ABNORMALITIES OF THE DEEP VEINS OF THE LEG By F. B. CocKIIrm, M.S., F.R.C.S. St. Thomas's Hospital, London The anatomy and pathology of the venous system of the leg has been, until very recently, a neglected subject. This is so, in spite of the fact that lesions resulting from diseases of these veins are among the commonest from which mankind suffers. To Homans (1917) must go the credit for awakening renewed interest in the subject, for he first clearly showed that the distressing ' ulcer and induration ' syndrome of the lower leg was a sequel to thrombosis of the deep veins; he also first showed that recanalization of these throm- bosed deep veins occurred in many cases. On the subject of anatomy and physiology of the veins of the leg, Gay's work in I867, and later the pains- taking studies of Turner Warwick (I931), gave a clear picture, although both authors received little attention at the time. During the last ten years, with the advent of safe techniques of venography, radioactive isotopes and accurate methods of measuring venous pressure in the veins of the foot, the growth of knowledge has been fast. In this article we will consider first the normal anatomy of the deep veins, secondly the physiology of venous return from the leg and thirdly how the effects of disease of the deep veins modifies the venous return and produces certain lesions and symptoms. Normal Anatomy Whereas the anatomy of the arteries is relatively constant, this is not so with the veins. Although the basic pattern of venous anatomy is constant one must be prepared for endless variations and duplications. These are part of normal anatomy and this variation in normal anatomy from patient to patient is the reason for many of the difficulties both in interpretation of venograms and in opera- tions upon the veins. A knowledge of the basic pattern and the normal variations is therefore essential to interpret, diagnose and treat the effects of venous incompetence. Fig. i shows the anatomy of the venous drainage of the calf and Fig. 2 shows the same thing in diagrammatic form. viw P.APO*A L.R ttL MlP FACICA SRuIHEr4eu& iitfoO FIG. i.-Dissection showing the anatomy of the venous drainage of soleus and the deep veins of the leg. Note particularly: (i) The relation of the ankle perforating veins, where they join the deep veins, to the muscular veins from soleus. (2) The peroneal vein takes little part in the venous drainage of the lower half of soleus. The venous drainage of the soleus and gastroc- nemius muscles, which constitute most of the calf, is very different. Soleus The soleus muscle has a series of large venous sinuses within it which are devoid of valves. These by copyright. on June 30, 2020 by guest. Protected http://pmj.bmj.com/ Postgrad Med J: first published as 10.1136/pgmj.30.348.512 on 1 October 1954. Downloaded from
Transcript
ABNORMALITIES OF THE DEEP VEINSOF THE LEG
By F. B. CocKIIrm, M.S., F.R.C.S.St. Thomas's Hospital, London
The anatomy and pathology of the venoussystem of the leg has been, until very recently, aneglected subject. This is so, in spite of the factthat lesions resulting from diseases of these veinsare among the commonest from which mankindsuffers. To Homans (1917) must go the credit forawakening renewed interest in the subject, for hefirst clearly showed that the distressing ' ulcer andinduration ' syndrome of the lower leg was asequel to thrombosis of the deep veins; he alsofirst showed that recanalization of these throm-bosed deep veins occurred in many cases. On thesubject of anatomy and physiology of the veins ofthe leg, Gay's work in I867, and later the pains-taking studies of Turner Warwick (I931), gave aclear picture, although both authors received littleattention at the time. During the last ten years,with the advent of safe techniques of venography,radioactive isotopes and accurate methods ofmeasuring venous pressure in the veins of thefoot, the growth of knowledge has been fast.
In this article we will consider first the normalanatomy of the deep veins, secondly the physiologyof venous return from the leg and thirdly how theeffects of disease of the deep veins modifies thevenous return and produces certain lesions andsymptoms.
Normal AnatomyWhereas the anatomy of the arteries is relatively
constant, this is not so with the veins. Althoughthe basic pattern of venous anatomy is constantone must be prepared for endless variations andduplications. These are part of normal anatomyand this variation in normal anatomy from patientto patient is the reason for many of the difficultiesboth in interpretation of venograms and in opera-tions upon the veins. A knowledge of the basicpattern and the normal variations is thereforeessential to interpret, diagnose and treat the effectsof venous incompetence.
Fig. i shows the anatomy of the venous drainageof the calf and Fig. 2 shows the same thing indiagrammatic form.
viw
P.APO*A L.R ttL
MlP FACICASRuIHEr4eu& iitfoO
FIG. i.-Dissection showing the anatomy of the venousdrainage of soleus and the deep veins of the leg.Note particularly: (i) The relation of the ankleperforating veins, where they join the deep veins,to the muscular veins from soleus. (2) The peronealvein takes little part in the venous drainage of thelower half of soleus.
The venous drainage of the soleus and gastroc-nemius muscles, which constitute most of the calf,is very different.
SoleusThe soleus muscle has a series of large venous
sinuses within it which are devoid of valves. These
October I954 COCKETT: Abnormalities of the Deep Veins of the Leg
Chk
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FIG. 2.-This diagram illustrates: (i) The differencein the venous drainage of soleus and gastrocnemius.(2) The arrangement and profusion of venous valvesin the leg veins. (Note that the venous sinus withinsoleus is devoid of valves.)
venous sinuses differ from subject to subject intheir size and degree of development and they areof importance, as it is in them that calf thrombosisstarts. They drain by a series of short but laxveins into the posterior tibial and peroneal veins asshown. This series of short lax veins are large andare grouped closer together in the upper part ofthe calf and in the position of rest assume atortuous appearance; this tortuosity, occasionallyseen on venograms, is sometimes mistakenly called' deep varicose veins,' but this appearance is, infact, normal here.The venous drainage of the lower half of soleus
is interesting and significant when we come toconsider the genesis of post-thrombotic ulcers.Firstly, it will be observed in Fig. i that nearly thewhole venous drainage of the lower half of the calfgoes into the posterior tibial vein. The peronealvein is quite small in the lower third of the leg andruns deep to the flexor hallucis longus origin fromthe fibula, close up against the interosseous mem-brane. In this region it receives one fairly constant
.d
FIG. 3.-Deep Varicose Veins. The tortuous dilatedveins seen in the upper part of this venogram arethe dilated gastrocnemial veins.
large lateral perforating vein (see Figs. i and 7).This vein as it winds round the fibula receives abranch from the soleus. This represents the onlycontribution from soleus in this region. In theupper half of the leg the peroneal vein emergesfrom under the flexor hallucis belly to lie in theposterior compartment and here it receives sevexiallarge lax veins from the lateral aspect of soleuswhich rapidly convert into quite a large vein beforeit unites with the posterior tibial to form, thepopliteal.Now turning to the posteriQr tibial veins in- the
I (7(a) (b) (c)FIG. 4.-The arrow represents the level of the adductor canal. For further description see text.
lower third, it will be observed that where theseveins receive the two lowest muscular veins fromsoleus they also receive two large perforating veinswhich perforate the deep fascia of the leg and drainthe subcutaneous tissues of the internal malleolarregion (the ulcer and induration area). Thisanatomical arrangement (see Figs. I, 2 and 6) isthe key to appreciating two things: (i) That thereis a direct anatomical pathway for the spread ofthrombus from calf sinuses to posterior tibialveins and then either outwards in the perforatorsand/or upwards in the posterior tibial veins. (2)The reason why the site of election for thecutaneous sequelae of deep thrombosis is so oftenthe inner side of the leg in the malleolar region andnot the outer side.
GastrocnemiusEach belly of gastrocnemius is drained by a
single large vein or pair of venae comitantes whichenter the popliteal vein in the lower part of thepopliteal fossa. These veins are often seen onvenograms of the region, are easily picked out andare accompanied by an artery and a nerve. Whenthe vales of the popliteal and femoral veins aredestroyed by the process of deep thrombosis andrecanalization these veins are subjected to an in-creased venous pressure and sometimes dilate and
become tortuous and varicose, constituting onetype of true deep varicose veins (Fig. 3).
The Popliteal and Femoral VeinsThe anatomy of the popliteal and femoral veins
is shown in Fig. 4; (a) represents the basic pattern;it is in fact most unusual for the popliteal andfemoral veins to be represented by one single largetrunk as depicted in most anatomy books; (b)represents a much commoner state of affairs wherethere is a main channel with numerous venaecomitante3; these venae comitantes are usuallyclosely applied to the accompanying artery andinter-communicate in a plexiform manner. Thusthe popliteal and femoral veins show every con-ceivable variation from, on the one hand, fairlyisolated single large channels (as depicted in text-books) to, on the other, a plexus of inter-com-municating venous channels in which one singledominant channel can scarcely be picked out. Re-duplication of venous channels in the poplitealfossa and Hunter's canal is thus the rule ratherthan the exception. One further point is of im-portance; in the region of the adductor canal theplexus of accompanying venae comitantes isusually particularly profuse and, at this point, ananastomosis with the profunda system takes placewhich is very constant. This anastomosis con-
October 1954 COCKETT: Abnormalities of the Deep Veins of the Leg S I S
120/ BOTHL\2O/01 ABSENT IN
200/0 OF1.. 6 5°/0 NORMAL
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FIG. 5.-Position of valves in the femoral and poplitelaveins.
stitutes an important avenue of collateral venousreturn when the femoral vein is blocked. Finally,Fig. 4 (c) represents a state of affairs found in about12 per cent. of legs (McLachlin and Paterson,195I; Cockett, 1953) where the lower part of theprofunda vein is large and unites directly with thepopliteal vein or popliteal venous plexus. In suchcases the profunda offers a large alternative path-way of venous return from the lower leg.
This variation in venous arrangement and in thenumber and profusion of available deep collateralsgives some clue to the apparently capricious wayin which the symptoms of deep venous obstructionarise and subside in different patients.
The ValvesThe venous valves of the leg veins are profuse
and of great importance in the pump mechanismwhereby blood is returned to the heart against
gravity in the upright position. In the venoussinuses of the soleus there are no valves, but in allthe muscular veins draining both soleus andgastrocnemius into the deep veins, valves arenumerous. The posterior tibial and peroneal veinsare profusely valved, having a pair of valves aboutevery inch. In addition all the perforating veins inthe lower part of the calf and all the veins con-necting the deep with the superficial veins in allparts of the leg, are so valved that blood can onlypass from superficial to deep veins and reflux out-wards from the deep to the superficial is preventednormally.The arrangement of valves in the large venous
trunks, the popliteal, femoral, common femoraland iliac veins is important in considering theaetiology of both superficial varicose veins and deepvenous incompetence. The arrangement has beenstudied by Eger and Casper (I943), Powell andLynn (I95i), Baamajian (I952) and Cockett (I953).The findings are summarized in the diagram(Fig. 5).The diagram shows the average sites where
valves are to be found. However, once again thereis considerable variation from case to case and thevariations must be known as they constitutenormal anatomy. In about 20 per cent. of casesno valve is to be found between the heart and theentry of the great saphenous vein. This may be ofsignificance in the aetiology of incompetence of thegreat saphenous system. In 2o per cent. of peoplethere is a valve in the external iliac and in about65 per cent. of people there is a valve in thecommon femoral. The most constant valve is thatwhich occurs just below the entry of the profundavein. There is usually another valve about themid-point of Hunter's canal and another in thepopliteal vein. However, the number of valves inthe segment of deep vein from inguinal ligament topopliteal may vary from two to nine. Occasionalcases are recorded (Bazmajian, 1952; Luke, I951)of congenital absence of valves in this entirestretch of vein although these are very rare. Evenin these cases the valves in the smaller veins arenormal.
The Superficial VeinsThe basic pattern of arrangement of the venous
drainage of the skin and subcutaneous tissues of thelower leg by the superficial veins must be men-tioned in order to understand how lesions of thedeep veins may affect the superficial tissues (Figs.6 and 7).
Figs. 6 and 7 show the venous arrangement onthe inner side and outer side of the limb. It willbe appreciated that in the erect position the venousdrainage of the ulcer bearing area of the ankle is tothe deep veins (posterior tibial) by the large fairly
FIG. 6.-This shows the essential anatomy of the venousdrainage of the skin and subcutaneous tissue onthe inner side of the limb. Note that the area whereulcers commonly occur is drained by the perforatingveins shown, and that there is a delicate venousarch connecting these perforating veins. Also notethat the saphenous vein itself has few branchesbelow knee level, the main groups of branches(i, 2 and 3) arise at or just below the knee. Thebranch labelled (3) is constant and important, as itmay connect the incompetent saphenous system tothe delicate venous arch connecting the perforatingveins.
constant perforating veins shown (see venousdrainage of soleus). The saphenous system takeslittle part in the venous drainage of this area in theerect position, although the effects of valvulardestruction and incompetence in this system mayreach the venous arch connecting the perforatingveins via the large posterior branch arising at kneelevel, shown in the diagram. The perforatingveins shown are large fairly constant ones; inaddition there are a number of much smallerinconstant, indirect ones scattered over the musclebellies of the limb.
The Physiology of Venous Return from theLegThanks to the intensive venographic investiga-
tions (Dow, '95'; Linton and Hardy, I948;Cockett, I953) and to the studies on venouspressure in the superficial veins and deep veins wehave now a fairly clear picture of the venous return
s is
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FIG. 7.-Shows the essential venous drainage of the skinand subcutaneous tissues on the outer side of thelimb. The large perforating vein shown, aboutone-third of the way up on the outer side, is veryconstant and usually connects directly with thesmall saphenous vein. If both this perforator andthe small saphenous are incompetent considerablevenous hypertension occurs in the subcutaneoustissues behind the malleoli.
from the lower limb. The soleus is a large power-ful muscle which, especially in its lower third, iscontained within a sheath of strong inelastic fascia.This arrangement of a large muscle within astrong inelastic fascial investment means that agreat rise of pressure occurs within the fascial en-velope when the muscle contracts. It is referredto as the ' calf pump.' The actual rise of pressurewithin the lower third of the calf pump on con-traction is from o to 90 mm. of Hg. (measured byWells, Youmans and Miller, 1938). Barcroft andDornhorst (1948) have also shown that this calfpump can overcome a resistance greater than0oo mm. Hg. Thus when the calf pump con-
tracts, blood is squeezed out of it with considerableforce in an upward direction, directed centrally andupwards only by the arrangement of the valves.Notice (diagram 8) that the arrangement of a pairof valves in each perforating vein effectively pre-vents the blood being forced outwards into the sub-cutaneous tissues as well, at each contraction. Tosome extent all the muscles both of foot, leg andthigh assist in this driving of the blood inwards
October 1054 COCKETT: Abnormalities of the Deep Veins of the Leg 517
towards the main deep vein, and upwards, whenthey contract.Now the veins in the subcutaneous tissues of
the leg and foot are also emptied very efficientlyinto the deep veins, in the erect position, bymuscular action, and exactly how this occurs hasbeen the object of several recent studies (Pollackand Wood, I949; Walker and Longland, 1950;Warren, White and Belcher, 1949; Hojensgardand Sturup, I949). In a person with a normalvenous system the pressure at rest in a sub-cutaneous vein in the dorsum of the foot is equal tothe pressure of a column of blood extending fromfoot to heart level. This is equivalent to a pressureof between 85 and go mm. Hg., according to theheight of the individual. As soon as the calfmuscles are put into action, however, this pressurerapidly falls to between o and io mm. Hg. Thusthe efficiency with which the subcutaneous veinsare drained into the deep by the systole anddiastole of the calf pump is truly remarkable.Hojensgard and Sturup moreover (I952), studyingsimultaneous pressure recordings of veins insideand outside the pump, showed that blood wasactively sucked into the deep veins inside thepump during the phase of diastole of the calf,when for a brief space the pressure in the veinswithin the calf became lower than that in the veinsoutside (i.e. in the subcutaneous tissues). Theroutes by which this blood from the skin enters thepump are the large direct perforating veins shownin Figs. 6 and 7 and by many much smaller indirectperforating veins.
Further interesting studies have been made byPayling Wright (I952) on the speed of venous flowin the leg under various conditions, using radio-active sodium as a tracer element. Briefly shefound that in the erect position at rest the flow wasextremely slow. At rest in the horizontal positionthe flow was doubled. If the legs and feet wereraised about io degrees then the flow rate wasdoubled again. These observations have beenconfirmed using pyelosil and observing its pro-gress in the veins under the screen.Thus the two most important factors in ensuring
a swift venous return from the leg and preventingvenous hypertension and venous stasis are (i)exercise of the calf muscles and (2) the position ofthe leg relative to the heart. The appreciation ofthese two factors is of supreme importance in theprophylaxis of post-operative or ' stasis' throm-bosis in the leg veins, which is such an importantand common problem.
Pathology of the Deep VeinsLesions of the deep veins may be classified as
traumatic and thrombotic.
FIG. 8.-This is an ascending venogram of a normalleg, made by the Valsalva technique. Note how thevalves show up with the use of the Valsalvamanoeuvre. Compare this with Figs. 9, IO and I i.
TraumaticUnder this heading the effects of surgical liga-
ture of normal deep veins at various levels must beconsidered. Ligature may be forced upon thesurgeon owing to trauma due to external woundingor accidental wounding at operation (the classicexample being injury to the common femoral veinduring a saphenous ligation operation). The
effects of such ligatures depend upon the anatomicalsituation and the availability of collateral channels;a glance at Fig. 4 will help in understanding this.Thus the effect of ligaturing the popliteal orfemoral vein distal t3 the poiat where the pro-funda joins it in the upper third of the thigh isslight. Mild oedema lasting a few days only maybe expected; after becoming ambulant slightoedema towards the end of the day may benoticed. Ligature of the common femoral be-tween the profunda origin and the inguinal liga-ment is followed by more severe effects, as isevident from Fig. 4, as far fewer deep venous col-laterals are available. More severe oedema oflonger standing can be expected. The externaliliac vein and the common iliac vein can heligatured without causing much swelling of thelimb, as profuse intrapelvic collateral channels tothe other side are available. Ligature of the in-ferior vena cava, however, as would be expected,is followed by prolonged and severe oedema ofboth lower limbs, which takes over six months torecede. Usually after ligature of a deep vein itremains patent on both sides of the ligature or atworst a short segmental thrombosis down and upto the next branch of the vein takes place. If, how-ever, more extensive distal thrombosis takes placethe sequelae are much more severe and oedema isgreater and of longer duration. Thus the aim oftreatment after such a ligature must be to try andprevent this extension thrombosis from takingplace. The first way to do this is to give everyaid to the venous return by simply raising the footof the bed until all oedema has subsided and bysupplying the patient with a firm elastic bandagefrom toes to knee and encouraging active calfexercises in the early days of ambulation. Ulcersand induration and chronic oedema of the lowerleg do not follow such ligatures unless they havebeen complicated by extensive distal thrombosisor have been actually done for calf thrombosis toprevent embolism.
ThrombosisThrombosis of the deep veins of the leg is
common. There are two main varieties. (i) Thesegmental or ilio femoral thrombosis (see Fig. 9).This thrombosis involves a segment of femoral oriliac vein extending from the vena cava or origin ofthe internal iliac branch above to a point near tothe origin of the profunda femoris. This type ofthrombosis usually follows some sort of directirritation of the vein wall in the vicinity of thepelvis by inflammatory or malignant glands or by alocal abscess due to diverticulitis or appendicitis orby gynaecological conditions. The thrombosismay spread retrogradely right down into the calf,when it differs in no way in its symptoms or
:......
FIG. 9.-Segmental ilio-femoral thrombosis. This veno-gram was done a few days after sudden considerableswelling of leg, and particularly the upper part ofthe thigh, occurred, following a long period ofsquatting on the grass watching a cricket matchwith the thigh fully flexed. Note how the deepveins end at mid-thigh and the venous returnfrom the leg is by the saphenous (the straight vessel)and its postero-medial tributary (the L-shapedvessel). Note also the tortuous collateral externalpudendal veins.
sequelae from the next group of deep thromboseswhich start in the calf. This ilio-femoral type ofsegmental thrombosis is much rarer than thenext variety; clinically it is characterized bysudden circumferential painful swelling andoedema of the leg which is most marked in thethigh; within two or three days numerous smallveins coursing over the inguinal ligament in frontand up round the fold of the buttock behind maketheir appearance-these are the collateral veins.The whole condition may subside within a month(if not due to a local malignant condition) andleave practically no sequelae. As the thrombosishas not involved the deep veins of the lower leg itis not followed by the ulcer and induration syn-drome. (z) Calf thrombosis (Fig. io). This is byfar the commonest variety. The thrombosis startsin the large venous sinuses of the calf (already re-ferred to in the section of anatomy), spreads byone or more of the numerous veins draining soleus
October I954 COCO{ET: Abnormalities of the Deep Veins of the Leg t9
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FIG. io.-White leg or femoral thrombosis. This venogram was done a few days after the development of a typicalwhite leg in a lady of 6o. The upper and lower leg pictures showing the maze of fine venous collaterals, bothsuperficial and deep, are very typical of the early phases of this condition.
into the posterior tibial vein where it may alsospread into the perforating veins; it may thenspread upwards involving in turn the popliteal,femoral and external iliac vein where it almostalways stops where the internal iliac vein joinsit. These various stages of spread of the throm-bosis are characterize4 by definite physical signsand clinical picture.
Stage i. Thrombosis confined to calf sinuses:Tenderness in lower third of the calf.
Stage 2. Early spread to posterior tibial:-Someslight oedema at inner side of ankle and localizedtenderness over the sites of the middle and/orupper perforating veins. The leg may feel warm.
Stage 3. Extensive involvement of posteriortibial veins and/or peroneal veins:-Obviousoedema of ankle and increase in diameter of calf.The leg and calf is warm. Fever up to I000 F.
Stage 4. Spread to popliteal vein:-Consider-able oedema of ankle and increase in size of calf.Fever.
Stage 5. Spread to femoral and iliac veins:-Classical picture of ' white leg.' Concentricswelling and tense oedema of whole leg and thigh.Leg is pale or slight dusky blue and is hot to thetouch. Fever up to IO0° F.
The Factors Responsible for Development ofCalf ThrombosisThese factors may be grouped under local and
general.
Local FactorsThe most important single factor is stasis. In
the section on physiology it was noted that whenthe legs are below the level of the heart and thecalf is at rest the venous flow in the leg is ex-tremely sluggish and, in fact, blood pools in thecalf. This is a common factor with any patientill in bed from whatever cause. The other localfactor is possibly trauma to the calf while underthe anaesthetic on the operating table.
General FactorsThere are certain general factors predisposing
to increased coagulability of the blood in disease.These include increased viscosity (polycythaemiaand dehydrated states), increased platelet count(post-operative and post-partum). There is alsothe undoubted fact that in certain cases of cancer(especially of the lung and pancreas) there is anincreased tendency to thrombosis, the cause ofwhich is so far unexplained.
FIG. i i.-Diagram of the effects of destruction of the valve in one of the large direct ankle perforating veins.
It follows from this consideration that the mostpowerful weapons in the prevention and treatmentof this form of thrombosis are elevation of the legsand the encouragement of calf movements. Theuse of anticoagulants is of entirely secondary im-portance to the above measures.
Calf thrombosis is nearly always bilateral,although the signs on one side may be consider-ably in advance of those on the other.
It is not proposed to discuss the question ofembolism in this paper.
The Sequelae of ThrombosisThe three main sequelae of thrombosis may
be:Chronic oedema of the leg and ankle.Induration, pigmentation and ulceration of the
lower third of the leg, the ' gaiter area.'Gravitational pain and aching in the calf and
leg.Two rarer sequelae are:-(I) A contracture of
the soleus leading to an acute equinus deformityof the foot. The tendo achillis may become soshort, due to this contracture, that the patientcannot put her heel to the ground and cannot wearlow-heeled shoes. (2) A hypertrophy and increasein girth of the upper part of the calf (probably dueto chronic intramuscular oedema) giving the ap-pearance of ' well-developed calves' and usuallyassociated with gravitational pain and aching.
These sequelae may appear all together or oneor two may occur without the others. Moreoverthere is a characteristic latent period before themost dreaded sequelae-induration and ulceration-appear. Many authors (Homans, Linton,Hojensgard and Cockett) have pointed out thatthe peak incidence of ulceration and induration isabout two years after the episode of thrombosis.This now becomes understandable if we considerthe effect of thrombosis on the physiology of thecalf pump and venous retum.The first important point is that once thrombosis
has occurred in a vein recanalization is the rule(Buxton and Collar, I945; Linton and Hardy,1947; Dow, 1951; Cockett, I953). This re-
canalization starts within a few weeks as fine bloodchannels growing into the clot which graduallycoalesce forming one or more large channels whichmay be as big as the original vein or bigger.Another way in which recanalization may occur isby retraction of the clot to the side of the vein andthen gradual organization. In either case the re-sult is that the venous valves are destroyed. In theaverage case this process is complete and leaveseffective large valveless deep channels in from oneto two years. It is from this time onwards that thesevere sequelae appear. Now it has been notedthat as the thrombosis spreads from calf toposterior tibial veins it also involves the perforatingveins (Cockett and Jones, I953). Thus when re-
Oct.ober 1954 COCKETT: Abnormalities of the Deep Veins of the Leg
v :q
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FIG. 12.-A Recanalized Deep Vein. The patient hadhad a post partum white leg eight years previouslyand she now had a small post-malleolar ulcer. Nosuperficial varicose veins were present. Thispatient had the deep vein tied in Hunter's canaland the next figure shows the appearance of thevein in cross-section.
canalization occurs not only are the valves in thedeep veins destroyed but also the valves of thelarge direct perforating veins in the lower leg (seeFigs. 6 and 7). These veins may then be regardedas ' leaks ' in the lower part of the calf pump,where the rise of pressure within the pump isgreatest on contraction. The effect on the sub-cutaneous tissues is shown diagrammatically inFig. ii.
....
FIG. 13.-Cross-section of a recanalized femoral vein.This is the same patient as in Fig. I2.
Thus the essential and basic pathologicalphysiology in the lower third of the leg is an un-relieved venous hypertension of the veins andvenules of the subcutaneous tissues. These veinsare fine and thin walled and are not intended tostand up against a venous pressure of go mm. Hg.indefinitely, so they gradually dilate. This sus-tained subcutaneous venous hypertension, un-relieved by exercise of the calf, has been demon-strated by many authors measuring the changes invenous pressure in veins of the foot on exercise incases of the post-thrombotic syndrome.
It is thus apparent that the well known sequelaeof deep thrombosis, induration, ulceration andoedema are primarily due to destruction by throm-bosis of the valve system within the calf pump.Destruction of valves in the whole popliteal andfemoral system is not further contributory towardsthis induration and uilceration. However, suchpatients with complete destruction of valves inpopliteal and femoral veins do often have moreoedema and more postural aching and pain in thecalf than people who have had calf thrombosisalone (see Figs. I2 and I3). This is particularlyso if their occupation is one which necessitatesheavy labour in the erect position. Such musculareffort causes a repeated rise in intra-abdominalpressure which is transmitted straight down thelarge valveless deep channel to the lower legcausing increased oedema and a deep aching painin the muscles of the calf (Gunnar Bauer's' burst-ing pain'). The classic occupational victim ofthis is the ' busy housewife.'
TreatmentThis brings us to a consideration of the treat-
ment of these sequelae of thrombosis. Preventionis better than cure and the most essential pointtherefore is the prophylaxis of post-operative andpost-partum thrombosis.
Once the post-thrombotic syndrome has beenestablished some regime of management is neces-sary. As the basic aberration in this disease is apersistent venous hypertension in the subcutaneoustissues round the ankle and malleoli, the mostnecessary part of treatment is the application ofstrong elastic pressure from outside which sup-ports and compresses the whole of the sub-cutaneous tissues and allows a massaging action totake place between deep muscles and elasticsupport. Such a system, to some extent, restoresthe efficiency of the calf pump. In the moreadvanced cases a firm webbing elastic bandageapplied over a dressing or cotton bandage, care-fully moulded round the malleoli and continuedup to just below the knee is required. This is puton before rising and discarded at night. Thepatient is instructed to sleep with the foot of thebed slightly raised. This simple regime, combinedwith local massage in advanced cases, will healmost post thrombotic ulcers and relieve most of thepain and control the oedema. When the ulcersare healed a strong elastic stocking can be sub-stituted. (Elasto net stockings are useless for thispurpose as they are not strong enough.) The greatadvantage of this form of treatment is that it isambulatory and does not interfere with thepatients' life or work.
Another simple way of lowering the venouspressure in the legs is to put the patient to bedwith the feet above the level of the heart. Undersuch circumstances venous ulcers rapidly heal.When they get up again support is vitally necessaryto prevent breaking down.
Local applications to ulcers are unimportantexcept that gross local surface infection must becontrolled (lotio streptomycin I/I,OOO is best forthis) and substances which induce irritation of thesensitive skin in these cases must be avoided.(This includes the penicillin creams, eusol used fora long time, and flavine.) Zinc cream is thesafest local application.
Surgical TreatmentSurgical treatment must be looked upon as an
episode in the general management of these cases.In older patients and those who are infirm fromany other reason conservative management withthe bandage routine is usually preferred. How-ever, there is a large group of younger people(under the age of 50) who are anxious to undergosurgical treatment to get rid of their ulcers andother symptoms and to stop them getting worse.The surgical treatment of a venous ulcer entails
first a careful evaluation of which group of veinsare at fault. Ulcers associated with gross andobvious incompetence of the great or small
saphenous systems should have these superficialveins ablated. This is so whether there is a historyof past deep thrombosis or not, as incompetentsuperficial veins are an encumbrance to the super-ficial circulation in any cas-Most ulcers (even those associated with super-
ficial venous incompetence) are essentially post-thrombotic in origin and the essential lesion under-lying them is destruction of the valves in the per-forating veins of the lower third of the leg. Theoperative treatment of these ulcers by the exposureand ligation of these veins is undergoing trial inthis country and America and is giving extremelypromising results (Linton, 1953; Wright, 1954;Cockett, I953).
Finally, the much discussed operation of deepvenous ligation (femoral or popliteal) must beappraised. From several follow-up studies nowpublished (Cockett, I953; Boyd, 1954; Goligher,1953; Moore, I953; Linton, 1953) it is nowapparent that deep venous ligation alone ha3 littleeffect on ulcers. The early glowing reports ofBauer have not stood the test of time. But this isnot to be wondered at because, as we have seenfrom the foregoing considerations, the essentialpathology of ulceration and induration is all in thecalf itself.
However, the effect of ligation of large in-competent deep venous trunks on gravitationalcalf pain is marked and definite. All authorsappear to be agreed on this. In performing thisoperation for pain, however, it is most essential tobe sure that it is being done for the right sort ofpain. Most patients with recent ulceration of theleg have pain and aching on standing up and thepain is in the lower third of the leg and in the ulcer.The true generalized aching of the calf muscles asthe day wears on is a much rarer complaint. Deepvenous ligation should not be contemplated untilit has been shown that a reasonable period of con-servative treatment (say six months) which healsthe ulcer, does not abolish or ease the calf pain.It must then be demonstrated, by a reliable veno-graphic technique, that the deep vein is in factlarge, valveless and pathological (Gryspeerdt andCockett, I953). In such circumstances ligation ofthe deep vein (either popliteal or femoral) willbring relief and a grateful patient (especially if thepatient has to be on his or her feet all day).Ligation of such recanalized incompetent deepveins has very little effect on the amount ofswelling present, neither increasing nordreasin gecit.
Sympathectomy alone does not control venousulceration or any of the symptoms, but it is auseful adjunct to appropriate venous ligation in theerythrocyanoid type of leg.Bihlinornbhv rnntin,,pd en ^naop AX
October 1954 FALLE, GILL AND POST: Chronic Disturbances of Bowel Function
BOCKUS, H. L. (I943), ' Textbook of Gastro-Enterology,'Vol. I, Philadelphia and London.
BOCKUS, H. L. (1944), Ibid., Vol. II.FRAZER, A. C., FRENCH. J. M., and THOMPSON, M.D.
(949), Brit. Y. Radiology, 22, 123.GILL, A. M., and FALLE, E. DE C. (I952), Lancet, ii, 356.GLAZEBROOK, A. J. (1952), Ibid., i, 895.GOLDEN, R. (1945), 'Radiological Examination of the Small
Intestine,' Philadelphia and London.GOLDEN, R. (I950), Brit. Y. Radiology, 23, 390.GRACE, W. J., WOLF, S., and WOLFF, H. G. (igsi), 'The
Human Colon,' New York and London.HALL, S. B. (I949), 'Psychological Aspects of Clinical Medicine,'
London.HARDY, T. L. (I934), Clin. _., 63, 407, 453.HARDY, T. L. (I945), Lancet, i, 5I9, 553.
HURST, A. F. (ixIi), Ibid., i, I05I, III9, II87.JORDAN, S. M., and KIEFER, E. D. (1929), J.A.M.A., 93, 592.JORDAN, S. M. (I932), Ibid., 99, 2234.MACPHEE, I. W. (I953), Lancet, i, 678.POSEY, E. L., and BARGEN, J. A. (i95i), Amer. J7. Med. Sciences,,
221, IO.RAY, B. R., and NEILL, C. L. (I947), Annals of Surgery, I26, 709-RYLE, J. A. (I928), Lancet, ii, iiiS.RYLE, J. A. (ir93I), Lincet, i, 737.SPRIGGS, E. I. (I93I), Q.J.M., 24, 533.WILSON, T. S. (1927), 'Tonic Hardening of the Colon,' London..WOLF, S. G., and WOLFF, H. G. (947), 'Human Gastric-
Function,' 2nd edition, New York.YOUMANS, W. B. (I949), ' Nervou3 and Neurohumorel Regulation,
of Intestinal Motility.' New York.
LLOYD ( LUKE
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