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usually be developed above and below the sapheno-femoral junction, allowing eventual
circumferential control of the junction, which can be divided and transfixed with a non-
absorbable suture. If the long saphenous vein is still present, identification of the proximal
end in scar tissue in the groin may be facilitated by passing a stripper up the
vein, proximally.
On completion of surgery, local anesthetic infiltration of groin and stripper retrieval
wounds with a preparation such as 0.5% Marcain reduces postoperative discomfort.
Use of Tourniquets
Some surgeons advocate use of a tourniquet to reduce postoperative haematoma caused by
stripping of the long saphenous vein (21,22). An autoclavable Boazul/Loefqvist-type
pneumatic tourniquet, inflated to 40–50 mmHg above systolic arterial pressure, can be
employed both to exsanguinate the leg during application and then, when secured at upper
thigh level, to prevent bleeding. Proponents suggest that this encourages the operating
surgeon to carry out more effective phlebectomies, but a Cochrane Database review found
only three prospective randomized trials, with small sample sizes, concluding that
although blood loss was reduced, there was no evident reduction in complications or
morbidity (23).
Short Sapheno-Popliteal Surgery
The sapheno-popliteal junction has a variable anatomical location (24–26). The short
saphenous vein terminates within 5 cm of the knee skin crease in approximately 60% of
subjects but at a higher level in the thigh, in the vein of Giacomini (12%) or in the femoro-
popliteal or other vein, in up to 40% of patients. Pre-operative marking of the sapheno-
popliteal junction with duplex Doppler ultrasound will allow the operating surgeon to
employ a smaller, appropriately placed incision.
With the patient lying prone, unless otherwise marked, a 2–3 cm transverse skin
incision is made in the skin creases of the popliteal fossa. The Short Saphenous Vein is
usually found beneath the popliteal fascia whose fibers run in a transverse plane. Some
surgeons advocate dividing this fascia longitudinally, allowing proximal and distal access
to the sapheno-popliteal junction. However, with confidence in the location of the
sapheno-popliteal junction inspired by ultrasound mapping, splitting the fascial fibers
transversely is the less disruptive surgical technique and facilitates subsequent repair.
Great care should be taken to avoid damage to the common peroneal nerve, (with the
potential consequence of foot-drop), which may be closely related to the short saphenous
vein as it courses through the popliteal fossa. The vein of Giacomini should be ligated
and divided.
Classical surgical teaching advocates dissection of the short saphenous vein to its
anastomosis with the popliteal vein at the sapheno-popliteal junction. However recent
comprehensive discussion at the Venous Forum of the Royal Society of Medicine in the
United Kingdom, a study undertaken by the Joint Vascular Research Group (JVRG), to be
published shortly, and a survey of members of the Vascular Surgical Society of Great
Britain and Ireland all indicate widespread variation in surgical practices with respect to
this part of the procedure (27).
The sapheno-popliteal junction can be difficult to access in a proportion of patients,
increasing risk of neurovascular damage if dissection is pursued. In these cases discretion
may be the better part of surgical valour and ligation of the short saphenous vein short of
the sapheno-popliteal junction may be advisable. Wherever possible a gastrocnemius vein,
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entering the short saphenous vein a short distance before its anastomosis with the popliteal
vein, should be ligated to eliminate a potential source of recurrence.
Discussion persists on whether to tie and divide the short saphenous vein alone,
excise a short segment, or strip to mid-calf or ankle, with greater potential risk of sural
nerve injury. However there is little in the way of prospective evidence to inform debate.
The prospect of a randomized trial of stripping versus no stripping, with sufficient power to
provide a definitive solution, may well be hampered by the potential impact of foam
sclerotherapy as a potential therapeutic alternative. Where stripping is undertaken, the
surgeon should attempt to ensure that the sural nerve is separated from the short saphenous
vein before the stripper is retrieved. Retrograde stripping may reduce risk of nerve injury.
Phlebectomies
Phlebectomies to remove troublesome varicosities are undertaken via fine stab incisions
in the skin creases, which are made with a pointed size 11 blade or an ophthalmic scalpel.
An “Oesch”-type or similar vein hook is used to pull a loop of the varicosity through the
incision. This is separated from adherent tissue, the afferent and efferent ends controlled
with fine haemostatic clips and the vein divided at the mid-point of the loop. Both ends of
the vein are then avulsed by gentle traction.
Care should be taken with avulsions to reduce risks of nerve injury. Areas
particularly prone to this risk include the path of the short saphenous vein in the posterior
calf where the sural nerve can be damaged, the region of the neck of the fibula laterally,
where the peroneal nerve is at risk, the long saphenous trunk and related saphenous nerve
in the calf and the nerves accompanying the anterior and posterior tibial arteries at
the ankle.
Ligation of cut ends of the vein with a fine absorbable tie is an alternative when
haemostasis is a particular concern. A short period of pressure over the phlebectomy site
usually quells bleeding and the incision is closed with an adhesive paper suture strip.
While placement of Steri-Strips
w
over phlebectomy sites may appear to be the most
innocuous part of the surgical procedure, application of these adhesive dressings by an
over-zealous assistant may result in “pinching” of skin if they are applied under tension.
This has resulted in friction burns, which can have a long-lasting, cosmetically debilitating
effect and has been a source for litigation. Any intolerance or allergy to adhesive dressings
should have been noted pre-operatively.
Post-operative bandaging after leg-elevation is carried out using either crepe, or
elastic bandages. The foot is included to prevent swelling. Pressure should be adequate to
staunch venous bleeding but not overly tight so as to compromise arterial circulation.
Pedal Varicosities
Traditionally many surgeons have shied away from surgical treatment of pedal varicosities
because of a perceived risk of associated cutaneous nerve injury. Venous hypertension
associated with such varicosities can cause significant skin changes including
haemosiderin pigmentation, varicose eczema and occasionally, a corona phlebectatica.
The patient may well complain of pain or swelling in the foot, particularly after prolonged
dependency or in association with venodilation, for instance after bathing. Pedal
varicosities can be dealt with via discrete stab incisions in the lines of the skin creases,
gentle extrusion of the varicosity with a vein hook and then by division, segmental
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excision and ligation of the divided ends of the veins with fine absorbable ties. This
reduces the volume of pedal haematoma postoperatively.
Perforator Surgery
Incompetent calf perforating veins may be abolished by superficial venous surgery in the
absence of specific perforator surgery (28). Specific perforator surgery should be reserved
for the few (2–3%) of patients with isolated perforator incompetence. Open surgery for
incompetent perforators was popularized by Linton, who described subfascial dissection
and ligation of perforating veins in the calf (29). Subsequently a number of modifications
to this procedure were introduced by surgeons, including Cockett, who described an
extrafascial approach, and Dodd (30,31). Popularity of open procedures, which entailed
long incisions with associated morbidity and high ulcer recurrence rates, has waned with
the advent of subfascial endoscopic perforator surgery (SEPS), which is described
elsewhere in this book.
Postoperative Care
Prior to discharge, bandages should be taken down and wounds inspected. Where
dressings or Steri-Strips
w
have lifted, these should be replaced and the leg cleaned.
Management protocols vary from surgeon to surgeon, but usually the patient will be asked
to wear a full-length elastic compression stocking continuously for one week and to
mobilise as soon as possible. Patients with ulcers may well require dressing changes in the
interim. Oral analgesia is prescribed and the patient should be given clear contact details of
who to contact in case of a query. In contrast to uncomplicated varicose vein surgery,
where it is rarely necessary to subject the patient to further formal outpatient follow-up,
patients with stigmata of chronic venous disease, or ulceration, will usually be reviewed
within four to six weeks after surgery.
KEY POINTS
† Chronic venous disease remains a major socio-economic problem in
modern healthcare.
† Surgical intervention should be directed at correcting underlying causes of
ambulatory venous hypertension.
† Superficial, or mixed superficial and deep incompetence, play a significant
part in the etiology of chronic venous disease.
† Appropriate superficial venous surgery in chronic venous disease is
associated with hemodynamic benefits, improved quality of life and reduced
ulcer recurrence rates.
† Risks of litigation specifically associated with superficial venous surgery can
be reduced by good communication, fully informed consent, scrupulous pre-
operative assessment and awareness of potential for nerve injuries.
† A future role for superficial venous surgery, in the context of alternative
potentially effective minimally-invasive therapies, remains to be seen.
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REFERENCES
1. Evans CJ, Fowkes FG, Ruckley CV, Lee AJ. Prevalence of varicose veins and chronic venous
insufficiency in men and women in the general population: Edinburgh vein study. J Epidemiol
Commun Health 1999; 53:149–153.
2. Lees TA, Lambert D. Prevalence of lower limb ulceration in an urban health district. Br J Surg
1992; 79:1032–1034.
3. Fowkes FG, Lee AJ, Evans CJ, Allan PL, Bradbury AW, Ruckley CV. Lifestyle risk factors for
lower limb venous reflux in the general population: Edinburgh Vein Study. Int J Epidemiol
2001; 30:846–852.
4. Bosanquet N. Costs of venous ulcers: from maintenance therapy to investment programmes.
Phlebology 1992; 7:44–46.
5. Kalra M, Gloviczki P. Surgical treatment of chronic venous insufficiency. In: Hallett JW,
Mills JL, Earnshaw JJ, Reekers JA, Mosby, eds. Comprehensive Vascular and Endovascular
Surgery, 2004:601–624.
6. Porter JM, Moneta GL. Reporting standards in venous disease: an update. International
consensus committee on chronic venous disease. J Vasc Surg 1995; 21:635–645.
7. Beebe HG, Bergan JJ, Bergqvist D, et al. Classification and grading of chronic venous disease
in the lower limbs. A consensus statement. Eur J Vasc Endovasc Surg 1996; 12:487–491.
8. Hanrahan LM, Araki CT, Rodriguez AA, Kechejian GJ, LaMorte WW, Menzoian JO.
Distribution of valvular incompetence in patients with venous stasis ulceration. J Vasc Surg
1991; 13:805–811.
9. Lees TA, Lambert D. Patterns of venous reflux in limbs with skin changes associated with
chronic venous insufficiency. Br J Surg 1993; 80:725–728.
10. Darke SG, Penfold C. Venous ulceration and saphenous ligation. Eur J Vasc Surg 1992; 6:4–9.
11. 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; 363:1854–1859.
12. Adam DJ, Bello M, Hartshorne T, London NJ. Role of superficial venous surgery in patients
with combined superficial and segmental deep venous reflux. Eur J Vasc Endovasc Surg 2003;
25:469–472.
13. MacKenzie RK, Allan PL, Ruckley CV, Bradbury AW. The effect of long saphenous vein
stripping on deep venous reflux. Eur J Vasc Endovasc Surg 2004; 28:104–107.
14. MacKenzie RK, Paisley A, Allan PL, Lee AJ, Ruckley CV, Bradbury AW. The effect of long
saphenous vein stripping on quality of life. J Vasc Surg 2002; 35:1197–1203.
15. Mackenzie RK, Lee AJ, Paisley A, et al. Patient, operative, and surgeon factors that influence
the effect of superficial venous surgery on disease-specific quality of life. J Vasc Surg 2002;
36:896–902.
16. Sam RC, MacKenzie RK, Paisley AM, Ruckley CV, Bradbury AW. The effect of superficial
venous surgery on generic health-related quality of life. Eur J Vasc Endovasc Surg 2004;
28:253–256.
17. Campbell WB, France F, Goodwin HM. Research and audit committee of the vascular surgical
society of Great Britain and Ireland. Medicolegal claims in vascular surgery. Ann R Coll Surg
Engl 2002; 84:181–184.
18. Onuma OC, Beam PE, Khan U, Malluchi P, Adiseshiah M. The influence of effective analgesia
and general anesthesia on patient’s acceptance of day-case varicose vein surgery. Phlebology
1993; 8:29–31.
19. Sarin S, Scurr JH, Coleridge Smith PD. Stripping of the long saphenous vein in the treatment of
primary varicose veins. Br J Surg 1994; 81:1455–1458.
20. Dwerryhouse S, Davies B, Harradine K, Earnshaw JJ. Stripping the long saphenous vein
reduces the rate of reoperation for recurrent varicose veins: five-year results of a randomized
trial. J Vasc Surg 1999; 29:589–592.
21. Robinson J, Macierewicz J, Beard JD. Using the Boazul cuff to reduce blood loss in varicose
vein surgery. Eur J Vasc Endovasc Surg 2000; 20:390–393.
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22. Sykes TC, Brookes P, Hickey NC. A prospective randomised trial of tourniquet in varicose
vein surgery. Ann R Coll Surg Engl 2000; 82:280–282.
23. Rigby KA, Palfreyman SJ, Beverley C, Michaels JA. Surgery for varicose veins: use of
tourniquet. Cochrane Database Syst Rev 2002;CD001486.
24. Moosman DA, Hartwell SW. The surgical significance of the subfascial course of the lesser
saphenous vein. Surg Gynecol Obstet 1964; 118:761–766.
25. Nabatoff RA. The short saphenous vein. Surg Gynecol Obstet 1979; 149:49–53.
26. Engel AF, Davies G, Keeman JN, von Dorp TA. Colour flow imaging of the normal short
saphenous vein. Eur J Vasc Surg 1994; 8:179–181.
27. Winterborn RJ, Campbell WB, Heather BP, Earnshaw JJ. The management of short saphenous
varicose veins: a survey of the members of the vascular surgical society of Great Britain and
Ireland. Eur J Vasc Endovasc Surg 2004; 28:400–403.
28. Gohel MS, Barwell JR, Wakely C, et al. The influence of superficial venous surgery and
compression on incompetent calf perforators in chronic venous leg ulceration. Eur J Vasc
Endovasc Surg 2005; 29:78–82.
29. Linton RR. The post-thrombotic ulceration of the lower extremity: its etiology and surgical
treatment. Ann Surg 1953; 138:415–433.
30. Cockett FB. The pathology and treatment of venous ulcers of the leg. Br J Surg 1955;
43:260–278.
31. Dodd H. The diagnosis and ligation of incompetent ankle perforating veins. Ann R Coll Surg
Engl 1964; 34:186–196.
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30
Surgical Therapies in Chronic Venous
Insufficiency: Deep Venous Surgery/
Valve Transplantation/SEPS
Michael C. Dalsing
Indiana University School of Medicine, Indianapolis, Indiana, U.S.A.
INTRODUCTION
Chronic venous disease is common in Western countries. Over 30 million U.S. citizens are
affected with some manifestation of venous disease while skin changes suggestive of the
disease are noted in about 6 million and venous ulcers are observed in up to 2% of those
with chronic venous insufficiency (about one half million patients) (1–3). Recent
population studies confirm these observations (4). The annual cost of treating venous
ulcers is estimated to be greater than one billion dollars in the United States (5).
Although many theories abound to explain the sequelae of chronic venous disease,
venous hypertension and the resulting stasis of venous blood are key to the pathophysiology.
The goal when treating significant chronic venous insufficiency is to diminish venous
hypertension on the target organ such that the sequelae of the disease is prevented or
minimized. External compression is the mainstay of conservative management even in
patients with venous ulceration but the recurrence rate is 70%–100% in non-compliant
patients and 30–40% in those who faithfully comply and in only a few years (6,7). In depth
evaluationis notrequired iftherapy isrestricted to conservativemeasuresbut if interventionis
contemplated then confirmatory diagnostic studies must differentiate those patients without
venous disease from those with superficial, perforator, deep disease or any combination
thereof. Valvular insufficiency accounts for 85% of symptomatic chronic venous disease
cases with the majority primarily superficial and 30% primarily deep venous insufficiency
(8,9). Isolated superficial and/or perforator venous insufficiency has been observed to cause
advanced manifestations of venous disease, but in approximately two-thirds of these
advanced cases, the deep system is insufficient alone, or more commonly, in association with
superficial/perforator disease (10–13). In patientswith superficial/perforator and deep venous
insufficiency, removal of pathologicsuperficialand/or perforator veins can resultin prolonged
venous ulcer healing (14). The hemodynamic importance of perforator vein insufficiency is
currently controversial but, in a clinical sense, the “ankle blow-out syndrome” has been
recognized for years in patients with advanced clinical disease (15,16). Certainly, in patients
with clinically advanced disease (C
5,6
), postoperative incompetent perforator veins are a risk
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factor for recurrence (17). Aboutone-third of patients with primary deep venousinsufficiency
and 70% of those with the post-thrombotic syndrome will experience ulcer recurrence after
removal of essentially all other significant insufficiency demonstrating the importance of the
deep venous component (9,14). Venous obstruction accounts for a minority of venous ulcers
observedin our practices (2–20%) (8,10,11), can bemanagedby variousinterventional means
and is not further considered in this chapter.
ETIOLOGY/PATHOPHYSIOLOGY OF VALVULAR DAMAGE
In the past, perforating veins were named for their discoverer (e.g., Crockett’s, Boyd’s
perforators) but more descriptive terms describing location are now preferred (18). The
anatomy of the perforating veins becomes extremely important when considering surgery
aimed at preventing reflux in the lower leg. For example, not recognizing the presence of
paratibial perforators can result in an unsuccessful operation aimed at preventing calf
perforator reflux (19). The etiology of perforator vein insufficiency mimics other major
venous tributaries in having similar primary and secondary causes.
Deep venous insufficiency is rarely due to a congenital absence of the valves (20).
Syndromes associated with venous abnormalities can have associated venous aplasia or
dysplasia. These syndromes are uncommon, and seldom require deep venous valvular
reconstruction. Primary deep venous insufficiency occurs as a result of a structural
elongation of the valve cusps or stretching of the vein wall without apparent histologic
damage (21,22). Floppy, redundant valves permit valve leaflet prolapse and poor
coaptation (21). Alternatively, an enlarged venous diameter can prevent a normal valve
cusps from coapting properly (23,24). On standing or with other causes of increased
intravenous pressure, blood refluxes through the architecturally preserved valve cusps. An
in situ repair is possible since all necessary valve architecture is available and competency
can be realized. Approximately 40% to 70% of deep vein valvular dysfunction occurs as
a consequence of DVT (deep venous thrombosis), whereas the remainder appear to be of
a primary etiology (8,21,25). As a result of the destructive process of thrombosis,
inflammation and scarring can cause shortening and fibrosis of the valve leaflets,
recannulation can result in small channels replacing the normal vein and valve, or valve
adhesions can cause luminal narrowing (21). This is the post-thrombotic syndrome. These
valves are often so damaged that an in situ repair is not feasible. This leaves only the
options of venous valve transplantation, transposition, or the use of “valve substitutes” to
address the pathologic reflux.
This classical differentiation between “primary” and “secondary” pathology is
fleeting whensubjected to direct observation of veins and valves at surgery. In fact, as noted
decades ago, the two conditions can be present in the same patient (26). In some cases during
surgery, the vein wall has been noted to be thickened/fibrotic at the valve station or there is
thickening of the valve cusps and/or intima. Pathologic study of eleven such veins
demonstrated post-thrombotic changes in six, but non-thrombotic phlebosclerosis was
found in the remainder (21). Preservation of a normal valve architecture can be explained if
“primary” reflux with resultant high pressure on the wall is the cause since stretching
without destruction could be the process of cusp incompetence. Another theory is that rapid
resolution of acute thrombi may leave the valves undamaged, or alternatively, the valve
itself may not have been directly involved in the thrombotic process (27–29). The fibrotic
process involves the vein wall only and the cusps become floppy because of a diminished
diameter consistent with a thickened, non-compliant vein wall (21). The valve remains
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architecturally intactand can be repaired surgical, a situation once thought impossible inthe
post-thrombotic patient (21).
DIAGNOSIS
Patients with chronic deep and/or perforator vein reflux present with signs and symptoms
typical of the sequelae of long standing venous hypertension. The patient may experience
dependent edema, leg fatigue and a feeling of “fullness” especially after long periods of
standing. There may be progression to skin changes such as eczema, cellulitis,
hyperpigmentation, lipodermatosclerosis, and stasis ulcers. During the physical examin-
ation all of these signs may be observed alone or in combination. The history should
concentrate on venous disease especially prior DVT, clotting abnormalities or prior venous
interventions. Someestimate of how the disease process is affecting the patient’s life should
be gathered. Significant arterial disease can generally be ruled in or out as a contributing
problem as can other causes of similar skin changes such as diabetic ulcers, simple eczema
or skin cancers. The CEAP (clinical (C), etiologic (E), anatomic (A), and pathophysiologic
(P))classification system should be used to describe patients as they currently present in the
spectrum of the disease process (30). An extension of the clinical classification can aid in
quantifying the disease process to allow evaluation of treatment response (31,32). Similarly,
the patients’ clinical outcome scores can be evaluated according to a grading scheme (31).
An improved method of determining the change in disease severity following intervention
has been developed but awaits overall utility in the clinical arena (32). Quality of life
surveys can quantify the impact of the venous disease on the patient’s life and effect of
therapy onthe patient’s overall well-being (33). Using these tools and the diagnostic studies
discussed below, the physician can precisely define the disease process and can formulate
a reasonable treatment plan.
Further diagnostic studies provide the surgeon with information to complete the
CEAP classification to its fullest extent. The venous duplex ultrasound study can clarify
the etiology (E of CEAP; congenital, primary, or secondary), better define the anatomic
location (A of CEAP;), and help to determine the pathophysiology (P of CEAP; reflux,
obstruction, or both) of the venous disease. Venous duplex imaging can provide rather
impressive imaging of individual valve cusps in many patients and can determine
the presence or absence of reflux past a given valve following provocative studies:
A prolonged reflux time of O0.5 seconds is considered abnormal and indicative of
pathologic reflux if a rapidly deflating distal cuff is used as the provocative test, while
O1.0 seconds is considered abnormal when manual compression is used (34,35). A recent
study suggests that these values may be appropriate for the deep calf veins but that
1.0 seconds should be the cut-off of the larger femoropopliteal veins even when using the
rapidly deflating distal cuff method (36). The examination is performed in the upright
position in these reports. Suffice it to say, many other provocative maneuvers to generate
venous reflux exists (Valsalva, standardized Valsalva, etc) in addition to performing the
test in different positions (15% Tredelenberg, sitting, etc.) (37). Each may be acceptable if
standardized for your laboratory. Incompetent perforating veins are generally larger in
diameter than normal perforators, thereby allowing a larger volume of blood flow during
reflux, and are considered to demonstrate reflux with a reflux time greater than 0.5 seconds
(38). There is some thought that this cut-off should be decreased to 0.35 seconds (39). Of
course, isolated deep venous valvular insufficiency may have little clinical impact on
a given patient and therefore clinicians have attempted to quantify the pathology by adding
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segmental disease, determining mean duration of reflux, determining peak reverse flow
velocity, etc. (34,40). Although, average scores and means do correlate with disease
severity, individual results have little predictive value and have not been widely adopted.
The issue of common standards for the performance and interpretation of venous duplex
studies still plagues efforts to defining venous disease (37), but many find duplex imaging
the most versatile and reproducible imaging device currently available in clinical use
(37,41). Imaging the entire lower extremity venous system, provides a detailed roadmap of
all veins and a means of determining if obstruction or valvular reflux is present.
Plethysmography can assess overall lower extremity venous hemodynamics.
Air plethysmography (APG) can measure several venous hemodynamic parameters and
is the most common device currently utilized in the clinical setting. A venous filling index
of 2 mL/s or less is indicative of a competent venous system and higher values suggest
venous insufficiency (42,43). The use of tourniquets to separate superficial from deep or
perforator disease has not been reliable (44), but it can be useful in specific cases.
The residual volume fraction is relatively equivalent to the ambulatory venous pressure
(5,44). Several other plethysmographic methods (impedance, photo, etc.) and even light
reflex rheography have evaluated similar venous parameters. These plethysmographic
methods can differentiate severe chronic venous insufficiency (class 3 or greater) from
disease absence but is unreliable in less severe disease (37). Because these studies do
not provide an anatomic image of the venous system or evaluate individual venous valve
function, most physicians combine one of these estimates of global hemodynamics with
ultrasonography to complete the non-invasive venous evaluation of patients with
advanced disease.
Although intravenous pressure measurements and venography were once the gold
standard for evaluating venous disease, duplex scanning and plethysmographic techniques
are the anatomic and functional tests of choice in current medical practice (42).
Patients with significant deep venous valvular reflux contemplating surgery
generally have a venographic study for proper operative planning. Ascending venography
is useful in demonstrating the anatomy of the deep venous system and helps eliminate
obstruction as a major contributing or confounding factor (21,45). It provides a road map
to allow selection of the most disease-free portion of lower extremity venous system for
valve transplantation if that becomes necessary. Simultaneous intravenous AVP
measurements can be obtained to provide an estimate of the magnitude of reflux (5).
The magnitude of the AVP correlates with the presence of venous ulceration such that
each 10 Torr increase above 30 Torr corresponding to a 10 to 15 percent increase in the
incidence of venous ulceration (46). If the VRT is less than 20 seconds, overall valvular
reflux throughout the lower leg is evident.
Descending venography is used to determine valve leaflet integrity, anatomic
location, and demonstrate the extent of reflux (47). Assessment of profunda femoris
venous system competence in addition to the femoral system is mandatory. Either
system may be a source of a competent valve for the transposition procedure, or may
indicate potential success with an isolated proximal femoral vein repair in the case of
profunda venous valve competence (48–50). It can fail in its attempt to determine the
presence or absence of a normal valve (21). Raju, et al. reports that the descending
venogram misrepresented the presence of a valve in 11% of cases (no valve was present
at operation), and missed an intact valve in 25% of cases (a valve thought absent was
present) (21). When combined with non-invasive venous imaging, descending
venography is the best method available to determine preoperatively if an in situ
reconstruction will be possible.
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INDICATIONS AND GOALS FOR SURGICAL INTERVENTION
In general, patients presenting for intervention of incompetent perforator and/or deep
venous insufficiency have attempted conservative measures to control the disease process
and have generally undergone superficial surgery if incompetence was also located there.
Likewise, proximal venous obstruction has usually been addressed. One study in patients
with combined superficial reflux and “segmental deep venous reflux” showed that
superficial venous surgery alone corrected deep venous reflux in about 50% of limbs
involved and allowed ulcer healing in 77% of limbs after one year of follow-up (51). This
study cannot be generalized to include patients with severe and extensive deep venous reflux
but it is interesting that treatment of superficial disease can impact the deep venous system in
such a positive manner. Failure of these measures, especially with recurrent symptoms of
advanced disease, requires consideration for further surgical intervention.
The precise candidate for the correction of perforator insufficiency is often difficult
to define since many reports in the literature have combined perforator surgery with
superficial saphenous ablation making comment on the effect of isolated perforator
incompetence hard to substantiate. Certainly, in those rather rare cases of isolated
perforator incompetence, treatment may be the only option available to correct venous
hypertension causing the sequelae such as venous ulceration. It is becoming increasing
evident that perforator vein incompetence is very common in patients with venous ulcers
being noted in about 60% of patients (12,13,52). It is clearly difficult to differentiate the
hemodynamic effect of perforator vein incompetence when deep disease is also present, as
it generally is in patients with advanced disease. Isolated perforator disease is really quite
unusual (12). It does appear, however, that incompetent perforators can result in
significant supramalleolar venous pressure with calf contraction (16). Furthermore,
increasing number and size of perforating veins does correlate with worsening chronic
venous insufficiency and, more importantly, the presence of incompetent perforating veins
is a risk factor for recurrent venous ulcers after attempted surgical correction of
hemodynamic derangements (17,38,53). Keeping in mind that the goal of therapy
is alleviation of venous hypertension on the target organ (the ankle skin), the data is
mounting that correction of perforator vein incompetence may be beneficial especially in
the patient with venous ulceration. The goal of treatment in perforator surgery is to remove
the influence of incompetent perforator veins on the lower leg and this implies removal of
all incompetent perforating veins.
Patients considered for deep venous valvular surgery generally are end-stage
patients with C5–C6 disease with only deep venous disease remaining untreated. How-
ever, as the results of surgery demonstrate improving long-term success, some surgeons
consider intervention in patients with disabling life-style symptoms like severe edema.
When the decision has been made to treat deep venous valvular incompetence, the goal is
to prevent axial reflux into the lower leg. If one ignores the rule of correcting all axial
reflux in patients with deep venous insufficiency, for example by ignoring reflux in the
profunda femoris vein, femoral vein valvular reconstruction alone will be clinically
unsuccessful and lower limb venous hemodynamics will not be improved (54). However,
with profunda femoris venous valvular competence, repair of femoral vein incompetence
alone can improve chronic lower limb venous hemodynamics (54,55). Tremendous
enlargement of the profunda femoris vein following femoral vein DVT has been clearly
demonstrated by venography and other methods, repair of both the femoral and profunda
vein valvular reflux is required for a successful outcome if both demonstrate
incompetence (56). The popliteal vein is the gateway through which all thigh venous
reflux must pass and, therefore, another way of correcting axial reflux may be to position
Surgical Therapies in Chronic Venous Insufficiency 397
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