Oxford Textbook of Fundamentals of Surgery

William E. G. Thomas (ed.) et al.

https://doi.org/10.1093/med/9780199665549.001.0001
Published: 2016 Online ISBN: 9780191810817 Print ISBN: 9780199665549

CHAPTER

2.7.3 Venous and lymphatic disease 

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Katy A. L. Darvall, Andrew W. Bradbury

https://doi.org/10.1093/med/9780199665549.003.0042 Pages 339–342

Published: July 2016

Abstract
Varicose veins (VV) are common and are part of a spectrum of disease known as chronic venous
insu ciency (CVI), with the more severe manifestations of CVI being skin changes and chronic venous
ulceration (CVU). The relationship between symptoms and VV is complex. Duplex ultrasound allows a
‘map’ of the abnormal veins to be obtained to guide treatment. Treatment has evolved from open
surgery to minimally invasive options such as endothermal ablation and ultrasound-guided foam
sclerotherapy. CVU has a prevalence of around 1%, frequently recurs, impairs quality of life, and has a
signi cant health and social care cost. The mainstay of treatment remains graduated multilayer
compression bandaging (having excluded arterial disease) and ablation of super cial venous re ux.
There are several causes of a chronically swollen limb, the most common being CVI and lymphoedema.
Lymphoedema can be primary or secondary. Lymphoedema is incurable and managed conservatively
with skin care, massage, and compression.

Keywords: chronic venous ulceration, lymphoedema, varicose veins, chronic venous insu iciency, leg
swelling, superficial venous surgery, endothermal ablation, foam sclerotherapy
Subject: Surgery, Vascular Surgery, Urology, Paediatric Surgery, Cardiothoracic Surgery, Peri-operative
Care, Trauma and Orthopaedic Surgery, Upper Gastrointestinal Surgery, Colorectal Surgery, Surgical
Oncology, Neurosurgery, Breast Surgery, Transplant Surgery, Surgical Skills
Series: Oxford Textbooks in Surgery

Varicose veins

Epidemiology
1
Varicose veins (VV) are common, a ecting up to 40% of the population. VV are part of a spectrum of
disorders usually called chronic venous insu ciency (CVI), although this term is often used to denote the
presence of ‘complicated’ VV including skin changes and chronic venous ulceration (CVU).
Aetiology and pathophysiology
The aetiology of VV is unclear. The most widely held view is that a defect in the vein wall (which may be in
part genetic), in addition to increased venous pressure (e.g. with obesity, prolonged standing, or
pregnancy), leads to progressive dilatation of the vein and secondary disruption of the venous valves
resulting in valvular incompetence. Valvular incompetence can occur in the deep veins but is usually
secondary to direct damage from deep vein thrombosis (DVT).

Normally, when ambulating, the calf muscles pump venous blood out of the leg and reverse ow with
gravity is prevented by valve closure. When the valves are damaged the pressure in the calf veins is

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increased, so-called ambulatory venous hypertension. In some cases the ambulatory venous hypertension is
caused by deep venous obstruction (out ow obstruction) secondary to DVT or, more rarely, extrinsic
compression.

Clinical presentation
The relationship between VV and various lower limb symptoms is complex. Some people with extensive VV
can be asymptomatic while, in others, quite minor VV are troublesome. The lower limb symptoms typically
related to venous disease include pain or ache, heaviness, itching, a feeling of swelling, heaviness, tingling,
1
and restless legs. Venous symptoms are typically worse at the end of the day and after prolonged standing.

The patient should be examined standing up, and viewed from in front and behind. Inspection may reveal
telangiectasia or spider veins (super cial in the dermis, < 1 mm), reticular veins (deep in the dermis, < 4
mm), and true VV (> 4 mm and palpable). The distribution (and likely source) may be obvious at this point,
that is, posterior calf VV from small saphenous vein (SSV) incompetence, medial thigh and calf VV from
great saphenous vein (GSV) incompetence, or anterior/posterior thigh VV. The lower leg should then be
inspected for the skin changes of CVI. Varicose (venous) eczema is red and intensely itchy.
Lipodermatosclerosis is indurated, hardened, and in amed. Haemosiderin deposition appears as brown
discoloration, usually in the gaiter area (Figure 2.7.3.1).

Fig. 2.7.3.1

Haemosiderin deposition, lipodermatosclerosis, eczema, and ulceration.

Palpation will con rm the ‘woody’ feeling of lipodermatosclerosis and will aid detection of VV which may
not be visible in the larger leg.

Investigations
Tourniquet tests are obsolete. Hand-held Doppler is also an inaccurate and incomplete examination
technique, which has been superseded by duplex ultrasound. Portable duplex machines used in clinic permit
a ‘one-stop’ diagnostic service. Recent guidance from the UK National Institute for Health and Care
Excellence (NICE) states that all patients with VV should have a venous duplex to aid diagnosis and

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2
treatment options.

Duplex ultrasound provides a ‘map’ of both the deep and super cial veins. Deep veins are assessed for
patency (including evidence of a previous DVT) and competency. Super cial veins, and their junctions with
the deep system (saphenofemoral junction, saphenopopliteal junction, and perforators), are also assessed
for patency and competency. Duplex ultrasound also helps to determine the most appropriate treatment for
an individual patient and is an integral part of endovascular interventions.

Other investigations such as plethysmography are only used as research tools, and invasive tests such as
venography are rarely indicated.

Management

Conservative
The mainstay of conservative management for VV has been compression hosiery and lifestyle modi cation,
including weight loss and avoiding prolonged standing. Compression hosiery, however, is only now
2
recommended by NICE when interventional treatment is unsuitable.

Surgery
Traditionally the mainstay of treatment for VV has been super cial venous surgery (SVS), but more recently
there have been many developments in endovenous techniques which seek to improve the side e ect pro le
of traditional surgery, shorten recovery times, and also to give greater durability.

SVS that aims to remove visible VV and correct axial super cial and perforator (deep to super cial)
incompetence has been considered the ‘gold standard’ for many decades, although recent NICE guidance
states that SVS should now only be performed in patients who are not suitable for either endothermal
2
ablation or ultrasound-guided foam sclerotherapy (UGFS).

In patients with GSV incompetence, the saphenofemoral junction is ligated and the GSV is stripped out from
the groin to the knee. In patients with SSV incompetence, the saphenopopliteal junction is ligated, but not
usually stripped to avoid damage to the sural nerve. Any remaining varices are removed through several tiny
stab incisions (avulsions or phlebectomies).
Endovenous ablation
The most frequently used, and studied, endovenous techniques are endovenous laser ablation,
radiofrequency ablation, and UGFS; all of which can be performed on an outpatient basis using local
anaesthesia. Endovenous laser ablation and radiofrequency ablation both utilize specialist bres and
catheters placed within the vein to be treated. Endothelial damage (leading to brosis) occurs as a result of
heat generation at the tip of the bre or catheter which is gradually withdrawn to treat the entire length of
vein.

UGFS involves injection of a liquid sclerosant, usually mixed with air, into the incompetent veins. The

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sclerosant acts immediately to cause endothelial damage that evolves to brosis.

Leg ulceration

Epidemiology
Up to 3–11% of patients with VV will develop the sequelae of severe venous insu ciency including
ulceration. The lifetime risk of developing CVU is usually quoted at 1% in Northern Europe, with an
3
estimated point prevalence of 0.1% (10% of those a ected will have an open ulcer at any one time).

The overall prognosis of CVU is poor, with delayed healing and recurrent ulceration being common. Venous
ulceration has a profound e ect on quality of life and social functioning, and the e ect on healthcare
spending is vast. It is estimated that up to 2% of the total annual healthcare budget in Western countries is
spent on the treatment of chronic venous disease—around £600 million per annum in the United Kingdom.
3,4
In addition, 22% of district nurses’ time is spent treating leg ulcers.

There are many risk factors considered to be associated with the development of CVI, including family
5,6
history, increasing age, obesity, parity, prolonged standing, physical inactivity, and previous leg injury.

Aetiology and pathophysiology

The term CVI encompasses the skin changes that occur as a result of ambulatory venous hypertension and
poor venous drainage. These are hyperpigmentation (haemosiderin deposition), lipodermatosclerosis
6
(subcutaneous tissue brosis), atrophe blanche (areas of devascularized skin), and eventually CVU.

There are a number of proposed pathophysiological mechanisms. The most popular of these are the brin
cu hypothesis and the white-cell trapping theory, which result in localized chronic in ammation, tissue
oedema, microcirculatory thrombosis, and hypoxia.

Clinical assessment
The majority of leg ulcers (>70%) are venous and a further 15–20% are of mixed arterial and venous
aetiology. Clinical assessment is essential in determining the likely aetiology of the ulcer, thus guiding
further investigations (Table 2.7.3.1, Figure 2.7.3.2). All patients should have their pulses assessed and an
ankle–brachial pressure index measured.
Table 2.7.3.1 Di erential diagnosis of leg ulceration

Clinical features Arterial ulcer Venous ulcer

Age and gender Usually men > 60 years O en women

Risk factors and Smoking, diabetes, dyslipidaemia, and hypertension; Previous DVT (confirmed or occult),
past medical o en a history of cardiovascular disease thrombophilia, VV
history

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Symptoms Severe pain is present (unless there is diabetic Pain only in about 30%, but usually not
neuropathy) and may be relieved by dependency severe and may be relieved with elevation

Site Usually on pressure areas (malleoli, heel, metatarsal Medial (70%), lateral (20%), or both malleoli
heads, 5th metatarsal base) and gaiter area

Edge Regular, ʻpunched-outʼ, indolent Irregular, with neo-epithelium (whiter than

mature skin)

Base Sloughy or necrotic with no granulation tissue; may Pink with granulation tissue; but may be
involve tendon, bone and joint covered in yellow-green slough

Surrounding skin Features of severe limb ischaemia, e.g. thin, dry skin, Lipodermatosclerosis, varicose eczema,
pallor, reduced temperature haemosiderin deposition

Veins Empty, ʻgutteringʼ on elevation Full, usually varicose

Swelling Usually absent O en present

Fig. 2.7.3.2

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Chronic venous ulceration.

Investigations
Investigations for venous ulcer are as for VV, with duplex ultrasound being the most useful modality.

Management
The management of patients with CVU requires a holistic approach: managing the ulcer in the context of the
whole leg, the leg in the context of the whole patient, and the patient in the context of their social and
cultural circumstances. Measures such as leg elevation to reduce oedema, weight loss, and exercise
programmes should be encouraged.

The mainstay of treatment for venous ulceration is elasticated, multilayer, graduated compression
7
bandaging, and it is very e ective at healing the majority of venous ulcers (Figure 2.7.3.3). After healing of
the ulcer with bandaging, the patient should be placed in graduated compression hosiery to reduce the risk
of recurrence. There is also evidence that when venous ulceration occurs in association with super cial
8
venous re ux, SVS can reduce the risk of recurrence.
Fig. 2.7.3.3

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Compression bandaging.

It is generally accepted that the type of dressing used has little e ect on healing. Larval therapy and
negative-pressure dressing systems improve debridement but do not shorten the time taken to healing (or
9,10
increase the number of ulcers that ultimately heal).

Swollen leg

Di erential diagnosis of the swollen leg

There are many di erent conditions that can cause chronic leg swelling (Box 2.7.3.1), but the two most
common are CVI and lymphoedema. Unilateral leg swelling is more likely to be due to a local cause than a
systemic condition.
 Box 2.7.3.1 Di erential diagnosis of chronic leg swelling

◆ Venous disease:

• Primary super cial and/or deep venous incompetence

• Previous DVT (post-thrombotic syndrome)

• Arteriovenous malformations

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• Venous out ow obstruction (intrinsic or extrinsic)

◆ Lymphoedema

◆ General disease:

• Congestive cardiac failure

• Pretibial myxoedema

• Hypoproteinaemia (e.g. nephrotic syndrome)

• Hepatic failure

• Lipoedema

• Dependency/disuse.

Lymphoedema

Epidemiology
11
Lymphoedema is a debilitating condition, has no cure, a ects up to 1–2% of the population, and is
characterized by the accumulation of protein-rich uid in the skin and subcutaneous tissues due to a defect
in the lymphatic system.

Aetiology and pathophysiology

Lymphoedema can be primary or secondary and should be di erentiated from other causes of limb swelling.
In primary lymphoedema the cause is unknown (or at least uncertain) and it can be classi ed based on the
age of onset. Women are more commonly a ected and it usually occurs in the lower limbs.

Lymphoedema congenita is present at birth and can be autosomally inherited (Milroy’s disease). It is more
likely to be bilateral and to involve the whole leg. Lymphoedema praecox presents up to the age of 35 years,
usually during adolescence. Most patients have unilateral limb involvement and it usually extends only to
the knee. Lymphoedema tarda presents after the age of 35 years and is often associated with obesity. All
subgroups of primary lymphoedema are likely to represent a spectrum of disease due to defective lymphatic
drainage (aplasia, hypoplasia, hyperplasia, or brosis).

Secondary lymphoedema is the commonest form and occurs when the lymphatic vessels become occluded
by an acquired pathology. The lymphatic channels distal to the obstruction become dilated and the
lymphatic valves secondarily incompetent. The commonest cause worldwide is lariasis caused by
infestation with the parasite Wuchereria bancrofti. The commonest cause in the Western world is neoplasia
and its treatment, resulting in damage or removal of lymph nodes, for example, post-mastectomy
lymphoedema of the upper limb.

The lymphatic system removes excess water and protein from the interstitial space and returns it to the
intravascular space. Failure of this mechanism results in stagnation of protein-rich uid in the interstitial
space, and the resultant oncotic pressure causes accumulation of more water, leading to dilatation of the
12
lymphatic vessels and lymphatic valvular incompetence.

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Clinical assessment
The initial presentation is with peripheral oedema. A detailed history and examination of the patient may
help to di erentiate primary from secondary lymphoedema, and exclude other causes of limb swelling.
Initially the oedema is pitting and shows diurnal variation, but over time it becomes non-pitting due to
brosis of the subcutaneous tissues. Unlike other forms of oedema, lymphoedema characteristically
involves the foot. As the oedema progresses, skin complications develop including bacterial and fungal
infection.

Investigations
Duplex ultrasound can be used to exclude concomitant venous disease but lymphoedema can usually be
diagnosed on the basis of history and examination alone. Investigation is usually only indicated if there is
uncertainty about the diagnosis, surgery is being considered, or there are concerns about underlying
malignancy.

Lymphangioscintigraphy (isotope lymphangiography) is the most commonly performed investigation. The

test involves injecting a radiolabelled colloid into a webspace and taking gamma-camera pictures at
intervals to determine lymphatic transit. If it is negative, lymphoedema is e ectively ruled out.
Lymphangioscintigraphy de nes anatomy, evaluates dynamics, and determines severity.

The main role of computed tomography is to diagnose malignancy, either primary or secondary, as a cause
of lymphoedema. Recurrent disease should be sought in patients with a previous history of pelvic or
abdominal malignancy. Magnetic resonance imaging can give clear images of the lymph channels and nodal
architecture. It can distinguish between lymphatic and venous swelling but gives less information than
lymphoscintigraphy.

Management
The treatment aims of lymphoedema management are to reduce limb swelling, reduce infection risk, and
improve function. Conservative measures are more likely to be successful when used early in the disease
process. Maintenance is an important part of the long-term management. Surgery is rarely indicated and is
11
palliative, not curative.

There is no cure for lymphoedema and this should be explained to the patient. General measures include
skin care to reduce infection risk, limb elevation and avoidance of tight clothing, exercise, weight reduction,
and simple massage. Manual lymphatic drainage is performed by specially trained therapists and uses
massage to stimulate the ow of lymph from an abnormal area to an adjacent normal area.

Graduated compression is used both in the initial treatment phase (usually achieved with multilayer
bandaging) and during the maintenance phase (usually compression stockings). Intermittent pneumatic
compression works best before subcutaneous brosis occurs. The a ected limb is placed in a sleeve that is
alternately in ated and de ated, to create a pressure gradient thereby moving uid out of the limb.

Surgery is only indicated in a very small proportion of patients in whom conservative measures have failed,
and there is severe disability or gross deformity, and can be by debulking or bypass.

Further reading
Burnand KG. The physiology and hemodynamics of chronic venous insu iciency of the lower limb. In Gloviczki P, Yao JS (eds)

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Handbook of Venous Disorders (2nd ed). New York: Arnold; 2011, 49–57.
Google Scholar Google Preview WorldCat COPAC

Eklof B, Rutherford RB, Bergan JJ, et al. American Venous Forum International Ad Hoc Committee for the Revision of the CEAP
Classification. Revision of the CEAP classification for chronic venous disorders: consensus statement. J Vasc Surg 2004; 40:1248–
52. 10.1016/j.jvs.2004.09.027
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Nicolaides AN. Investigation of chronic venous insu iciency: a consensus statement. Circulation 2000; 102:e126–
63. 10.1161/01.CIR.102.20.e126
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