# 62 Venous disorders

# AXILLARY VEIN THROMBOSIS

AXILLARY VEIN THROMBOSIS

Thrombosis of  the axillary vein (Paget–Schrotter disease) may occur following excessive exercise in a patient with an anatomically abnormal thoracic outlet, but is also associated - with excessive muscle bulk as found in weight lifters. The vein may be compressed by a cervical rib if  this is present early stage, the thrombus can be disrupted by thrombolysis delivered through one of  the arm veins. The vein must then be imaged to see if  there is any compression on elevation of  the arm. If  this is confirmed, thoracic outlet decompression can be carried out by resecting the cervical rib or first rib.

# Aetiology

Aetiology

The three factors described by Virchow over a century ago are still relevant in the development of  venous thrombosis. These are: /uni25CF contact of  blood with an abnormal surface (e.g. endothelial damage); /uni25CF abnormal flow (e.g. stasis); /uni25CF abnormal blood (e.g. thrombophilia). - There are many predisposing causes for VTE. These are listed in Table 62.2 . The most important factor is a hospital admission for treatment of  a medical or surgical condition. Injury , especially fractures of  the lower limb and pelvis, pregnancy and the oral contraceptive pill are other well - recognised predisposing factors. Endothelial damage is now known to be critically important. The interaction of  the endothelium with inflammatory cells, or previous deep vein damage, renders the endothelial surface hypercoagulable and less fibrinolytic. Stasis is a predisposing factor seen in man y of  the conditions described in Table 62.2 , especially in the postoperative period, in patients with heart failure and in those with arterial ischaemia. - ) and 

(a)
diagnostic venogram;
(b)
therapeutic
Figure 62.30
Post-thrombotic leg demonstrating features of eczema,
pigmentation and mild lipodermatosclerosis.

/uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF A number of  conditions are associated with increased coagulability of  the blood (thrombophilia) ( Table 62.3 Deficiencies of  antithrombin, activated protein C and protein S have all been shown to predispose to venous thrombosis in young patients. Activated protein C deficiency is associated with inheritance of  the factor V Leiden gene and may account for the higher incidence of  venous thrombosis in white populations (being present in 6–7%). It results in a small increase in the risk of  VTE, although it may act in concert with some of  the other predisposing factors. A thrombophilia should be excluded in any patient presenting with an episode of  VTE who gives a family history of  VTE or in whom there is no other predisposing factor. Although the development of  DVT is probably multifac torial, immobility (and hence stasis) remains one of  the most important factors. DVT is recognised as a complication of long-haul flights and other forms of  travel. 

Patient factors
Age
Obesity
Varicose veins
Immobility
Pregnancy
Puerperium
High-dose oestrogen therapy
Previous deep vein thrombosis or pulmonary embolism
Thrombophilia (see
Table 62.3
)
Disease or surgical procedure
Trauma or surgery, especially of pelvis, hip and lower limb
Malignancy, especially pelvic, and abdominal metastatic
Heart failure
Recent myocardial infarction
Paralysis of lower limb(s)
Infection
In
/f_l
ammatory bowel disease
Nephrotic syndrome
Polycythaemia
Paraproteinaemia
Paroxysmal nocturnal haemoglobinuria antibody or lupus
anticoagulant
Behçet’s disease
Homocystinaemia

# CLINICAL FEATURES OF VENOUS HYPERTENSION OF THE LE

CLINICAL FEATURES OF VENOUS HYPERTENSION OF THE LEG

The following clinical features are commonly seen: /uni25CF Varicose vein: subcutaneous dilated vein 3 /uni00A0 mm in diameter or larger. They are frequently elongated and tortuous, with intermittent ‘blowouts’, but are defined by the presence of  reflux and may be straight and uniform tubes morpho logically ( Figure 62.3 ). /uni25CF Telangiectasia (thread veins, spider veins and hyphen webs): represent tiny intradermal venules less than 1 /uni00A0 mm in diameter ( Figure 62.4 ). Maurice Klippel , 1858–1942, neurologist, La Salpêtrière, Paris, France. Paul Trénaunay , 1875–1938, French neurologist. Klippel and Trénaunay described this condition in a joint paper in 1900. A gaiter is a leather or cloth covering for the lower leg and ankle. The name is derived from the French ‘guetre’ for the same piece of  clothing. /uni25CF Reticular vein: small dilated ‘bluish’ subdermal vein 1–2.9 /uni00A0 mm in diameter, usually tortuous, can be di ffi cult to distinguish this from a normal subdermal vein in someone with white thin transparent skin. /uni25CF Saphena varix ( Figure 62.5 ) is a (usually painless) groin swelling apparent on standing. /uni25CF Corona phlebectatica (malleolar flare): a fan-shaped pat - tern of  telangiectasia on the ankle or foot. This is an early , sign of  advanced venous disease. /uni25CF Oedema: increased volume of fluid in the skin and soft tis - sues of  the leg. Commonly starts distally and moves more proximally with increasing venous dysfunction. Classically this is ‘pitting oedema’, with firm digital pressure leaving an indentation in the soft tissues. /uni25CF Eczema: an erythematous dermatitis, often appears minor, although it may be associated with significant itching and discomfort. In extreme cases it may progress to blistering and weeping ( Figures 62.6–62.8 ). /uni25CF Pigmentation (haemosiderosis): a brownish discoloration of  the skin, usually permanent. It is usually seen around the ankle, but is also seen in proximity to varicose veins and - incompetent perforators ( Figures 62.7 and 62.9 ). /uni25CF Lipodermatosclerosis (LDS): chronic inflammation and fibrosis of  the skin and subcutaneous tissues, resulting in a tight, contracted, ‘woody’ leg on examination. It occa - sionally results in significant contractures of  the Achilles 

(c)
varicose veins in the

tendon. This is a sign of  severe chronic venous disease ( Figures 62.6 and 62.9 ). /uni25CF Atrophie blanche: localised areas of  atrophic, white skin, often surrounded by telangiectasia and pigmentation. Some authors distinguish this from the white scarring left by ulceration; others do not. Either way , this is a sign of severe chronic venous disease ( Figure 62.6 ). /uni25CF V enous ulcer: full-thickness skin loss, usually around the ankle, which fails to heal spontaneously and is propagated by continuing venous hypertension and the changes associ ated with chronic venous disease ( Figure 62.10 ). 

Figure 62.4
Telangiectasia and reticular veins.
Figure 62.5
A saphena varix.

# CONGENITAL VENOUS ANOMALIES

CONGENITAL VENOUS ANOMALIES

There are four main types of  anomaly: /uni25CF aplasia; /uni25CF hypoplasia; /uni25CF duplication; /uni25CF persistence of  vestigial vessels. Aplasia is most commonly seen in the inferior vena cava and has a similar presentation to the post-thrombotic limb. Membranous occlusion of  the left common iliac vein (May– Thurner syndrome) often develops where the v ein passes behind the right common iliac artery (iliac vein compression syndrome). This leads to an iliac vein thrombosis, which most commonly a ff ects the left common and external iliac veins. Membranes may also narrow the hepatic veins, which can become totally occluded, leading to a Budd–Chiari syndrome. Hypoplasia results in a narrow vein, which frequently o ff ers little significant venous function and amounts to a functional venous occlusion, being circumvented by enlarged collateral venous tributaries. Duplications are quite common, with dou b le vena cava, femoral and renal veins; they often present as an incidental finding.

# Classification system

Classification system

The descriptive CEAP (Clinical–aEtiology–Anatomy–Patho physiology) classification for chronic venous disorders is widely utilised. - - 

Figure 62.6
Advanced skin changes: lipodermatosclerosis, eczema
and atrophie blanche.
Figure 62.7
Pigmentation (haemosiderosis) and mild eczema.
Figure 62.8
Severe eczema.
Figure 62.9
Haemosiderosis and mild lipodermatosclerosis of the calf
skin.

For clinical classification: /uni25CF C0: no signs of  venous disease; /uni25CF C1: telangiectasia or reticular veins; /uni25CF C2: varicose veins; /uni25CF C3: oedema; /uni25CF C4a: pigmentation or eczema; /uni25CF C4b: LDS or atrophie blanche; /uni25CF C4c Corona phlebectatica /uni25CF C5: healed venous ulcer; /uni25CF C6: active venous ulcer. Clinical class can be further characterised as symptomatic (s), asymptomatic (a) or recurrent following previous successful treatment or healing (r), e.g. C2a, C2s, C6r. For aetiological classification: /uni25CF Ec: congenital; /uni25CF Ep: primary; /uni25CF Es: secondary (post-thrombotic); /uni25CF En: no venous cause identified. For anatomical classification: /uni25CF As: superficial veins; /uni25CF Ap: perforator veins; /uni25CF Ad: deep veins; /uni25CF An: no venous location identified. For pathophysiological classification: /uni25CF Pr: reflux; /uni25CF Po: obstruction; /uni25CF Pr,o: reflux and obstruction; /uni25CF Pn: no venous pathophysiology identifiable. In clinical practice, patients are normally categorised as having ‘varicose veins’ or ‘venous ulcers’. Cases of  varicose veins may be uncomplicated or complicated. Complications may be chronic (as discussed above) or acute, including superficial vein thrombosis (thrombophlebitis) and bleeding. Uncomplicated varicose veins may be asymptomatic or symptomatic. 

Figure 62.10
Venous ulcer.

# Clinical features

Clinical features

The ulcer must be carefully examined. A venous ulcer usually has a gently sloping edge and the floor contains granulation tissue covered by a variable amount of  slough and exudate. Any significant elevation of  the ulcer edge should indicate the need for a biopsy to exclude a carcinoma (usually a squamous cell). V enous leg ulcers characteristically develop in the skin of the gaiter region, the area between the muscles of  the calf  and the ankle. This is the region where many of  the Cockett perfo rator s join the posterior tibial vein to the surface vein, known as the posterior arch vein. The majority of ulcers develop on the medial side of the calf, but may develop anywhere in the gaiter area. Extension onto the foot or into the upper calf  is uncommon and, if  there is ulceration at these sites, other diag noses should be seriously considered. Ulcers often develop in response to minor trauma; many patients notice some itch ing, perhaps associated with mast cell degranulation, before the ulcers develop . Almost all venous ulcers have surr ounding haemosiderosis (seen as pigmentation) and the more chronic ulcers develop LDS with associated fibrosis of the subcuta neous tissue ( Figure 62.10 ). This is manifest as thickening, pigmentation, inflammation and induration of  the calf  skin. The pigmentation comes from haemosiderin and melanin and the haemosiderin itself  may be an important factor in ulcer development. A full examination of  the front and back of  the limbs with the patient standing should be carried out to assess the presence of  varicosities and truncal incompetence of  the saphenous systems (note that venous ulcers are not always accompanied by varicose veins). All patients should hav e their pulses palpated and, if  there is any doubt, their arterial Doppler pressures should be measured. Sensation and proprioception should be assessed to exclude neuropathy , especially in patients with diabetes. A careful examination of  the hand and other joints may confirm the presence of rheumatoid arthritis or osteoarthritis. Frank Bernard Cockett , 1916–2014, surgeon, St Thomas’s Hospital, London, UK. Jean-Nicholas Marjolin , 1780–1850, surgeon, Paris, France, described the development of  malignant ulcers in scars in 1828. Most vascular surgeons will carry out a duplex scan when the patient with an ulcer is first seen to assess the status of  the deep and superficial veins. The presence of  reflux in these veins does not confirm a venous ulcer, but supports the diagnosis in the absence of  another cause and helps direct treatment. V enous ulcers are characteristically di ffi cult to heal; how - ever, persistence may indicate that there is another or coex - isting cause (e.g. malignancy , rheumatoid arthritis or arterial ischaemia). Biopsies are indicated if  malignancy is suspected and it is important to remember that a Marjolin’s type of ulcer (a squamous cell or basal cell carcinoma) can develop in a chronic longstanding venous ulcer ( Figure 62.28 ). Patients with atypical or with ulcers not responding to treatment should have a full blood count, blood glucose, erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) assessment as well as a sickle cell test if  the y have an appropriate ethnic background. Anaemia can both cause ulcers (e.g. sickle cell disease and pernicious anaemia) and be a result of ulceration (e.g. iron deficiency anaemia and the anaemia of  chronic disease). Polycythaemia is a rare cause of ulceration. An antibody screen should be obtained if  the ulcer appears ‘atypical’ or if  there is any suggestion of  joint disease (e.g. rheumatoid arthritis). All patients presenting with a new ulcer should have their Doppler pressures measured unless the - foot pulses are easily palpable and have been confirmed as such by a vascular specialist.

# Cystic degeneration

Cystic degeneration

As in the peripheral arterial system, cystic degeneration of  the vein wall is an uncommon cause of  venous occlusion. It may be detected by ultrasound. The cyst may be deroofed or the venous segment excised. -

# Diagnosis

Diagnosis

The most common presentation of  a DVT is pain and swelling, especially in the calf, usually in one leg; however, bilateral DVTs are common, occurring in up to 30%. When the swelling ) . - - 

Figure 62.31
An organised thrombus.

is bilateral, DVT must be di ff erentiated from other causes of systemic oedema, such as hypoproteinaemia, renal failure and heart failure. Some patients have no symptoms of  thrombosis and may first present with signs of  a pulmonary embolus, e.g. pleuritic chest pain, haemoptysis and shortness of breath. Patients may also develop shortness of  breath from chronic pulmonary hypertension. Sometimes the leg appears cellulitic and very occasionally it may be white or cyanosed: phlegmasia alba dolens and phlegmasia cerulea dolens ( Figure 62.32 indicates venous pressures that are so high they are impeding tissue perfusion. Patients who present with venous gangrene ( Figure 62.33 ) often have an underlying neoplasm. Clinical examination for DVT is unreliable. Physical signs may also be absent. Mild pitting oedema of  the ankle, dilated surface veins, a sti ff calf  and tenderness over the course of  the deep veins should be sought. Leg pain occurs in about 50% of patients with DVT but is non-specific. Homans’ sign – resistance John Homans , 1877–1957, Professor of  Clinical Surgery , Harvard University Medical School, Boston, MA, USA, a founding member of  the Society f Surgery . Philip Wells , contemporary , physician, University of  Ottawa, Ottawa, ON, Canada. specific and should not be elicited. Tenderness occurs in 75% of patients but is also found in 50% of  patients without objectively confirmed DVT . The pain and tenderness associa ted with DVT does not usually correlate with the size, location or extent of the thrombus. Clinical signs and symptoms of pulmonary embolus occur in about 10% of  patients with confirmed DVT . A low-grade pyrexia may be present, especially in a patient who is having repeated pulmonary embolus. Patients may have signs of  cyanosis, dyspnoea, raised neck veins , a fixed split sec - ond heart sound and a pleural rub if  they have pulmonary emboli causing right heart strain, although these signs may be subtle or absent. 

Figure 62.32
Phlegmasia cerulea dolens.
Figure 62.33
A foot with venous gangrene. The gangrene is symmet
rical, involving all of the toes. There is no clear-cut edge and there is
marked oedema of the foot.

# Epidemiology

Epidemiology

The adult prevalence of  visible varicose veins is between 30% and 50%. Factors a ff ecting prevalence include: /uni25CF Gender: the vast majority of  studies report a higher preva - lence in women than in men, though community preva - lence may di ff er. /uni25CF Age: the prevalence of  varicose veins increases with age. In the Edinburgh V ein Study , the prevalence of trunk vari - cosities in the age groups 18–24 years, 25–34 years, 35–44 years, 45–57 years and 55–64 years was 11.5%, 14.6%, 28.8%, 41.9% and 55.7%, respectively . /uni25CF Ethnicity: does seem to influence the prevalence of  vari - cose veins. /uni25CF Body mass and height: increasing body mass index and height may be associated with a higher prevalence of  vari - cose veins. /uni25CF Pregnancy: increases the risk of  varicose veins. /uni25CF Family history: evidence supports familial susceptibility to varicose veins. /uni25CF Occupation and lifestyle factors: there is inconclusive evi - dence regarding increased prevalence of  varicose veins in smokers, in patients who su ff er constipation and in those with occupations that involve prolonged standing.

# FURTHER READING

FURTHER READING

Barwell JR, Davies CE, Deacon J et al. Comparison of  surgery and compression with compression alone in chronic venous ulceration (ESCHAR study): randomised controlled trial. Lancet 2004; 1857–60. Brittenden J, Cotton SC, Elders A et al. Clinical e ff ectiveness and cost e ff ectiveness of  foam sclerotherapy , endovenous laser ablation and surgery for varicose veins: results from the Comparison of  LAser, Surgery and foam Sclerotherapy (CLASS) randomised controlled trial. Health T echnol Assess 2015; 19 (27): 1–342. Carradice D, Mekako AI, Mazari FA et al. Randomized clinical trial of  endovenous laser ablation compared with conventional surgery for great saphenous varicose veins. Br J Surg 2011; 98 (4): 501–10. Carradice D, Mekako AI, Mazari FA et al . Clinical and technical outcomes from a randomized clinical trial of  endovenous laser ablation compared with conventional surgery for great saphenous varicose veins. Br J Surg 2011; 98 (8): 1117–23. Carradice D, Wallace T , Gohil R, Chetter I. A comparison of  the e ff ectiveness of  treating those with and without the complications of superficial venous insu ffi ciency . Ann Surg 2014; 260 (2): 396–401. Coleridge-Smith P , Labropoulos N, Partsch K et al. Duplex ultrasound investigation of  the veins in chronic venous disease of  the lower limbs: UIP consensus statement. Eur J Vasc Endovasc Surg 31 : 83–92. Comerota AJ, Kearon C, Gu CS, et al . Endovascular thrombus removal for acute iliofemoral deep vein thrombosis. Circulation 2019; 1162-73. Gohel MS, Epstein DM, Davies AH. Cost-e ff ectiveness of  traditional and endovenous treatments for varicose veins. Br J Surg 97 (12): 1815–23. Gohel MS, Heatley F , Liu X et al . A randomized trial of  early endovenous ablation in venous ulceration. N Engl J Med 378 : 2105–114. Lurie F , Passman M, Meisner M, et al . The 2020 update of the CEAP classification system and reporting standards. J Vasc Surg Venous 363 : - Lymphat Disord 2020; 8 (3): 342-52. Erratum in: J Vasc Surg Venous Lymphat Disord 2021; 9 (1): 288. Michaels JA, Campbell WB, Brazier JE et al . Randomised clinical trial, observational study and assessment of  cost-e ff ectiveness of  the treatment of  varicose veins (REACTIV trial). Health T echnol Assess 2006; 10 (13): 1–196. National Institute for Health and Care Excellence. Venous thromboembolism in over 16s: reducing the risk of  hospital-acquired deep vein thrombosis or pulmonary embolism . NICE Guideline 89. London: NICE, 2018. Available from https://www .nice.org.uk/guidance/ 2006; ng89. National Institute for Health and Care Excellence. Varicose veins: diagnosis and management . NICE Guideline 168. London: NICE, 139 (9): 2013. Available from https://www .nice.org.uk/guidance/cg168. Shalhoub J, Lawton R, Hudson J et al . Graduated compression stockings as an adjuvant to pharmaco-thromboprophylaxis in 2010; elective surgical patients (GAPS study): randomised controlled trial. BMJ 2020; 369 : m1309. ‘VEIN’ supplement. Phlebology 2015; 30 (2 suppl): 3–52. 2018; Watson L, Broderick C, Armon MP . Thrombolysis for acute deep vein thrombosis. Cochrane Database Syst Rev 2016; Issue 11, Art. No. CD002783. 

Figure 62.40
(a)
Venous angioma of the leg;
(b)
magnetic resonance
imaging showing extensive angioma (white) throughout the super
/f_i
cial
tissues and anterior and posterior compartments of the left leg in a
different patient.
Figure 62.41
Inferior vena cava containing a
/f_i
lling defect from a
leiomyosarcoma (arrow).

# Introduction

INTRODUCTION

Up to 40% of  the adult population in resource-rich countries have diseases of  the veins of  the leg. This extraordinary prevalence along with the associated impairment in health- related quality of  life make it a very important area of  surgical practice. Surgical intervention has been revolutionised by /uni00A0 the development of  endovenous techniques, and level 1 evidence has demonstrated that treatment can be associated with very high clinical- and cost-e ff ectiveness. Despite the considerable importance placed on lower limb function during the manage ment of  orthopaedic and arterial diseases, venous diseases are often forgotten or dismissed as cosmetic practice. An under standing of  the nature and management of  venous disease is critical to address this imbalance and improve the quality of patients’ lives.

# Investigation

Investigation

Tourniquet tests and the use of  hand-held Doppler have now been abandoned. There is good evidence to support the policy of  duplex ultrasound scanning for all patients with varicose veins prior to any intervention. The best clinical results come from clinicians who are personally very skilled in the use of duplex ultrasound and use it to design a bespoke treatment for each individual patient, based upon their unique anatomy . A high-frequency linear array transducer of 7.5–13 /uni00A0 MHz is appropriate for the majority of  lower limbs in order to obtain good quality images. The B-mode settings (depth, focal zone, overall gain and dynamic g ain) should be optimised to ensure that the area of  interest is in the centre and occupies the major ity of  the image, and that the lumen of  the vein appears as a dark void in the subcutaneous and deep tissues. The pulsed wave spectral or colour Doppler settings should be optimised for the low-flow velocities encountered within veins. It is conventional to use blue to represent antegrade venous flow towards the heart and red for the reverse. Visible venous flow can be augmented by a calf  squeeze. The aim of  the duplex scan in a patient with varicose veins is to establish: /uni25CF the presence of  reflux in the deep and superficial venous system; /uni25CF the exact distribution and extent of reflux in the superficial venous system, including a ff ected junctions and perfora tors; /uni25CF the presence of  obstruction in the deep venous system; /uni25CF the suitability of  the incompetent superficial veins for the di ff erent treatments available (based upon diameter, extent, tortuosity , saphena varix); Christian Johann Doppler , 1803–1853, Professor of  Experimental Physics, Vienna, Austria, enunciated the ‘Doppler principle’ in 1842. Antonio Valsalva , 1666–1723, anatomist, Bologna, Italy . Also described the Eustachian tube and aortic sinuses. /uni25CF - an indication of  a pelvic source of  reflux or obstruction. In order to standardise measurements of venous diameter and reflux, it is recommended that examination of  the super - ficial veins is performed with the patient standing. Superficial or crural vein reflux is defined as retrograde flow in the r everse direction to physiological flow lasting for 0.5 seconds or more. The pr oximal deep veins require a duration of  1 second or more to be classified as incompetent. Reflux may be elicited by release of  a calf  or foot squeeze for proximal or calf  vari - cosities, respectively , manual compression over varicosity clus - ters, pneumatic calf  cu ff deflation, active foot dorsiflexion and relaxation or the Valsalva manoeuvre. The patient should stand facing towards the examiner with the leg rotated outwards, heel on the ground and w eight on the opposite limb ( Figure 62.11 ). The use of  a platform, ideally - with a handle or support bar for the patient and a stool tha t can drop to a low height, will improve the ergonomic com - fort of  both the sonographer and the patient. The scan should commence in the groin, using a transverse view to identify the GSV and CFV lying medial to the common femoral artery (the ‘Mickey Mouse’ sign; Figure 62.12 ). SFJ competence is assessed in the transverse view and potential destinations for reflux, including the GSV , the AAGSV and other major thigh tributaries superficial to the saphenous fascia, are noted. Any indication of  a pelvic source of  reflux suggests the need for more proximal imaging. The full length of  the GSV within its fascial compartment should be examined ( Figure 62.13 ), and its diameter measured if  required. The groin is next examined - - 

Figure 62.11
Patient position for venous duplex examination of the
great saphenous system.

for reflux or obstruction in the CFV , superficial femoral vein and SFJ using spectral and/or colour Doppler ( Figure 62.14 A loss of  phasic flow with respiration in the CFV suggests upstream obstruction and the need for proximal imaging. The presence and competence of  thigh and calf  perforators should be noted and the crural veins examined for reflux or obstruc tion. F or examination of  the SSV and posterior thigh extension of  the SSV (Giacomini vein), the patient is positioned facing away , knee slightly flexed, heel on the ground and the weight taken on the opposite leg. If  the SPJ is incompetent, the level of the SPJ in relation to the knee crease and whether the SSV joins the popliteal vein posteriorly , medially or laterally is noted if  open surgical ligation is to be entertained. In the transverse view , the SSV vein is followed distally , checking its competence and diameter in the proximal, mid- and distal calf. Finally , the patency and competence of  the popliteal vein is assessed. Pelvic and iliac veins may be investigated using transabdominal or transvaginal duplex. V ery occasionally investigations other than duplex are required, and these may be non-invasive, suc h as magnetic resonance (MR) venography , or invasive, such as contrast venography or intravenous ultrasound (IVUS). The use of  varicography has become ). historical ( Figure 62.15 ). 

Figure 62.12
‘Mickey Mouse’ transverse B-mode image of the right
(R)
common femoral vein (CFV) and artery (CFA), great saphenous
vein (GSV) and saphenofemoral junction.
Figure 62.13
‘Saphenous eye’ transverse B-mode view of the great
saphenous vein in fascial compartments of the thigh. The fascial line
above the vein is the saphenous fascia. A true great or small saphe
nous vein will not cross this line, although the fascia may become
discontinuous around the knee. The line deep to the vein is the fascia
lata, with the muscle beneath.
Figure 62.14
Spectral Doppler trace of the saphenofemoral junction
showing antegrade and retrograde
/f_l
ow. The downward spike on
the trace is the antegrade augmented
/f_l
ow and this is followed by
approximately 4 seconds of retrograde
/f_l
ow.
-
Figure 62.15
Varicogram. (This is now a historical investigation.)

Investigation

The diagnosis of DVT and pulmonary embolus should be established by special investigations as the symptoms and signs are non-specific and may be absent. In addition, treatment with anticoagulation is not without risk and the diagnosis must be made with reasonable certainty . Many centres direct investigations based upon the modi - fied Wells score ( Table 62.4 ) , with further imaging dictated by these results. These scores can be unreliable though, especially in hospital inpatients, and should only be considered a guide. V enous duplex ultrasound is commonly performed to look for evidence of  thrombosis throughout the deep or superficial venous system. Ideally , this should be performed by an expe - rienced vascular sonographer, but the v olume of  cases is such that compression ultrasound is frequently being performed by non-specialists. Compression ultrasound involves applying pressure with the ultrasound probe over the common femoral ). This or Vascular 

TABLE 62.4
Modi
/f_i
ed Wells criteria for predicting deep
-
vein thrombosis (DVT).
Variable
Score
Lower limb trauma or surgery or immobilisation in a
1
plaster cast
Bedridden for >3 days or surgery in last 4 weeks
1
Tenderness along the line of femoral or popliteal veins
1
Entire limb swollen
1
Calf >3
/uni00A0
cm larger circumference than other side 10
/uni00A0
cm
1
below tibial tuberosity
Pitting oedema
1
Dilated collateral super
/f_i
cial veins (not varicose veins)
1
Previous DVT
1
Malignancy (including treatment up to 6 months ago)
1
Intravenous drug abuse
3
Alternative diagnosis more likely than DVT
–2
Low probability (5%) of DVT (score –2 to 0); moderate probability
(17%) of DVT (score 1 or 2); high probability (17–53%) of DVT (score
>2).

will compress tightly shut. In the presence of  DVT they will not fully compress. It is rapid to both learn and perform, but not ideal and most importantly misses calf vein thrombosis. Calf  vein thromboses may propagate to form a more extensive thrombus, which may in turn embolise. The optimal manage ment of calf vein thrombosis when detected is not clear; some units use surveillance, with others anticoagulating such patients upon detection. Ascending venography , which shows a thrombus as a fill ing defect, is now rarely r equired unless thrombolysis is being considered ( Figure 62.34 ). MR venography may also be used. Pulmonary embolus is diagnosed definitively by computed tomography (CT) pulmonary angiogram, which will demon stra te the presence of  filling defects in the pulmonary arter ies ( Figure 62.35 ). Pulmonary angiography is rarely required unless thrombolysis is being considered. The di ff erential diagnosis of  a DVT includes a ruptured Baker’s cyst, a calf muscle haematoma, a ruptured plantaris muscle, a thrombosed popliteal aneurysm and arterial isch aemia. Duplex scanning will detect many of these conditions but often patients present with non-specific pain in the calf that resolves with no firm diagnosis being made. The di ff eren tial diagnosis of a pulmonary embolism includes m yocardial infarction, pleurisy , pneumonia and aortic dissection.

# Klippel–Trénaunay syndrome

Klippel–Trénaunay syndrome

This is a combined anomaly of  a cutaneous naevus, persistent vestigial veins with varicose veins and soft-tissue and bone hypertrophy . The condition is a mesodermal abnormality that is not familial ( Figure 62.36 ). Segments of  the deep veins are hypoplastic or aplastic and there may be an associated obstruction of  the lymphatics. The condition must be distinguished from the Parkes-Weber syndrome, in which there ar e multiple arteriovenous fistulae causing venous hypertension, ulceration and high-output cardiac failure. Virtually all patients with Klippel–Trénaunay syndrome should be treated conservatively with compression hosiery; however , some will benefit from laser ablation of  the naevus, stapling of  the bones to avoid leg length discrepancy and occa sional removal of  large superficial varicose veins, provided the George Budd , 1808–1882, Professor of  Medicine, King’s College Hospital, London, UK, described this syndrome in 1845. Hans Chiari , 1851–1916, Professor of  Pathological Anatomy , Strasbourg, Germany (Strasbourg was returned to France after the end of  the First World War, in 1918), gave his account of  this condition in 1898. Frederick Parkes-Weber , 1863–1962, physician, The German Hospital, Dalston, London, UK. Sir James Paget , 1814–1899, English surgeon and pathologist, best known for his description of  Paget’s disease of  the bone. Leopold von Schrotter , 1837–1908, Austrian physician and laryngologist, Chair of  Laryngology , University of  Vienna, Vienna, Austria. deep veins are patent. LMWH should be given to all patients having surgery as this syndrome is associated with an increased risk of  VTE. - 

Figure 62.36
Two patients with Klippel–Trénaunay syndrome.
(a)
This
patient has a longer leg and a capillary naevus;
(b)
this patient has a
large lateral anomalous axial vein.

# Learning objectives

Learning objectives

To understand: Venous anatomy and physiology • The pathophysiology of venous hypertension • The clinical signi /f_i cance and management of super /f_i cial • venous re /f_l ux

# Leiomyoma and leiomyosarcoma of the vein wall

Leiomyoma and leiomyosarcoma of the vein wall

These are extremely rare tumours that are usually slow growing. They present with pain and a mass with signs of venous obstruction, e.g. oedema and distended veins. Duplex scanning, CT ( Figure 62.41 ) and magnetic resonance imaging (MRI) show a filling defect within the vein wall. Treatment is by resection with replacement by autogenous vein taken from another site. Rarely , a PTFE graft is required. When the tumour a ff ects the vena cava it must be resected and replaced with a prosthetic graft.

# Management

Management

Many patients with asymptomatic varicose veins do not progress - to develop complications, although a significant proportion do, and there is no clear confirmatory evidence that treating such patients prevents the development of  future complications. There is clear evidence, however, that those with symptoms and/or complications see a significant quality-of-life benefit from treatment to remove or ablate refluxing superficial veins. When interventional treatment is planned there are con - siderable variations in practice and treatment strategies. A detailed description of  the nuances, merits and criticisms of the various options is beyond the scope of  this chapter; how - ever, a description of the basic treatment modalities available is presented below . An experienced surgeon will have his/her own preferred methods, but will frequently employ several or all methods in chosen circumstances, not infrequently in the same patient. Compression hosiery relies on graduated external pressure to improve deep venous return and reduce venous pressures. It may be knee length or thigh length; there is no evidence which length of  stocking is more e ff ective and hence below-knee stockings are usually prescribed as they are easier to don and have much better patient acceptance. Compression hosiery is classified according to the pressure it exerts: the British classifi cation class 1 stockings exert pressure of  14–17 /uni00A0 mmHg, class 2 exert 18–24 /uni00A0 mmHg and class 3 exert 25–35 /uni00A0 mmHg. Compression hosiery significantly improves varicose vein symptoms but is not popular with patients, with compliance rates and long-term tolerance being univ ersally poor. There is no evidence to suggest that compression hosiery prev the occurrence or progression of  varicose veins. Further more, incorrect application of  compression hosiery can have serious consequences (pressure necrosis, tourniquet e ff ects); thus assessment, prescription and application of  compression hosiery should be limited to those with the appropriate skills and training. Ther e are level 1 trial data to demonstrate that interventional treatment o ff ers superior improvements in qual ity of  life and is cost-e ff ective. Compression is therefore to be regarded as an adjunct to assessment or treatment, unless by patient choice. Endothermal ablation Endothermal ablation technologies replaced surgical ligation and stripping as the gold standard treatment once randomised trials demonstrated that they were marginally safer, have extremely high technical e ffi cacy , o ff er superior quality of  life post procedure (with a rapid recovery) and equivalent improve ments in quality of  life in the longer term. The techniques are cost-e ff ective as they can be performed as an outpatient under local anaesthetic. The basic concept is that a treatment device is inserted into the incompetent axial vein percutaneously . The vein is surrounded by tumescent local anaesthetic solution. This compresses the vein onto the treatment device, emptying it of blood. It also hydro-dissects tissues such as nerves away from the zone of  injury . Finally , it acts as a heat sink, mopping up excess thermal energy to prevent remote damage. The treat ment device then produces thermal energy that destroys the structure of  the vein, resulting in permanent occlusion. Two broad technologies exist: laser ablation and radiofrequency ablation (RFA). Laser ablation Endovenous laser ablation (EVLA) utilises a small flexible glass fibre that is inserted into the vein. Laser energy (typically at a wavelength of  1470 /uni00A0 nm) is transmitted down the fibre and is absorbed at the point of  treatment at the end of  the fibre. Absorption of  this radiation results in a vigorous generation of thermal energy . The tip of  the fibre may be bare, focusing the energy in a very small area; divergent forward firing, spreading the energy over a larger area; or divergent side or radial firing. It is postulated that the last two designs allow a more even distribution of  energy , reducing vein wall perforations that Friedrich Trendelenburg , 1844–1924, Professor of  Surgery successively at Rostock (1875–1882), Bonn (1882–1895) and Leipzig (1895–1911), Germany . The Trendelenburg position was first described in 1885. bruising. There is no clear evidence to support one design over another. This procedure is very good for treatment of  any v ein that will allow the passage of  a guidewire. No technique has reported a higher technical e ffi cacy rate. The procedure begins with ultrasound-guided marking of the truncal vein to be treated and the site of proposed cannulation. T he varicosities are also marked at this stage if - concomitant treatment (phlebectomy or foam sclerotherapy) is to be undertaken. The patient is then positioned on the procedure couch in the reverse Trendelenburg position. For the GSV , the patient is supine with the hip of  the leg to be treated externally rotated and slightly flexed. A pillow under the contralateral hip/lower back may improve patient comfort. ents For the SSV the patient is positioned in the prone position. - The vein is then cannulated percutaneously under ultrasound guidance, at the lowest point of  reflux. Some devices allow passage of  the fibre directly through a short sheath, while others use a wire first, allowing passage of  a catheter that then carries the laser fibre. The former is slightly faster with fewer steps; the latter allows greater success with more tortuous - veins. Accurate positioning of  the fibre tip with ultrasound is crucial ( Figure 62.16 ), but the exact location is controversial, with some surgeons positioning the tip several centimetres distal to the junction and others aiming for a flush occlusion. Proponents of the former cite that this strategy protects the deep vein from inadvertent damage and/or thrombosis. Proponents of  the latter argue that neoreflux in junctional tributaries is a common pattern of  recurrence and that in expert hands the rate of  deep vein injury is no di ff erent and the thrombosis rate may be lower (presumably as there is minimal patent stump - in which to form thrombus). Following the administration of perivenous tumescent anaesthesia ( Figure 62.17 ), the ablation can be performed. Practice varies as to the power of  the laser and the withdrawal speed, but commonly an energy delivery - 

Deep vein
Figure 62.16
Endovenous laser ablation; B-mode longitudinal imaging
during catheter tip positioning at the saphenofemoral junction. The
saphenofemoral junction is highlighted (in blue) with an arrow pointing
to the catheter.

There is no clear evidence to guide the optimal power and pullback speed. Compression is usually applied following treatment, but /uni00A0 there is no consensus over the method, degree or duration, and this is true of  postprocedural compression with all techniques. Radiofrequency ablation RFA uses the same treatment principles, but an electromag netic current is used to create the thermal energy . A range of di ff erent devices have been created but the most popular, which has the most supportive evidence, is the ClosureFast™ device (Medtronic) ( Figure 62.18 ). This device has a wire coil on the end of  a treatment catheter. The generator passes an electrical current through the coil until the surrounding temperature reaches 120°C. This is then maintained for a treatment cycle of  20 seconds. The coil is then withdrawn for a set length and another treatment cycle is commenced. Coils of  3 /uni00A0 cm and 7 /uni00A0 cm are produced, with the latter increasing the speed of  treatment, while still being suitable for most anatomies. RFA. The evidence is generally equivocal, with both treat - ments having relative advantages and disadvantages; choice often comes down to personal preference. Both are excellent treatment options and can be applied successfully to the major - ity of  patients. There hav e been a range of studies comparing EVLA and RFA. The evidence is generally equivocal, with both treat - ments having relative advantages and disadvantages; choice - often comes down to personal preference. Both are excellent treatment options and can be applied successfully to the major - ity of  patients. Some summary points: /uni25CF Both treatments have a very high e ffi cacy (>95% closure rate) and are suitable for treatment of  the vast majority of patients presenting with superficial vein reflux in associa - tion with superficial axial incompetence. /uni25CF V eins that are very tortuous may still be suitable for endo - thermal ablation but require a guidewire and in the case of  EVLA, a catheter-based, rather than direct fibre system. Both techniques o ff er this. 

(a)
(b)
Figure 62.17
(a)
Ultrasound-guided in
/f_i
ltration of perivenous tumes
cent anaesthetic via a long spinal needle. The anaesthetic solution
is in
/f_i
ltrated using an electronic foot-operated pump;
(b)
ultrasound
image of a perivenous ‘halo’ of anaesthetic solution around the vein
and catheter in transverse section.
-
Figure 62.18
Radiofrequency ablation with ClosureFast™ introducing
the treatment catheter through a sheath. The distal 7 cm of this device
comprises a metal coil.

allowing direct and targeted delivery of  adjuvant foam sclerotherapy , e.g. to ablate areas of  neovascularisation. This is more di ffi cult with radiofrequency catheters due to a smaller lumen (0.018 versus 0.035 /uni00A0 in), but it is still possible. Advantages in favour of  RFA over EVLA include: /uni25CF The core skill set to plan and perform these procedures is the same; however, EVLA requires an understanding of  power settings and pullback speeds, whereas a radio- frequency device typically has a set treatment cycle on a single button press. This reduces the device-specific learn ing curve and the possibility of  a novice making a mistake with the energy delivery . /uni25CF The automatic treatment cycle also frees the surgeon’s fo cus, allowing better communication with the patient and with care, concurrent treatment, e.g. infiltrating local an aesthetic into the tributaries and performing phlebectomy , reducing procedural times . /uni25CF EVLA requires specific laser safety protocols including the design and function of  the room as well as specific training for the operator and theatre team. This can have an im pact on the set-up and flexibility of  the service. /uni25CF RFA may be associated with a marginal reduction in pain and bruising, although this has not been shown to impact on periprocedural quality of  life or recovery . Advantages in favour of  EVLA over RFA include: /uni25CF When it comes to veins that are very large in diameter (>15 /uni00A0 mm) EVLA can be a better option, allowing an increase in energy delivery and higher e ffi cacy rates. /uni25CF EVLA consumables are typically much less expensive; however, costs vary by device and market and the price di ff erence has reduced over time. /uni25CF A standard EVLA fibre may be used to treat perforators, whereas a specific additional device is typically required for Lorenzo Tessari , b. 1949, physician, Trieste, Italy . for perforator management remain uncertain. As endothermal ablation treats only junctional and truncal incompetence, debate exists regarding the management of  var - icosities. These can be managed concomitantly or sequentially by either phlebectomy or sclerotherapy . Concomitant phlebec - tomy ( Figure 62.19 ) results in a more rapid improvement in disease-specific quality of  life, and allo ws the vast majority of patients to complete treatment in a single visit. Non-endothermal , non-tumescent ablation Endothermal ablation was a large step forwards in the - management of  superficial incompetence; however, all tech - niques require the injection of  tumescent local anaesthetic solution and this can be uncomfortable for the patient. Other - techniques that avoid injection are being developed. - Ultrasound-guided foam sclerotherapy Sclerotherapy is the original non-endothermal, non-tumes - cent technique and has been performed for over 100 years. It involves the injection of  a sclerosing agent directly into the superficial veins. The most commonly used is sodium - tetradecyl sulphate. The direct contact with detergent causes cellular death and initiates an inflammatory response, aiming to result in thrombosis, fibrosis and obliteration (sclerosis). Blood deactivates the action of  the sclerosing agent and the doses administered need to be limited to avoid adverse e ff ects, causing a trade-o ff between poor e ffi cacy and safety . This led to the development of  ultrasound-guided foam sclerotherapy (UGFS). The use of  foam increases the e ff ective volume of the agent, maximising endothelial contact and displacing any blood that deactivates it. The procedure commences with the patient standing, and the sites of  venous cannulation are selected and marked using ultrasound. With the patient supine, the major venous trunks and superficial varicosities to be treated are then all cannulated using ultrasound guidance prior to any injection ( Figure 62.20 ). Once all injection sites are cannulated the foam can be prepared. The most widely used method is that of Tessari; this utilises two syringes connected using a three-way 

Figure 62.19
Phlebectomy performed under tumescent anaesthesia
following endothermal ablation.
Figure 62.20
Foam sclerotherapy; cannulation of veins during ultra
-
sound-guided foam sclerotherapy.

tap. A 1:3 or 1:4 ratio mixture of  sclerosant and air is drawn into one syringe, and is then oscillated vigorously between the two syringes about 10 or 20 times ( Figure 62.21 ). The foam produced in this way is stable for about 2 minutes so it should be injected as soon as it has been made. The leg is then elevated to empty the veins of blood, and injection of foam commences first with superficial varicosities and ends with injection of  the GSV or SSV . Only 1–2 /uni00A0 mL of  foam should be injected at a time and the distribution of  the foam should be monitored and massaged with the ultrasound probe. When the foam is visu alised at the site of  junctional incompetence no further foam should be injected. The maximum volume of  foam that should be injected at a single session should not exceed 10–12 /uni00A0 mL as the incidence of complications is dir ectly related to the volume of  foam injected. Compression is then applied as following endothermal ablation. While it is postulated that compression may have a larger e ff ect upon e ffi cacy for this treatment, prac tice is not informed by evidence and a wide variation exists. Outside of  a small number of  centres, the e ffi cacy of  UGFS is significantly worse than for endothermal ablation, leading to high reintervention rates, and the rates of complications such as phlebitis and pigmentation can be high. UGFS does how ever carry some significant advantages: /uni25CF It avoids tumescent anaesthetic and is therefore a less pain ful procedure (although postoperative pain is probably similar). /uni25CF No axial or tributary veins are too tortuous. /uni25CF It also allows the treatment of  calf  veins with overlying skin damage or ulceration without the need to pierce through damaged skin. /uni25CF Consumable treatment costs are very low . These factors mean that many surgeons using endothermal techniques also use foam sclerotherapy as an adjunct in specific circumstances. Catheter-directed sclerotherapy and mechanochemical ablation The e ffi cacy of  sclerotherapy relies on endothelial contact with fresh, undiluted sclerosant. Some have therefore experimented with catheter-delivered sclerotherapy rather than trying to milk the sclerosant down the vein lumen. There is no good evidence to date that this increases e ffi cacy and the technique is not in widespread use. A related technology that has shown more promise is mechanochemical ablation ( Figure 62.22 ). This involves a led wire from the end. treatment device that deploys an ang This attaches to a motorised handle. The catheter is placed within the vein lumen as for endothermal ablation. The trigger - on the handle is depressed, spinning the wire around and liquid sclerosant is infiltrated via the catheter simultaneously during catheter withdrawal. It is thought that the spinning wire causes physical damage to the endothelium and allows a deeper pen - etration of  the sclerosant into the vein wall. The technique is possible in most cases without tumescent anaesthesia, although a small number of  patients find the procedure uncomfortable - and the device can ‘snag’ on the vein, tearing it or rarely strip - - ping it altogether. Comparative studies with endothermal abla tion suggest similar early e ffi cacy rates but increased medium-/ long-term recanalisation rates. The axial ablation is usually less painful than endothermal ablation, but this advantage is - lost when it is combined with phlebectomy of  the tributaries; efore, it is uncertain whether it can replace endothermal ther ablation, unless axial ablation is to be performed in isolation. - Treating longer veins can also be challenging owing to limita - tions in catheter length and the safe dose of  sclerosant. It is a good choice for a patient with needle phobia who is happy to forgo treatment of  varicose tributaries. Endovenous glue The final non-tumescent technique is the endoluminal appli - cation of  cyanoacrylate adhesive ( Figure 62.23 ). Again, this involves a treatment catheter placed within the vein lumen. A handle is used to infiltrate the adhesive in 0.1-mL applications via the catheter. The vein is then compressed, sealing the results are similarly promising and lumen closed. Early e ffi cacy patients experience minimal intraprocedural pain. Long-term results and the optimal management of tributaries are unknown (similar to mechanochemical ablation). The consumable costs are currently the highest for any venous ablative technique. 

Figure 62.21
Foam sclerotherapy; Tessari method of foam sclerosant
preparation.
Figure 62.22
Mechanochemical ablation device (reproduced with
permission from Vascular Insights).

Open surgery The principles of  traditional ligation and stripping are to fully dissect the point of  junctional incompetence and to remove the refluxing axial vein and dilated tributaries. The operation is usually performed under general anaesthesia but locoregional anaesthesia is used by some; the infiltration of tumescent local anaesthesia around the axial vein prior to stripping may have some advantages, but is not widely used. The role of  open surgery as a primary treatment of  a reflux ing superficial axis has been considerably reduced with the development of the minimally invasive techniques described above, the long-term results of which are at least comparable to open surgery but with significantly less morbidity and faster recovery . Experienced endovenous surgeons do still use open surgery in some circumstances and a venous surgeon needs to be trained and experienced in this area. Surgical adjuncts including phlebectomy and, occasionally , perforator ligation are much more commonly used, and the former has been shown to have a significant impact upon out come. Saphenofemoral ligation and great saphenous stripping An oblique groin incision is made at the level of, and lateral to, the pubic tubercle, ideally above the groin crease. The GSV is identified and dissected to the SFJ, which should be clearly established before the vein is divided to avoid disastrous inadvertent transection of the superficial femoral vein. The anatomy is often variable but six GSV tributaries may be encountered close to the SFJ: /uni25CF Laterally: /uni25CF superficial inferior epigastric vein; /uni25CF superficial circumflex iliac vein. /uni25CF Medially: /uni25CF superficial external pudendal vein; /uni25CF deep external pudendal vein. /uni25CF Distally: /uni25CF anterior accessory of  the great saphenous vein; /uni25CF posteromedial thigh vein. Classically , these are ligated distal to their divisions. A flush SFJ ligation is then performed and the GSV retrogradely stripped to around the knee ( Figure 62.24 ). Phlebectomy is perfor med as discussed above. Closure of  the cribriform fascia, with sutures or synthetic patches over the ligated SFJ, does not reduce groin recurrence. - - Stripping to the lowest point of  reflux may improve results, but at a cost of  increased saphenous nerve complications and is not widely performed. More recently , some surgeons have argued that surgical trauma and subsequent inflammation in the groin are associated with neovascularisation, which in turn may lead to recurrence. Furthermore, others hypothesise that it is the loss of  the normal groin tributaries that may be responsible for driving the process of  neovascularisation. These concepts have led some to believe that ligation of  the refluxing vein should be distal to the tributaries and that the junction itself should be left untouched. There is no clear clinical evidence to support these hypotheses. 

Figure 62.23
Endovenous glue device (reproduced with permission
from Medtronic Inc.).
Femoral
vein
Ligature
Point of division
Great saphenous vein
Figure 62.24
Saphenofemoral junction ligation and great saphenous
vein stripping.

Saphenopopliteal junction ligation and small saphenous stripping Preoperative duplex to mark the position of  the SPJ is highly recommended ( Figure 62.25 ). The patient is positioned in the prone position, a transverse incision is made over the premarked SPJ, the fascia is divided and the SSV is exposed. The SPJ can then be formally dissected with a flush ligation or the SSV can be gently retracted and ligated as proximally as possible. No good evidence exists to favour one technique over the other; proponents of  the flush ligation would argue that it avoids leaving a stump of  SSV , a common source of  recur rence, while proponents of  the simple SSV ligation technique argue that it reduces the incidence of  the most common serious complications – nerve injury and popliteal vein injury . The SSV can then either be stripped or the proximal sec esected. Those who strip argue that tion of  the vein can be r it reduces the incidence of recurrence, while opponents feel it increases the incidence of  sural nerve injur y . There are no randomised trials comparing these techniques. Once again, phlebectomy is then performed. Adjunctive surgical techniques Phlebectomy This may be performed following treatment of  junctional incompetence and axial vein reflux, or as a sole treatment under local anaesthetic in patients with isolated tributary incompetence, or possibly in very early axial reflux, which duplex ultrasound. Phlebectomy is usually performed through small stab incisions using small mosquito forceps and/or phle - bectomy hooks that have been demonstrated to be superior – in terms of  bruising , pain and generic quality of  life – to transilluminated-powered phlebectomy ( Figure 62.19 ). Perforator ligation The majority of  studies assessing the role of  perforator ligation have been in patients with venous ulcers, analysing the e ff ects on ulcer healing; even in this situation randomised data are lacking. The role of  perforator ligation in patients with uncom - plicated varicose veins is even less clear. In uncomplicated varicose veins perforators may be ligated through a small, duplex-guided incision, while in patients with skin changes subfascial endoscopic perforator ligation may be preferred, although the benefits are unproven. Perforators can also be ablated with endovenous techniques. Complications of standard varicose vein surgery Complications (minor and major) are reported in up to 20% of patients who undergo traditional varicose vein surgery . Wound infections, the most common complication, are reduced by prophylactic antibiotics. Nerve injury is the most common serious complication. The incidence of  saphenous nerve neuralgia is up to 7% following GSV stripping to the knee (the incidence is higher with stripping to the ankle). The incidence of  sural nerve neuropraxia and common peroneal nerve injury may be as high as 20% and 4%, respectively , following SSV surgery . The incidence of  venous thromboembolic complications is approximately 0.5% following varicose vein surgery; however, patient risk factors must be individually assessed and appropriate prophylaxis administered according to guidelines. Recurrent varicose veins Approximately 10–20% of  patients who present to hospital with varicose veins have had previous intervention. Prospective data on long-term results following intervention for recurrent varicose veins are sparse and the criteria for defining recur - - rence are variable. Significant clinical recurrence 5–10 years following vari - cose vein surgery occurs in 10–35% of  patients, but minor/ duplex-detected recurrence is much more common, being of - the order of  70%. Causes of  recurrence include: neovascu - eflux in the residual axial vein, inadequate initial larisation, r surgery and new junctional reflux. Neovascularisation is the development of  new veins within postsurgical tissue. These er time can span the tissue between veins lack valves and ov a ligated junction and nearby tributary veins. If significant in size and/or number, these may contribute to recurrent venous hypertension. Recurrence is more common following SSV surgery than following GSV surgery , and in patients with high body mass index, while stripping of  the incompetent axial vein reduces ence rates. Limited data suggest that recurrence rates recurr following endovenous thermal ablation may be lower than 

Figure 62.25
Preoperative marking of the saphenopopliteal junction
and small saphenous vein mapped using duplex scanning.

atypical distribution and duplex assessment is mandatory ( Figures 62.26 and 62.27 ). Open surgery for recurrent varicose veins is associated with a high (40%) complication rate, the most common being lymph leak and wound infection, thus endovenous interventions would seem to o ff er an attractive alternative, where feasible. Summary box 62.1 Varicose veins /uni25CF /uni25CF /uni25CF /uni25CF 

Are one of the most common conditions causing a physical
impairment in quality of life
Interventional treatment improves quality of life and is highly
cost-effective
Anatomical and physiological assessment using duplex
ultrasound is invaluable in the diagnosis and planning of
treatment
Ultrasound-guided endovenous ablation has revolutionised
treatment, minimising procedural morbidity while being highly
effective
Figure 62.26
Recurrent anterior abdominal wall varicose veins follow
ing saphenofemoral junction ligation complicated by iliac deep vein
thrombosis.

Management

- The very best results are seen in specialist multidisciplinary ulcer services. The cause of  a venous leg ulcer is venous hyper - - tension and the keystone of  management is to decrease this hypertension using venous ablation and compression therapy . - 

Figure 62.28
A Marjolin’s ulcer (a squamous cell cancer arising in a
chronic venous ulcer).

In patients with venous leg ulcers, treatment of  superficial venous incompetence has been demonstrated to accelerate healing and reduce recurrence; therefore, expeditious referral to a vascular service for assessment is recommended. Compression The most clinical and cost-e ff ective compression regimes are two-layer compression hosiery or four-layer compression bandaging. The latter includes: /uni25CF Orthopaedic wool: distributes the pressure and reduces undue pressure on sensitive areas susceptible to pressure damage. Also helps to absorb excess exudate that escapes the primary dressing. /uni25CF Cotton crepe: smooths the wool and holds it in place. /uni25CF Elastic bandage: first compressive layer, contributes about one-third of  the interface pressure. /uni25CF Cohesive bandage: second compressive layer, increases sti ff ness and adds approximately two-thirds of  the inter face pressure. The ideal interface pressure in pure venous ulceration is 35–40 /uni00A0 mmHg. Skilled application of  these dressings is essential for both safety and e ffi cacy , and the best results come from specialist nursing teams based either in secondary care or in the community . Compression in mixed ulcers is controversial, but emerging evidence suggests that it is both safe and e ff ective when performed and monitored appropriately . With an ankle–brachial pressure index (ABPI) of  0.5–0.8 modified compression with an interface pressure of  30 mmHg is safe and e ff ective and pressures of  up to 40 mmHg have been described in studies using inelastic bandages without ill e ff ect. Contrary to conventional thinking, studies have shown an increase in perfusion in patients treated in this way , presumably by a reduction in capillary back pressure. Patients do see respectable healing rates in this group, but they remain lower than in those patients with an ABPI >0.8. It is not clear whether revascularisation followed by full compression yields better results, but this is common practice. Patients with an ABPI <0.5 or an ankle pressure <60 /uni00A0 mmHg must undergo revascularisation prior to any compression treatment. Other treatments Pentoxifylline, which increases microvascular perfusion by decreasing plasma cellular viscosity and cytokine inhibition, has been demonstrated to be a useful adjunct to compression by augmenting ulcer healing. Horse chestnut seed extract has been shown to be a safe and e ffi cacious treatment for chronic venous hypertension, improving symptoms and reducing leg volume. A number of  biological dressings hav e been developed, including fetal keratinocytes and collagen meshes, which have been shown to improve healing; however, they ar cost-e ff ective for the majority of  ulcers. Pinch grafts and ulcer excision with mesh grafting have been shown to provide good early healing with moderate long-term results (50% healed at 5 years). cellulitis and all other specific ulcer-healing drugs are of  dubi - ous validity . A large range of  topical therapies and primary dressings have similarly failed to have an impact. Management

As with all traumatic injuries, the management priorities are the assessment and management of  issues a ff ecting the airway , then breathing and then circulation. V enous injuries have the potential to threaten life through massive bleeding and patients require vascular access, circulatory support and blood products. Trauma patients with life-threatening haemorrhage are at risk of  hypothermia, acidosis, functional and consumptive coagu - lopathy and paradoxical thrombosis, and these issues need to be prevented where possible and managed when present. V enous pressures are low and so, where there is access to the site of injury , pressure will control bleeding and in most cases o ff er definitive management. Intervention is required where pressure cannot be applied, or where the loss of venous function itself  threatens life or limb. Intervention can include reduction and stabilisation of  a fracture (e.g. pelvis), endo - venous embolisation or stent grafting. A small proportion of  venous injuries will require formal exploration and ligation or repair. Di ff erent types of  repair are shown in Figure 62.39 ; the type of  r epair carried out depends on the extent of  the venous injury , including how much venous wall has been lost or damaged. Lateral sutures and vein patches are ideal methods of  repair and end-to-end anastomosis is sat - isfactory , provided that it is not carried out under tension. A jump graft may be required. V ein replacement should be by autogenous tissue whenever possible, using vein harvested from another site, e .g. the internal jugular vein or the GSV from an undamaged limb. Artificial grafts, such as polytetrafluoroethylene (PTFE) g rafts, are at risk of  infection and have given poor results in recent conflicts. The use of  anticoagulants and an arteriovenous fistula to reduce the risk of  thrombosis in the vein graft are controversial and depend on the associated injuries that are present. In 

-

contaminated wounds, tetanus toxoid and antibiotics should be given. A fasciotomy should always be considered if  there is a concomitant arterial and venous injury . 

(b)
(c)
(d)
Figure 62.38
Types of venous damage:
(a)
incision;
(b)
transection;
(c)
irregular laceration;
(d)
avulsion of a tributary.

# PEL VIC CONGESTION SYNDROME

PEL VIC CONGESTION SYNDROME

Pelvic congestion syndrome (PCS) is among the di ff erential diagnoses to be considered in female patients presenting with chronic pelvic pain and may be significantly underdiagnosed. PCS su ff erers are typically premenopausal, multiparous women aged 20–45 years, who present with severe dull aching pelvic pain thought to be the direct result of  ovarian and pelvic varicosities. The pain is usually non-cyclical, and may be precipitated by prolonged standing. Other symptoms include dysmenorrhoea, menorrhagia, rectal discomfort or urinary frequency . Signs may include tenderness over the uterus/ovaries, vulval varicosities and haemorrhoids. There may be vulval and atypically distributed thigh varicosities. The road to a diagnosis of  PCS is often a long and laborious one, usually only made following extensive investigations to exclude e not other more common causes of  pelvic pain. Abdominal, pelvic and transvaginal duplex examination allows dynamic visualisation of  pelvic blood flow and should be the initial investigation of  choice, as these are rapid, readily accessible outpatient procedures that are also valuable in excluding other pathologies. Alternatives include MR venography and diagnostic venography . Medical treatments for PCS include psychotherapy , progestins, danazol, gonadotropin receptor agonists (GnRH) with hormone replacement therapy , and non-steroidal anti inflammatory drugs (NSAIDs). Historical open surgical pr ocedures (extraperitoneal resection of  ovarian veins) have now largely been superseded by percutaneous pelvic vein embolisation ( Figure 62.29 ), reducing peri- and post- procedural morbidity while maintaining high success rates. 

Figure 62.29 (a, b)
Left ovarian vein incompetence supplying the pelvic and pudendal varicosities:
embolisation.

# Pathology

Pathology

The thrombus commences as a platelet aggregate. Subse quently , fibrin and red cells form a mesh until the lumen of the vein wall occludes. The coralline thrombus then progresses Hulusi Behçet , 1889–1948, Turkish dermatologist, described a disease of  inflamed blood vessels in 1937. /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF as a propagated loose red fibrin clot containing many red cells ( Figure 62.31 ). This is likely to extend up to the next large venous branch and it is possible for the clot to break o ff and embolise to the lung as a pulmonary embolus. In this situation the embolus arising from the lower leg veins becomes detached, passes through the large veins of  the limb and vena cava, through the right heart and lodges in the pulmonary arteries. This may totally occlude perfusion to all or part of  one or both lungs. This results in a clinical spectrum from tachycardia and pain, through respiratory failure (despite adequate ventilation) to cardiovascular collapse and death. Moderate-sized emboli can cause pyramidal-shaped infarcts on imaging. 

(thrombophilia) that lead to an increased risk of venous
thrombosis.
Congenital
De
/f_i
ciency of antithrombin III, protein C or protein S
Antiphospholipid antibody or lupus anticoagulant
Factor V Leiden gene defect or activated protein C resistance
Dys
/f_i
brinogenaemias
Acquired
Antiphospholipid antibody or lupus anticoagulant

# Pathophysiology of ulceration

Pathophysiology of ulceration

The exact pathophysiology of  ulcer development has not been established. Originally , it was thought that static blood within the superficial veins led to hypoxia, which caused tissue death (stasis ulcers). This was not confirmed by investigation of venous oxygen saturation, which was found to be higher in ulcerated limbs. This led to the concept of  arteriovenous fistulae, which were thought to develop in response to the high venous pressure; however, this could not be confirmed. High venous pressure was found to be associated with a pericapil - lary infiltrate. This includes fibrin and other proteins, which are known to lead to fibrosis. It was hypothesised that these ‘cu ff s’ could act as an impediment to di ff usion of  oxygen and nutrients. Leukocytes were found to be reduced in the blood retur ning - from legs with venous hypertension. This decrease in leukocyte passage was shown to increase if  short-term venous hyperten - sion was induced by application of  a tourniquet. This led to the conce pt of  white cell ‘trapping’, which, however, has not been confirmed by further investigation. Polymor phonuclear leuko - cytes were not found within the tissues, but increased numbers of  mast cells, monocytes and lymphocytes have been found in - periulcer tissues. Reactive oxygen species are increased in the ulcer environ - ment and these may generate fr ee radicals, leading to tissue 

-

the fibroblasts in the ulcer surrounds are also abnormal, being in a ‘senescent’ state. Growth factors may be inhibited, leading to poor repair, and their absence may also lead to ulceration. It is debated whether these factors are the cause or e ff ect of an ulcer. At present, ambulatory venous hypertension is the only accepted underlying cause of  venous ulceration. This also explains why venous ulcers are never seen in the upper limb. It is important to try to define the exact mec hanism of  ulcer development. V enous hypertension may be the result of  primary valve incompetence of  the saphenous veins, incompetence of the perforating veins or incompetence or obstruction of  the deep veins.

# Prevention of recurrence

Prevention of recurrence

Once an ulcer has healed the patient must be re-evaluated in an attempt to prevent recurrence. If  not already performed, patients should undergo treatment for their superficial venous incompetence. Class 2 below-knee graduated compression stockings should be prescribed for all patients with residual reflux or deep venous occlusion, or those with recurrent ulceration despite not being in this group. These should be worn for life.

# Prognosis

Prognosis

Nearly all venous ulcers can be healed, but, even in those who have successful ablation or wear their stockings religiously , - there is a 20–30% incidence of  reulceration by 5 years. The greatest risk of  reulceration is in the post-thrombotic leg. Summary box 62.2 Venous leg ulcer /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF 

Is associated with a profound impairment in quality of life
Ulcers are not infrequently dif
/f_i
cult to heal and prone to
recurrence
The treatment of these chronic wounds is associated with high
costs to healthcare systems and patients
The mainstay of treatment is the reduction in venous
hypertension, with ablation of super
/f_i
cial venous
incompetence and compression
Early endovenous ablation of super
/f_i
cial re
/f_l
ux almost halves
the time to healing of venous leg ulcers, reduces ulcer
recurrence rates and is cost-effective

Prognosis

It is now recognised that repair of  a major vein can be carried out with a 70–80% success rate, reducing the morbidity of  a combined arterial and venous injury considerably (especially limb loss). Complex repairs should not, however, be carried out if  a patient’s life is at risk, when ligation may have to su ffi ce in the short term.

# Prophylaxis

Prophylaxis

Prophylactic methods can be divided into mechanical and pharmacological. A variety of  mechanical methods have been tried, but only the use of  graduated elastic compression stockings and external pneumatic compression have been William Morrant Baker , 1839–1896, surgeon, St Bartholomew’s Hospital, London, UK, described these cysts in 1877. - - - - - shown to be worthwhile by reducing the incidence of  throm - bosis. Newer devices, such as electronic nerve stimulators, lack evidence of  e ffi cacy to date. More recent emerging evidence is - casting some doubt on the benefit of  mechanical prophylaxis in surgical patients and ther e are further studies underway . Compression-based prophylactic measures should be avoided in patients with peripheral vascular disease. Pharmacological methods are more e ff ective than mechanical methods at risk reduction, although they carry an increased risk of  bleeding. In the past, low-dose unfractionated heparin was used both intravenously and subcutaneously . In the absence of renal impairment, most centres currently use low-molecular-weight heparin (LMWH) given subcutaneously . This is given once daily , does not require monitoring and has a lower risk of  bleeding complications. Patients who are being admitted for surgery may be graded as low , moderate or high risk for pulmonary embolism and VTE ( Tables 62.5 and 62.6 ). Patients in the medium- or high-risk groups should be considered for pharmacological 

Figure 62.34
An ascending venogram of a deep vein thrombosis seen
as
/f_i
lling defects (arrows) with contrast passing around the thrombus.
Figure 62.35
A computed tomography pulmonary angiogram show
-
ing pulmonary emboli as
/f_i
lling defects (arrow) in the pulmonary artery.
TABLE 62.5
Modi
/f_i
ed Wells criteria for predicting
pulmonary embolism (PE).
Variable
Score
Clinical signs and symptoms of DVT (minimum of leg
3
swelling and pain on palpation of deep veins)
Alternative diagnosis less likely than PE
3
Heart rate >100
/uni00A0
bpm
1.5
Immobilisation >3 days or surgery within past 4 weeks
1.5
Previous DVT or PE
1.5
Haemoptysis
1
Malignancy (treatment or palliation within past 6
1
months)
A score of <4 means PE is unlikely (12.4%); >4 is suggestive of PE
(37.1%).
bpm, beats per minute; DVT, deep vein thrombosis.

/uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF prophylaxis with an anticoagulant medication. Recent level 1 evidence suggests that the addition of  mechanical prophylaxis in such patients a ff ords no additional benefit. 

for venous thromboembolism.
Low
Minor surgery <30 minutes; any age; no risk factors
Major surgery >30 minutes; age <40; no other risk factors
Minor trauma or medical illness
Medium
Major surgery; age 40+ or other risk factors
Major medical illness: heart/lung disease, cancer, in
/f_l
ammatory
bowel disease
Major trauma/burns
Minor surgery, trauma, medical illness in patient with previous
DVT, PE or thrombophilia
High
Major orthopaedic surgery or fracture of pelvis, hip, lower limb.
Major abdominal/pelvic surgery for cancer
Major surgery, trauma, medical illness in patient with DVT, PE or
thrombophilia
Lower limb paralysis (e.g. stroke, paraplegia)
Major lower limb amputation
DVT, deep vein thrombosis; PE, pulmonary embolus.

# Signs

Signs

The presence of  tortuous dilated subcutaneous veins is usually clinically obvious. These are confined to the GSV and SSV systems in approximately 60% and 20% of  cases, respectively . The distribution of  varicosities may indicate which superficial axis is defective; medial thigh and calf  varicosities suggest GSV incompetence ( Figure 62.3a ), posterolateral calf  varicosities are suggestive of  SSV incompetence ( Figure 62.3b ), whereas anterolateral thigh and calf  varicosities may indicate isolated incompetence of  the AAGSV ( Figure 62.3c ). Any of  the clin ical features above may be present. Large, dilated veins around the SFJ may present as a (usually painless) lump, emergent when standing and disappearing when recumbent. This is a saphena varix ( Figure 62.5 ). Gentle palpation over the varix during coughing may elicit an impulse and it ma y be mistaken for a groin hernia.

# Symptoms

Symptoms

Varicose veins frequently cause symptoms. Patients describe aching, heaviness, throbbing, burning or bursting over a ff ected areas and sometimes the whole limb. Such symptoms typically increase throughout the day or with prolonged standing, and are relieved by elevation or compression hosiery . Itching is also commonly described, though this is more frequent in the presence of  complications, as is swelling of  the ankle. V enous symptoms in the absence of complications can be vague and it may be di ffi cult to ascertain from history alone whether they are truly venous in origin and, therefore, whether treatment will help. A trial of  compression hosiery can help as venous symptoms should show some beneficial improvement. Symptoms can be very severe and interfere with a patient’s daily activities such as work, recreation and caring for children and adults. Such symptoms are independent of  the degree of v enous incompetence or the presence of complications, including skin changes short of  ulceration. Studies have also shown that symptoms are associated with a significant deficit in health-related quality of  life, and significant improvements are seen with treatment to remove or ablate the refluxing veins. The maximal benefit is seen in those with uncomplicated symptomatic varicose veins, as skin changes and a proportion of  the associated morbidity are frequently irreversible. reticular veins occur very commonly in the absence of  sig nificant reflux or obstruction and in the vast majority do not cause any physical symptoms, though cosmetic treatment is commonly sought.

# THE ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB

THE ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB

The venous system of  the lower limb can be divided anatomi cally into the superficial venous system , which is located within the superficial tissues, and the deep venous system beneath the deep fascia of  the leg, accompanying the arterial tree. The superficial veins drain into the deep system, either at junctions or via fascial perforating veins, and the deep veins then return blood to the right atrium of  the heart. V enous anatomy is characteristically variable. The terminology used below is consistent with international consensus. The deep veins of  the lower limb ( Figure 62.1a ) include three pairs of  venae comitantes, which accompany the three crural arteries (anterior and posterior tibial and peroneal arter ies). These six veins intercommunicate and come together in the popliteal fossa to form the popliteal vein, which also receives the soleal and gastrocnemius veins. The popliteal vein passes up through the adductor hiatus to enter the subsartorial canal as the femoral vein, w hich receives the deep (profunda) femoral vein (or veins) in the femoral triangle before passing behind the inguinal ligament to become the external iliac vein. The internal iliac vein combines with the external iliac vein in the pelvis to form the common iliac vein. The left common iliac vein passes behind the right common iliac artery to join the right common iliac vein on the right side of  the abdominal aorta to form the inferior vena cava, which goes on to the right atrium. Far more anatomical variations exist within the superficial veins of  the lower limb, but there are almost always two trunks - or axes – the great and small saphenous veins ( Figur e 62.1b,c ). These lie superficial to the fascia lata (deep fascia) but deep to - the saphenous fascia, in the saphenous ‘envelope’. As the sole of  the foot is often placed under significant pressure, the majority of  the venous drainage of  the foot is into the dorsal venous arch, running in the subcutaneous tissues over the metatarsal heads. T he medial end of  this arch drains into the first axis: the great saphenous vein (GSV). This is the longest vein in the body and is the most frequently a ff ected by superficial incompetence. The GSV passes anterior to the - medial malleolus and ascends the leg accompanied by the saphenous nerve in the superficial tissues medial to the tibia, , looping posteriorly at the level of the medial condyle of the femur and continuing in the medial thigh. In the groin, it unites with tributaries corresponding to the arterial branches of  the common femoral artery , before piercing the cribriform fascia covering the saphenous opening (approximately 2.5 /uni00A0 cm below and lateral to the pubic tubercle, but often somewhat higher) and terminates by draining into the common femoral vein (CFV) at the saphenofemoral junction (SFJ). Throughout its course the GSV unites variably with other superficial - tributaries. /uni00A0 The anterior accessory of  the great saphenous vein (AAGSV)  is one of  the most common. This is often seen originating around the lateral border of  the knee, although it sometimes originates as low as the lateral end of  the dorsal venous arch. Occasionally , this vein may also course up the medial aspect of  the thigh, anterolateral to the GSV and 

The management of venous ulceration
•
Venous thromboembolism
•

following its course. In this instance, its origin is typically a confluence of  small tributaries around the knee. There is usually an in-line GSV axis passing uninterrupted from the foot (in some cases this may be hypoplastic), but this pattern of  AAGSV is commonly mistaken for the GSV itself  (some surgeons will call this a duplex GSV; a true duplex GSV is rare). The AAGSV may drain into the GSV in the thigh, but is typically at or near the junction itself. The small saphenous vein (SSV) originates from the lateral side of  the dorsal venous arch and accompanies the sural nerve as it passes posterior to the lateral malleolus, then upwards in the posterior midline of  the leg. In the proximal calf  it is usually found sitting in the groove between the two muscular heads of gastrocnemius. Its termination commonly occurs by piercing the fascia of  the popliteal fossa to drain into the popliteal vein at the saphenopopliteal junction (SPJ). However, this junction is highly variable and the vein may terminate as low as the mid-calf. The SSV may extend cranially beyond the SPJ, in which case it is known as either a cranial extension of  the SSV , which terminates by piercing the fascia in the posterior thigh to drain into the deep system, or the Giacomini vein, which communicates with the GSV system occasionally joining the GSV at or about the SFJ. In some cases, the SSV does not terminate at or below the popliteal fossa at all, but continues on as described above. In the calf  and thigh there are a number of  valved perforat ing (communicating) veins that join the superficial to the deep veins at inconstant sites and which allow blood to flow from the superficial to the deep venous system. The most important of these are the direct perforating veins of  the medial and la calf  and the communicating veins around the knee and in the mid-thigh. Carlo Giacomini , 1840–1898, anatomist, Turin, Italy . On his death he left his skeleton to the Anatomical Museum in Turin. Ernest Henry Starling , 1866–1927, physiologist, University College, London, UK. 

femoral vein
Saphenofemoral
junction
Super
/f_i
cial
Profunda femoral
femoral vein
vein
Popliteal vein
Anterior tibial veins
Posterior tibial veins
(usually paired)
(usually paired)
Peroneal veins
(usually paired)
Figure 62.1
(a)
Anatomy of the deep veins of the lower limb;
(b)
omy of the super
/f_i
cial veins of the lower limb (great saphenous axis);
(c)
anatomy of the super
/f_i
cial veins of the lower limb (small saphenous
axis).
Great saphenous vein
Posteromedial thigh
Anterior accessory
tributary
of the great
saphenous vein
Anterior tributary
of the leg
anat
-
(c)
Cranial extension
of small saphenous
(Giacomini) vein
Saphenopopliteal
junction
Small saphenous vein

# Treatment

Treatment

Deep vein thrombosis The management of  DVT has in the past been focused upon reducing the risk of  pulmonary embolus. Patients who are confirmed to have a DVT on duplex imaging should be rapidly anticoagulated with a ‘treatment dose’ of  subcutaneous LMWH. Patients with significant renal impairment should be commenced on intravenous unfractionated heparin. Patients who have a sensitivity towards heparinoids, such as those with heparin-induced thrombocytopenia, should commence on another anticoagulant, such as fondaparinux (an indirect factor Xa inhibitor) or bivalirudin (a direct thrombin inhib itor). This will achieve rapid anticoagulation and reduce the risk of  embolisation. Typically , patients will then commence on oral anticoagulation for at least 3 months (or longer depending upon the persistence of  risk factors or in recurrent cases). Oral anticoagulation using new or ‘novel’ anticoagulants (NOACs), which directly inhibit either factor Xa (rivaroxaban and apixaban) or thrombin (dabigatran), is recommended as they are equally e ff ective as vitamin K antagonists (warfarin) in preventing recurrent symptomatic VTE but are associated with less major bleeding complications. Patients who cannot be safely anticoagulated (usually because of  bleeding risks) should be considered for a tempo rary inferior vena cava filter, until either they are safe to be Leo Buerger , 1879–1943, Professor of Urologic Surgery , The New Y ork Polyclinic Medical School, New Y ork, NY , USA, described thromboangiitis obliterans in 1908. the filter may be retrie ved. Endovascular surgery aiming to restore patency , including thrombus removal, lysis and stenting tec hniques, are increasingly /uni00A0 used in patients with acute DVT aiming to reduce the risk of  chronic post-thr ombotic syndrome. Research suggests this may be beneficial in selected patients, for example those with iliofemoral thrombosis. Pulmonary embolus Most pulmonary emboli can be treated by anticoagulation and observation, but severe right heart strain and shortness of  breath indicate the need for thrombolysis or radiologically guided catheter embolectomy . Superficial vein thrombosis This condition was previously known as thrombophlebitis. An abnormal endothelium is a much more common precip - itating factor than in most DVTs. Common causes include external trauma (especially to varicose veins), venepunctures and infusions of  hyperosmolar solutions and drugs. The presence of  an intravenous cannula f or longer than 24–48 hours often leads to local thrombosis. Some systemic diseases such as thromboangiitis obliterans (Buerger’s disease) and malignancy , especially of the pancreas, can lead to a flitting thrombophlebitis (thrombophlebitis migrans), a ff ecting di ff er - ent veins at di ff erent times. Finally , coagulation disorders such as polycythaemia, thrombocytosis and sickle cell disease are often associated, as is a concomitant DVT . The surface vein feels solid and is tender on palpation. The overlying skin may be attached to the v ein and in the early stages may be erythematous before gradually turning brown. A linear segment of vein of  variable length can be easily palpated once the inflammation has died down. A full blood count, coagulation screen and duplex scan of the deep veins should usually be obtained. Any sugges - tion of  an associated malignancy should be investig ated using Summary box 62.3 Venous thromboembolism - /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - 

May be unprovoked, in which case an association with an
inherited thrombophilia should be considered
Is much more commonly seen as a complication of illness or
surgery
Is associated with both quality-of-life impairment and a risk of
mortality
All healthcare professionals should actively assess the
risk and consider preventative measures where this risk is
increased
Management should involve measures to reduce the risk
of extension and/or embolisation, typically with systemic
anticoagulation
Early thrombus removal is increasingly being used aiming to
prevent chronic post-thrombotic syndrome, and rarely for limb
salvage

inal CT scan. Most patients are treated with NSAIDs and topical heparinoid preparations and the condition resolves spontaneously . Proximity to a deep venous junction or long a ff ected length are indications for short-term anticoagulation and interv al duplex assessment. Rarely , infected thrombi require incision or excision. Ligation to prevent propagation into the deep veins is almost never required. Associated DVT or thrombophilia is treated with anticoagulation.

# VENOUS ENTRAPMENT SYNDROMES

VENOUS ENTRAPMENT SYNDROMES

The axillary vein and the popliteal vein are the two veins that are most commonly compressed. The former is compressed at the thoracic outlet between the �rst rib and the clavicle, where it usually presents as an axillary vein thrombosis (see Axillary vein thrombosis ) ( Figure 62.37a ). The latter is compressed by an abnormal insertion of  the gastrocnemius muscles. Entrapment may cause discomfort and swelling of  the limb during exercise before thrombosis develops. Treatment is by surgical decompression, excising the �rst rib or dividing the abnormal musculature of  the gastrocnemius insertion.

# VENOUS INJURY

VENOUS INJURY

Blunt or penetrating trauma almost always damages some small and medium-sized veins, which can be safely ignored or ligated without causing any problems. Larger axial venous recognised that these axial veins should be repaired whenever possible to reduce subsequent morbidity (pain and swelling in the tissues being drained) and limb loss when associated with a concomitant arterial injury . Many venous injuries remain undiagnosed at the time of  injury (e.g. crural vein damage associated with a fractured tibia) and only present many years later when post-thrombotic changes become apparent. V enous injuries occur from both civilian and military trauma but the incidence of  venous military injuries has been particularly well documented. In total, 40–50% of  arterial injuries have concomitant venous injuries, especially in the popliteal fossa. The mechanism may be laceration, contusion or avulsion ( Figure 62.38 ). Iatrogenic injuries result from damage at the time of  surgery and from punctures caused by catheter inser - tion. Thrombosis , haemorrhage and embolisation are all com - mon complications and arteriovenous fistulae may develop when there is a local concomitant arterial injury . Associated injuries to soft tissue, arteries and bones often overshadow the venous injury . Massive haemorrhage from the pelvic bones or the inferior vena ca va can rapidly lead to hypovolaemic shock and death if left untreated. Haematomas are common and engorgement, cyanosis and swelling are also indicative of  a major venous injury . 

(a)
(b)
Figure 62.37
Thoracic outlet syndrome:
(a)
cervical ribs on plain
radiograph;
(b)
elevation of the arm causes occlusion of the axillary
vein with collaterals. The patient has had previous surgery to decom
press the left side (arrow in
(a)
).

# VENOUS LEG ULCER

VENOUS LEG ULCER

V enous disease is responsible for around 85% of  all chronic lower limb ulcers in resource-rich countries. Community-based prevalence is 0.1–0.3% in adults (2–4% in the elderly). V enous leg ulcer has a disproportionate cost to society , with profound impairment in health-related quality of  life for both patients and their carers; the dressings alone account for 1–3% of  west ern healthcare expenditure. Furthermore, 15–30% of  patients with ‘venous’ leg ulcers have concomitant arterial occlusive disease. This is termed a ‘mixed’ ulcer. T here are many other causes of  leg ulcers and these must be excluded in any patient presenting with ulceration. Causes of  leg ulceration include: /uni25CF venous disease: superficial incompetence, deep incompe tence or obstruction; /uni25CF arterial ischaemic ulcers; /uni25CF vasculitic ulcers; /uni25CF traumatic ulcers; /uni25CF neuropathic ulcers; /uni25CF neoplastic ulcers; /uni25CF infections, especially in low and middle income countries. 

Figure 62.27
Recurrent varicose veins secondary to an incompetent
thigh perforator.

# VENOUS PATHOPHYSIOLOGY

VENOUS PATHOPHYSIOLOGY

The purpose of  the venous system is primarily to return blood back to the heart so that it can be delivered into the pulmonary circulation. The venous system contains approximately 60% of the total blood volume, with an average pressure of around 5–10 /uni00A0 mmHg. Mechanical factors, alongside the autonomic nervous and endocrine systems, control the rate at which - blood is delivered to the right atrium. Through its e ff ects upon myocardial contractility via the Starling mechanism, venous return is one of  the factors responsible for determining cardiac output. teral Blood enters the lower limb through the femoral arteries before passing through arterioles into the capillaries, which have a pressure of  about 32 /uni00A0 mmHg at their arterial ends. This pressure is reduced along the course of  the capillaries and is approximately 12 /uni00A0 mmHg at the venular end of  the capillary . The pressure continues to fall in the main veins, and is as low as 5 /uni00A0 mmHg at the upper end of  the vena cava where it enters the right atrium. The venous pressure in a foot vein on standing is equiv alent to the height of  a column of  blood extending from the heart to the foot, e.g. approximately 100 /uni00A0 mmHg. To enable blood to be returned against gravity in the standing position a pressur e gradient must exist between the veins in the leg and those in the chest. This gradient is created in two ways. First, the increase in thoracic volume during inspiration decreases intrathoracic pressure. Second, the pressure in the veins of the leg is increased by compression by the surrounding mus cles (the ‘calf  muscle pump’) and to a lesser extent the tone of  the venous wall. The deep veins of  the calf  are capacious and are joined by blind-ending sacks called the soleal sinusoids, which force b lood into the popliteal and crural veins during calf  muscle pump contraction, e.g. walking. The foot pump also ejects blood from the plantar veins during walking. As the calf  muscles contract, the veins are compressed and the valves only allow blood to pass in the direction of  the heart. The pressure within the calf compartment rises to 200–300 /uni00A0 mmHg during muscle contraction. Rapid blood flow in the deep veins at junctions and perforators draws blood from the superficial veins, driving this up the deep veins also. During muscle relax ation, the pressure falls and further blood from the superficial veins enters the deep vein. Each time this occurs the pressure falls in the superficial venous compartment until a thr is reached, when the venous inflow keeps pace with ejection from the deep veins. This is normally around 30 /uni00A0 mmHg, a fall of approximately two-thirds of the resting venous pressure. The net reduction in the pressure of  the superficial system is Rudolf Virchow , 1821–1902, pathologist, Charité Hospital, Berlin, Germany , was the first to be credited with describing iliac vein compression. It was not until 1957 that May and Thurner (Innsbruck, Austria) clearly described compression of  the left common iliac vein by the right common iliac artery . leg and the thorax and a patent and compliant venous system containing competent valves ( Figure 62.2 ). An absence of  one or more of these results in venous hypertension, which leads to further vein wall damage, including loss of  compliance, thickening, dilatation and valvular dysfunction. This venous damage goes on to reduce the function of  the a ff ected veins, worsening the venous hypertension in a vicious cycle. When exposed to high venous and capillary pressures chronically , the soft tissues of  the leg will be damaged, causing a spectrum of  damage that becomes irreversible. The causes of  venous hypertension are listed in Table 62.1 . /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF The majority of  patients with venous disease have a problem primarily with the vein wall structure and in most this is confined to the superficial veins. Little is known about the mechanism of  initiation of  the changes in the vein wall. These changes are complex, but are typified by valvular failure allowing retrograde flow within the vein with gravity - (venous incompetence). It is no longer thought that venous incompetence is caused by a primary mechanical valvular failure. eshold The vein wall changes include inflammatory cell infiltration and activation, dysfunctional smooth muscle cell proliferation, collagen deposition, decreased elastin content and increased matrix metalloproteinases. These e ff ects typically lead to loss 

limb
Standing
80
70
60
50
40
30
Normal limb
20
Foot vein pressure (mmHg)
10
Walking
Standing
0
0
10
20
30
40
Time (seconds)
Figure 62.2
Effect of exercise on the super
/f_i
cial venous pressure in
health and disease. The light blue line demonstrates the reduction in
pressure primarily related to the action of the calf muscle pump. The
dark blue line demonstrates how venous dysfunction is associated
with reduced net antegrade
/f_l
ow during exercise, resulting in a relative
increase in venous pressure when compared with normal (venous
hypertension).
TABLE 62.1
Factors causing venous hypertension.
Pressure gradient dysfunction
Increased abdominal or thoracic pressure
COPD
Pregnancy
Obesity
Large tumour
Constipation
Decreased calf muscle pump function
Immobility
Ankle joint fusion
Paralysis
Dysfunction of the venous system
Venous structural de
/f_i
cit
Valvular agenesis
Valvular incompetence
Venous dilatation
Venous tortuosity
Loss of vein wall compliance
Loss of venous tone
Arteriovenous
/f_i
stula
Venous occlusion
Agenesis
Thrombosis
Iatrogenic/trauma
Venous compression
May–Thurner syndrome
Pelvic/abdominal tumour
Pelvic/abdominal radiotherapy
COPD, chronic obstructive pulmonary disease.

of  compliance, dilatation, elongation (causing tortuosity) and secondary valvular dysfunction. This process can be initiated anywhere in the venous tree. Secondary varicose veins may develop in patients with post-thrombotic limbs and in patients with congenital abnormalities such as the Klippel–Trénaunay syndrome or multiple arteriovenous fistulae. The extent and number of  incompetent veins governs the extent of  the venous hypertension and correlates with the severity of  the soft-tissue complications seen. Importantly however, neither the reflux burden nor the presence of  skin changes, short of  ulceration, correlate with the presence or degree of  symptoms. 

Figure 62.3
Varicose veins:
(a)
left leg varicose veins in the distribution of an incompetent great saphenous vein (marked for intervention);
/uni00A0
(b)
right leg varicose veins in the distribution of the small saphenous system with a recent episode of phlebitis;
distribution of an isolated incompetent anterior accessory of the great saphenous vein with associated gaiter area skin changes.

# VENOUS THROMBOEMBOLISM

VENOUS THROMBOEMBOLISM

V enous thromboembolism (VTE) is an important condition within surgery , and autopsy studies suggest that it is the most common direct cause of  death in surgical patients. V enous thrombosis is the formation of  a semisolid coagulum within the venous system and may occur in the superficial system (super ficial vein thrombosis [SVT] or ‘thrombophlebitis’) or the deep system (deep vein thrombosis [DVT]). V enous thrombosis of the deep veins of the leg may be complicated by the immediate risk of pulmonary embolus and sudden death. Subsequently , patients are at risk of  developing PTS ( Figure 62.30 venous ulceration. While DVT may occur in the upper limb, it is the leg that gives rise to the vast majority of  the morbidity and subsequent complications of  this condition.

# VENOUS TUMOURS Venous malformation cavernous angio

VENOUS TUMOURS Venous malformation cavernous angioma/haemangioma

These malformations are common, representing one end of a spectrum of  arteriovenous malformations. They often a ff ect the skin but also extend into the deep tissues, including bones and joints. They usually present with variable swelling and dilated veins beneath the skin. Occasionally , there is no visible mass and the complaint is one of  pain. Haemorrhage and thrombophlebitis may exacerbate the pain. A soft compressible mass, which is venous in colour especially if  it is under the skin, is usually present ( Figure 62.40a ). A dark-blue tinge is often apparent, even if  the malformation is deeply situated. Nodules within the mass usually represent previous episodes of thrombosis. The size and extent of  the haemangioma are best visualised by nuclear MR with a short tau inversion recovery (STIR) sequence ( Figure 62.40b ) or CT scanning with contrast enhancement. V enography rarely shows an abnormality , but direct puncture with contrast injection shows the connections of  the malformation. Treatment is a highly specialised area. Treatment options nowadays rarely initially involve surgical excision as once this Alexis Carrel , 1873–1944, a French surgeon who emigrated to work at the University of  Chicago, Chicago, IL, USA. He was awarded the Nobel Prize in Physi ology or Medicine in 1912 for pioneering vascular suturing techniques. is done future embolisation and sclerotherapy are very di ffi cult. No treatment is entirely curative because it is di ffi cult to remove all of  the angiomatous tissue or sclerose the angioma com - pletely . Sclerosis can be dangerous when the veins connect to the deep system, particularly near the central nervous system. 

(b)
(c)
(d)
(e)
Figure 62.39
Types of venous repair:
(a)
lateral suture (risk of ste
-
nosis);
(b)
patch graft;
(c)
Carrel triangulation technique of venous
anastomosis;
(d)
panel graft;
(e)
spiral graft.