Varicose ulceration: herbal treatment and case studies

Ulcers are a common hazard of the elderly. They are not considered 'serious' illness but
are readily immobilizing and thus can severely restrict the quality of life.

Ulceration of the lower limb affects about 3.6% of the adult population over 65 years
old in Britain1. They tend to recur and are estimated to cost between £294 and £650
millions2.

More that 90% of all leg ulcers are venous, arterial or neuropathies, with 85% of the
total being venous ulcers. Given that 6 million UK women have varicose veins and over
11 million suffer aching or swollen legs3, these risk factors indicate the numbers of
women predisposed to varicose ulcers.

th
Types of ulcer (Ref: Hamilton Bailey's Physical Signs 17 ed 1986)

VENOUS OR VARICOSE ULCER

Due increased hydrostatic pressure giving oedema, low oxygen exchange and
metabolite availability thus proneness to anoxia and infection on slight trauma. Either
coexist with incompetent superficial veins (varicose veins) or with incompetent
perforating veins (ie. Anastomotic veins penetrating deep tissues linking with deep
veins) (or chronic venous insufficiency) or incompetent deep veins. Small % VU occur
without varicosities and are due to deep vein thrombosis (post thrombotic ulcer).

Shallow, never penetrating the deep fascia, and has irregular deep, shelving edges
often with thin blue line of growing epithelium. Base of ulcer can be pink or grey
granulation or slough. One or more of large feeding veins may visibly encroach into
edge of ulcer. Site of ulcer constant to 'gaiter region', which is almost pathognomic. And
is more common on medial side (long saphenous vein) than lateral (short saphenous
vein).
Most are painless (cf arterial ulcers), but involvement of saphenous nerve in infection
causes the pain.
Haemosiderin pigmentation from extravasion of blood corpuscles and their
disintegration due to stasis.

Early signs of latent ulceration is the fine splay of fine venules from the medial (usually
but can be the lateral) malleolus distally towards the heel. "Gravitational" or venous
'eczema', often appears 3-18 mths before ulceration occurs.

Brown pigmentation (Haemosiderin from breakdown for RBCs extruded through

capillary walls in diapedesis in increased intercapillary pressure) is a sign of venous
stasis

1
N J London and R Donneley (2000) ABC of Arterial and venous disease: Ulcerated
lower limb. BMJ 320:15891591
2
Laing W (1992) Chronic venous diseases of the lg. OHE, London.
3
Purcell S (2000) Show a leg. Chem and Drug Nov 2000.
Normal venous pressure is 30 mm Hg, but when the deep vein pressure is sufficient to
return the venous blood to the heart, pressure in the superficial veins can rise to 60-
80mm Hg. This creates a back pressure that forces stretching of the capillary walls,
damaging them and allowing leakage. One theory is that fibrinogen is extruded where it
polymerises to fibrin, collecting around the capillaries as an impenetrable layer4.

POST-THROMBOTIC ULCER

Pain is usually constant. Site and appearance almost identical to VU. Here the ulcer
follows clear evidence of DVT, and suspected if history of pregnancy, leg trauma or
abdominal surgery. Often presents with extensive induration extending up the leg to the
bulk of the gastronemis, giving an 'inverted beer bottle’ effect. Dorsiflexion of the foot
elicits pain.
Otherwise is not distinguishable from varicose ulcer.

ARTERIAL ULCER

Rare (< 10% all leg ulcers) but extremely painful. Varicose veins usually absent but
their presence does not contradict the diagnosis. Occur after trauma of pressure points
(shin, malleolus, dorsum of foot) where flow of blood through capillaries in reduced
critically by either arteriosclerosis of additional point pressure, poor gaseous exchange
with adjacent tissues results is ulceration.

Arterial ulcers are DEEP cf VU and may penetrate the deep fascia with tendons
exposed in base. Pedal and medial malleolus pulses usually absent and pigmentation
of foot either pale or cyanosed. The foot is cold cf VU where it is warm or hot.
Intermittent claudication common.

NOT to be treated with compression bandaging.

NEUROTROPHIC ULCER

Most common cause is diabetic neuropathy, but also due to tabes dorsalis, spinal
dysraphism, and spinal and sciatic nerve lesions. Usual distribution is the metatarsal
heads. DD includes arterial ulcers, but latter generally have no pedal pulses.

Cautions with ulcers

NEVER use compression on arterial ulcers.
Long standing VU can develop carcinomas (basal cell, squamous commonly). Look for
everted edge and enlarged lymph nodes in groin.

DIAGNOSIS

An essential element of treatment is careful differential diagnosis of ulcers of the lower

limb. The different pathologies require different approaches.

History is essential to clarify diagnosis and appropriate management. Duration and size
are important (research shows the recidivist ulcers are those of greater size and
4
Robinson B (1988) Aetiology and treatment of leg ulcers. Supplement to Mims
magazine. July 2-3.
longest duration..). Pain is relevant. Neuropathic ulcers are generally painless. Location
gives significant clues as to aetiology.

Systemic disease is relevant. Inflammatory and auto-immune states are involved in

vasculitic ulcers (RA, SLE, PAN)

Examination noting presence of haemosiderin pigment, presence/absence of pulses,

signs of varicosities, oedema, MS examination for neuropathopies, diabetes.
Doppler ultrasonography for arterial stenosis and occlusion.
Ankle brachial pressure index (comparison of systolic BP at ankle and brachial artery):
should be at least 90% of brachial. If ankle systolic is <55mm, ischaemia may not heal
easily.

Management

Orthodox treatment is controversial. It relies on various forms of graduated

compression bandaging. Usually no drugs are applied to the lesion, except a moist
emollient under a non-adherent dressing under the bandaging. Antibiotics are rarely
used and steroids may be applied to the adjacent varicose eczema.

1
Evidence suggests that if only the long or short saphenous veins are incompetent,
then surgical treatment can help. But if the deep veins are compromised, compression
bandaging is the only option.

Healing is not always successful and recidivism is common. One study5 suggested that
only 13% of ulcers larger than 5cm diameter and present for more than 6 months
before treatment healed successfully. Healing was assessed after 12 months of
therapy.
The 5 year recurrence rate is about 40%, which probably emphasises the influence of
1
the physical damage underlying the pathology rather than any comment of treatment .

The high recurrence is the probable reason for so many presentations to medical
herbalists.

Herbal management

Accurate assessment is essential. Confusing arterial or neuropathic ulcers with

varicose/venous ulcers can have serious consequences. This emphasises the
importance of clinical skills AND cooperation with orthodox health workers.

Most patients would have been seen and usually treated by orthodox GP or nurses. In
my experience it is usually the long-standing and 'unhealed' ulcers that present to
herbalists. The Heroic failure syndrome.

5
Margolis DJ, et al (2000) Which venous ulcers will heal with limb compression
bandages? Am J Med 109: 15-19
Co-operation is essential for details of:
• circulation (Venograms?, Doppler assessment?)
• diabetic assessment
• treatment history
• and especially continuing skilled bandaging.

Herbal competence centres on:

• arresting varicosity progression
• promoting circulation/reducing oedema
• promoting healing of the wound
• strengthening surrounding skin
• encouraging secondary prevention (treatment and lifestyle)

Arresting varicosity progression includes:

• appropriate compression bandaging/stockings (grade ! or II)
• leg elevation
• exercises to promote calf contraction (primary pump)
• weight bearing on feet (secondary pump)

Promoting circulation
Herbal treatment included systemic use of :
Aesculus hippocastenum (anti-inflammatory and anti-oedematic)
Achillea millefolium
Zanthoxylum spp
Centella asiatica
Crateagus spp
Ginko biloba
Zingiber officinalis

A recent systematic review of 13 placebo controlled trials 6 of treatment of Chronic

Venous Insufficiency (CVI) with Aesculus hippocastenum showed clearly the superiority
of Aesculus over placebo. The herb led to reduced oedema at calf and ankle. Leg pain
and pruritis were reduced. One comparative study suggested that Aesculus could
replace compression bandaging. The dose was 100-150 mg of the saponin aescin,
equivalent to 2-3g seed.

6
Pittler MN, Ernst E (1998) Horse-chestnut seed extract for chronic venous
insufficiency. A criteria based systematic review. Arch Derm. 134: 1356-1360.
Healing the wound
Although some evidence suggests poor response from use of antibiotics, evident
infection should be treated herbally and the wound protected from re/infection.

Melaleuca leucadendron EO. 1-3 gtt dropped into centre of the wound bid. Has been
found effective in my clinic.
Otherwise the wound can be washed over with a lotion of Calendula officinalis infusion
(15g flores/ 300ml) and let air dry before reapplying dressing.

Around the wound, a cream of :

Symphytum officinale 30ml
Calendula officinalis 30ml
Melaleuca eo 15gtt

Or:

Washing around the wound (leaving clear margin of 1.5cm) with lotion of Calendula tr
90% with 1% Melaleuca, depending on the degree of dryness or exudative quality of
the varicose eczema.

Strengthening the surrounding skin

The vulnerable varicose eczema that can extend around half skin area of the lower leg
can be made less vulnerable to the slight traumas that 'trigger' ulceration by 'toning'
with the Calendula 90% lotion above and moisturised with the Symphytum/Calendula
cream above.
Ultimately, improving blood flow through the leg is essential and the combination of
compression, leg raising and exercise, as appropriate, are concomitants of any topical
treatment.

Case study 1

An 83 year old male presented with left leg, medial calf, 4cm dia. venous ulcer. This
was a recurrence 12 mths ago of a previous ulcer that followed an RTA in 1968.
Following the original RTA, he developed phlebitis and required hospitalisation. The
ulcer developed within three months and persisted until 1981, when a skin graft was
attempted and superficial varicosed veins were 'stripped'. The ulcer healed. And was
stable until July 1997 when a scratch from a dog claw erupted into an ulcer at the same
site. Compression made no impact. He had CHD and had a successful bypass and
aortic valve replacement in '93 and '94 respectively. He was otherwise a healthy, with
nothing relevant in his PMH. He was on Zocor and 1/2 a 75mg Aspirin a day since the
bypass surgery in '94.

The patient was no longer using compression bandages when he presented. They had
been dropped over 6 months ago. The history could suggest arterial and/or venous
factors behind the ulcer. On examination he showed no signs of arterial compromise.
Pedal pulses were patent, the leg and feet were warm and there was no sign of
cyanosis. He showed visible varicosities and slight ankle oedema that pitted. The
assumption was to initiate treatment as varicose ulceration. BP 150/80 pulse 68
Treatment included:

1/ Tr as:-
Achillea millefolium 1:3 20
Aesculus hippocastenum 1:3 30
Zanthoxolum a. 1:3 10
Glycyrrhiza glabra FE 15 sig: 10ml bid
Ginko biloba 1:3 40
Capsicum minimum 1:10 1
101

2/ cream for surrounding tissue

Calendula cr. 30ml
Symphytum cr. 30ml

60ml

3/ lotion

Calendula officinalis 90% 1:3100ml

Melaleuca eo. 1%

Patient returned 4/52 with healed ulcer. Surrounding skin was pink rather than red, the
centre of the ulcer was dry, free of slough and showing good granulation. Patient
supplied further two weeks medication and discharged with request to report back on
month.

Case study 2

A 70 year old woman presented with a history of poor circulation, Raynaud's in hands
and feet and a DVT history as diagnosed by her GP. She was seen in November and
reported an infection on her right shin in the summer, with hot, inflamed and
erythematous skin. Both legs were very pruritic during that summer. She reported
SOBOE and restless legs at night. The GP had treated with steroids to no effect.
Patient also had ankle oedema and stiffness in the legs. PMH included bronchitis every
winter, chilblains since age 16. Her father had 'poor circulation' and her mother had
diabetes and arthritis. She had had breast cancer 5 years ago and after radiotherapy
was put on Tamoxifen. She was on Betnovate for her leg erythema.

On examination she had varicose veins in both legs, erythema over the lateral legs
below the knee and a 'cuff' around the ankles. She has signs of scratching and slight
ankle oedema. Both legs were hot and pulses patent.

This patient appeared to have compromised venous return and evidence of

gravitational eczema. Despite the Raynaud's, evidence of arterial shortfall was lacking.
Her SOBOE restricted even walking exercise and she spent hours each day sitting
watching TV.

Management aimed at getting her vertical and doing exercise that included her
standing on toes and back to heels, as well as walking about the house and garden
followed by 30 minutes in front of the TV but with legs elevated by sitting along her
sofa.
Herbal treatment consisted of:

Ginko biloba 1:3 40

Melilot 1:3 10
Zanthoxylum 1:4 20 sig 10 ml bid.
Aesculus hippocastenum 1:3 50
Viburnum opulus 1:3 10
Achillea millefolium 1:3 20
Zingiber officinalis 1:10 5

155

Diuretic tea of:

Taraxacum officinale herba 50g
Achillea millefolium 50g 3 tsp/mug, 3 mugs per
100g Day, last mug before
5pm

Return in two weeks showed less pruritis, and tenderness of legs with reduced
swelling. Erythema was reduced. There had been no episode of Raynaud's despite
o
being O C when she visited. Last seen in January 7 weeks on and still improving.