, dismissing true cellulitis as "just eczema."
• Missing acute lipodermatosclerosis and treating it as cellulitis, phlebitis, or panniculitis with antibiotics it does not need.
• Recommending diuretics for pure venous edema — diuretics are indicated for volume-overload states (heart failure, hepatic or renal disease), not for edema caused by venous reflux and valvular incompetence, and do not address the underlying mechanism.
• Advising rest or inactivity for painful legs, when calf-muscle activation through walking and ankle exercises is actually beneficial and directly addresses one of the three core disease mechanisms.
• Presenting venoactive drugs (phlebotonics) generally as a proven substitute for compression, when Cochrane-level evidence shows this class does not improve ulcer healing and carries more adverse events than placebo.
• Skipping the "put it on before you get out of bed" counselling point — a garment applied over a leg that has already swollen through the day is both harder to don and less effective.
• Assuming a non-healing ulcer at some fixed follow-up point automatically represents a treatment failure, rather than recognizing that a substantial minority of venous ulcers remain unhealed at 24 weeks even with genuinely optimized care.

How to use this table: this catalogues the drug options relevant across the full CVI spectrum, organized by role — venoactive adjuncts, symptomatic/analgesic support, topical anti-inflammatory therapy for stasis dermatitis, antibiotics for genuine secondary infection, anticoagulants for concurrent thrombosis, and the sclerosant used in procedural sclerotherapy. None of these substitute for correctly selected, correctly worn compression, which remains this chapter's central intervention. Doses shown are typical adult doses only and require patient-specific confirmation. Select any drug name to open its complete Pharmasist Drug Database page.

Venoactive Agents (Phlebotonics)

Evidence quality genuinely differs within this class — see Choose Initial Treatment. Diosmin/hesperidin (MPFF) and horse chestnut seed extract have no Drug Database entry under any plausible slug (independently verified); pentoxifylline does.^[1][7]

Anti-Inflammatory and Analgesic Adjuncts

For pain related to superficial thrombophlebitis, acute lipodermatosclerosis, or general symptom control; none of these treat the underlying venous pathology.

Topical Corticosteroids for Stasis Dermatitis and Lipodermatosclerosis

Treat the eczematous/inflammatory skin changes, not the underlying venous hypertension — compression remains the definitive treatment.

Antibiotics for Secondarily Infected Ulcers and Cellulitis

Reserved for clinical infection (spreading erythema, warmth, fever, purulence) — not for bacterial colonization of a chronic wound, which does not itself need systemic antibiotics.^[1]

Anticoagulants for Concurrent Venous Thromboembolism

Relevant when CVI coexists with, or is complicated by, deep or extending superficial vein thrombosis — not a treatment for CVI itself.

Sclerosing Agent for Procedural Management

Administered by a trained proceduralist as part of sclerotherapy — not a community-pharmacy-dispensed product, but worth knowing to counsel patients accurately about a referral.^[6]