Professional Documents
Culture Documents
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)
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.
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.
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.
DIAGNOSIS
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.
Management
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
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.
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
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.
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.
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
60ml
3/ lotion
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.
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:
155
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.