254

animal breathing with an arterial PC02 at 40 mm. Hgis the same as its standard bicarbonate determinedin-vitro. However, as is well known, the in-vivoand in-vitro curves are different .21-11The Astrup system is widely used to calculate the

theoretical " amount of NaHCOg required to correcta base deficit by the formula 24:

NaHCOs (mmol)=base deficit x 0-3 X body-weight (kg.).

Use of this formula can lead to the overestimationof the amount of NaHC03 required to correct a

metabolic acidosis by as much as 50% 25 or to patientswith pure CO2 retention being described as havinga base deficit requiring " correction " by many milli-moles of NaHC03.26

If it is considered helpful to use nomograms to

follow acid-base changes in acutely ill patients (e.g.,undergoing intermittent positive-pressure respiration)then it is better to use ones based upon the in-vivo

blood-CO2 titration curves such as the Pco2-pHnomogram of Stoker et al .21 which is shown withS.I. units in the figure. However, owing to individualvariations in a and carbonic-acid pK’, patients onventilation should not be expected to follow exactlythe in-vivo titration lines given in the figure.

H+ ( nmole per litre)

CO, titration curves in vivo in man at different values of non-respiratory H+ (blood H+ concentration at P$co, 53 kPa,40 mm. Hg) with H+ activity on the abscissa and C02 on theordinate.

Data from Stoker et al. 2 6

CONCLUSIONS

The Henderson-Hasselbalch equation as widelyused in clinical acid-base work applies only to" normal " human serum, and equilibrium conditions.Since the serum carbonic acid pK’ and CO2 solubilitycoefficient can vary rapidly and unpredictably in

pathological states all nomograms based upon a

fixed Henderson-Hasselbalch equation are theoreti-

cally unsound.The Astrup scheme based upon both the

Henderson-Hasselbalch equation and the similarityof in-vivo and in-vitro CO2-blood titration curves is

doubly unsound. It is possible that patients couldbe given up to 50% too much NaCHO if the amountcalculated to be necessary by the Astrup scheme werein fact given.

Assessment of acid-base balance is best made

clinically by the " physiologic " approach of Schwartzand Relman .6 Acid-base nomograms, if used at all,should be based upon in-vivo blood-CO2 titrationcurves with H+ and CO2 reported in S.I. units.

REFERENCES

1. Campbell, E. J. M. Lancet, 1962, i, 681.2. Owen, J. A., Dudley, H. A. F., Masterton, J. P. ibid. 1965, ii, 660.3. Whitehead, T. P. ibid. 1965, ii, 1015.4. Lennon, E. J., Lemann, J. Ann. intern. Med. 1966, 65, 265.5. van Ypersele de Strihou, C., Frans, A. Presse méd. 1967, 75, 1797.6. Schwartz, W. B., Relman, A. S. New Engl. J. Med. 1963, 268, 1382.7. Bunker, J. P. Anœsthesiology, 1965, 26, 591.8. J. clin. Path. 1970, 23, 743; 1973, 26, 729.9. Broughton, P. M. G. (editor) Quantities and Units in Clinical

Biochemistry: Ass. Clin. Biochem. Tech. Bull. 1970, no. 20.10. Lancet, 1965, ii, 1010.11. Flenley, D. C. ibid. 1971, i, 961.12. Henderson, L. J. Am. J. Physiol. 1908, 21, 427.13. Hasselbalch, K. A. Biochem. Z. 1917, 78, 112.14. van Slyke, D. D., Sendroy, J., Hastings, A. B., Neill, J. M. J. biol,

Chem. 1928, 78, 765.15. Guye, P. A., Pintza, A. Mem. Soc. Phys. nat. Hist. Geneva, 1908,

35, 569.16. van Slyke, D. D., Sendroy, J. J. biol. Chem. 1928, 79, 781.17. Hastings, A. B., Sendroy, J., van Slyke, D. D. ibid. 1928, 79, 183.18. Severinghaus, J. W., Stupfel, M., Bradley, A. F. J. appl. Physiol.

1956, 9, 197.19. Trenchard, D., Noble, M. I. M., Guz, A. Clin. Sci. 1967, 32, 189.20. Astrup, P., Jorgenson, K., Siggaard-Andersen, O., Engel, K.

Lancet, 1960, i, 1035.21. Cunningham, D. J. C., Lloyd, B. B., Michel, C. C. J. Physiol.,

Lond. 1962, 161, 26P.22. Cohen, J. J., Brackett, N. C., Schwartz, W. B. J. clin. Invest. 1964,

43, 777.23. Norman, J., Linden, R. J. Br. J. Anœsth. 1966, 37, 290.24. Mellemgaard, K., Astrup, P. Scand. J. clin. Lab. Invest. 1960, 12,

187.25. Zimmet, P. Z., Taft, P., Ennis, G. C., Sheath, J. Br. med. J. 1970,

iii, 610.26. Stoker, J. B., Kappagoda, C. T., Grimshaw, V. A., Linden, R. J.

Clin. Sci. 1972, 42, 455.27. Davenport, H. W. The ABC of Acid-base Chemistry. Chicago,

1958.28. Bradley, A. F., Stupfel, M., Severinghaus, J. W. J. appl. Physiol.

1956, 9, 201.

Special Article

REALISTIC GOALS FOR SMOKING AND

HEALTH

A CASE FOR SAFER SMOKING

M. A. H. RUSSELL

Addiction Research Unit, Institute of Psychiatry,Maudsley Hospital, London SE5

Summary Evidence is presented demonstratingthe crucial role of nicotine in the

generation and maintenance of cigarette dependence,the potency of which ensures that almost anyone whosmokes at all becomes dependent. It is suggestedthat this high dependence-producing potency and theuniversal appeal of the effects of nicotine lie behindthe past failures of smoking-control programmes. Inthis context, the goal of abstinence and the abolitionof all smoking is unrealistic and doomed to fail. Themore realistic goal of safer smoking is explored. It is

argued that the carbon monoxide (CO) yield of

cigarette brands should be added to the official tar

and nicotine tables and that the safer cigarette is likelyto be the one with low tar and CO yields but a high,rather than low, nicotine yield. However, the ultimategoal of acceptably safe, light to moderate, controlledsmoking will probably require the virtual elimination

255

of cigarette smoking in favour of non-inhaled smokingof pipes or medium to large cigars. With the com-bined effects of health education coupled to selectivetaxation directed at this more realistic goal, successis not only possible but probable.

INTRODUCTION

THE health hazards of cigarette smoking are now aswidely recognised as is our failure at a national levelto do anything to reduce them substantially. Tradi-tional methods of health education, treatment at

clinics and antismoking propaganda have so far beenuniformly ineffective.1 I suggest that the aims of mostnational smoking-control programmes are not

realistic and that the goal of " safer " smoking is more

realistic than the goal of " no smoking ".

REALITIES OF CIGARETTE DEPENDENCE

The first reality for health educationists is the

degree to which cigarette smoking is dependenceproducing. Three out of four smokers either wishto or have tried to stop smoking, yet only about onein four ever succeeds in becoming a permanent ex-smoker.2 Thus most people smoke not because theywish to, but because they cannot easily stop. Thisstate is one of the features of a dependence disorder.Giving up smoking is an aim of middle and later life:only about 15 % of smokers succeed in stopping per-manently before the age of sixty,3 by which time manyof the harmful effects have already been incurred.

Cigarettes are far more dependence producing thanalcohol or barbiturates. Most people who drinkalcohol or take sleeping pills are able to limit them-selves to intermittent use and to tolerate periods freeof the chemical effect. Not so with cigarettes; smokingis seldom a take-it-or-leave-it activity practised inmoderation on special occasions. Intermittent or occa-sional smoking is rare-about 2% of smokers.2 Withalcohol use it is a small minority who become depen-dent but with smoking it is a small minority who avoiddependence. Furthermore, dependence on alcohol orbarbiturates usually occurs only in a setting of

psychological or social difficulty. This is not the casewith smoking. If he smokes at all, the most stablewell-adjusted person sooner or later becomes a

regular dependent smoker. The virtual inevitabilityof this escalation to regular dependent smoking is

brought out by McKennell and Thomas’s finding thatof those teenagers who smoke more than a singlecigarette only 15% avoid becoming regular dependentsmokers .2 If we bear in mind that only about 15 % ofsmokers succeed in giving up permanently before theage of sixty, it follows that of those teenagers whosmoke more than a single cigarette, over 70 % willcontinue smoking for the next forty years; despite thefact that within ten years of starting most of them wishto stop.But to establish that cigarette smoking is a life-long

dependence disorder does not explain how it is con-tracted. This has been discussed elsewhere,3 and theargument will not be repeated here other than to saythat after initiation to smoking has been mediated byvarious psychosocial motives, the pharmacological

effects of nicotine take over as prime reinforcers ofsuch strength and universal appeal that eventual

dependence is almost inevitable. Thus most peopleend up smoking not because they want to look" tough " or " grown-up " or because " most of theirfriends smoke", but simply because they have becomedependent on nicotine.

CRUCIAL ROLE OF NICOTINE

Cigarette smoking allows the absorption of about50-150 gg. nicotine per puff or 1-2 mg. per cigarette.’Smokers who do not inhale still absorb some nicotine

through the nasal and buccal mucosa. There is littledoubt that if it were not for the nicotine in tobaccosmoke people would be little more inclined to sm’kethan they are to blow bubbles or light sparklers. Whatevidence is there for this statement?

Since its introduction to Europe in the 16th century,tobacco use has fluctuated between chewing, snuffing,and smoking-but no population has dispensed with oneform of tobacco use without replacing it with another.The only time the British gave up smoking was in the18th century when, for almost 100 years, they switchedto snuff. The common factor here is nicotine. Buttobacco has never been used as a substance of ingestion,possibly because with absorption via the portal systemmuch of the nicotine would be metabolised by the liverto cotinine which is psychopharmacologically inert. Thushistorical evidence shows that we have used tobacco onlyin ways which allow the nicotine absorbed to bypass theliver and enter the brain in an active form.

Apart from this historical evidence, there are severalstudies which demonstrate convincingly the crucial roleof nicotine as a determinant of smoking behaviour. For

instance, most smokers are just not satisfied and mayeven suffer withdrawal effects after ’ blind " substitutionof low-nicotine or nicotine-free cigarettes.-,6 A singlestudy has shown that the craving of cigarette withdrawalcan be relieved by nicotine injection.’ Two independentstudies have clearly shown that smokers unconsciouslymodify their puff-rate to regulate their nicotine intake.When smoking a high-nicotine cigarette they puff less

frequently and when smoking a low-nicotine cigarette theyincrease their puff-rate thus compensating for the lownicotine yield.8.9 Under natural conditions too, smokingis modified to regulate nicotine intake. On switching tolow-nicotine cigarettes consumption, in terms of the weightand number of cigarettes smoked, is increased while on

switching to high-nicotine cigarettes it is decreased."Another study showed that people in an experimental wardunconsciously changed and reduced their smoking whengiven intravenous nicotine. While the intravenous dripcontained saline they smoked in their usual way, but whennicotine was added to the saline drip not only did theylight up fewer cigarettes but those that were lighted werepuffed less frequently and discarded earlier, showingclearly that when there was an alternative source of nico-tine there was less need to obtain it from cigarettes."Monkeys and rats will learn to self-inject nicotine for

its own sake,’’,,13 indicating that it has some action which

they find rewarding. This quality of acting as a primarybut " unnatural " reinforcer of behaviour is shared withother dependence-producing drugs. There is no evidencewhatsoever that other components of tobacco smoke such astar and carbon monoxide are intrinsically rewarding. Itis not known which of the many actions of nicotine are

the ones which humans and animals find rewarding, butthere are a number of these actions, peripheral and central,which have potential for behavioural reinforcement.3

256

DEPENDENCE AND RATE OF NICOTINE ABSORPTION

Whatever the action involved, much of the dependence-producing potency of nicotine is likely to be due to theextremely rapid intravenous-like effect which followsinhalation. The slower effect after buccal absorption maybe less dependence-producing; more akin say to that ofalcohol or barbiturates taken by mouth.

Buccal absorption of nicotine is pH dependent.14 It

happens with the alkaline smoke (about pH 8-5) of theair-cured tobaccos used in pipes and cigars, but does notoccur with the acidic smoke (about pH 5’S) of flue-curedtobaccos present in most brands of British cigarette.Thus while pipes, cigars, and cigarettes may all be inhaledso as to make dependence almost inevitable, it is possibleto get a nicotine effect from pipes and cigars withoutinhaling them and without incurring, therefore, the samehigh risk of dependence. The reason that small cigarsand the air-cured brands of Continental cigarettes are

more likely to be inhaled than pipes and large cigarsmay possibly be due to the fact that they are too smallto give an appreciable nicotine effect from slow buccalabsorption. More research is required to answer these

important questions.SWITCH TO FILTERS

It is unlikely that any single measure has savedmore lives or done more to reduce smoking-relateddisease than the switch from plain to filter-tippedcigarettes which began in the late 1950s and continuedthroughout the 1960s. In 1955, less than 2% of allcigarettes smoked were filter-tipped; by 1960 the figurewas about 16% and in 1970 it was over 78 % .15 Thusover a fifteen-year period which saw little sustainedchange in smoking prevalence or per caput cigaretteconsumption, there has nevertheless been this massiveshift in the type of cigarettes smoked.This is perhaps more surprising when it is realised

that during this period health-education efforts werechiefly directed towards persuading people to stopsmoking or, failing this, to reduce consumption.There was no deliberate programme to induce peopleto switch to filter-tipped cigarettes. So while health-education programmes were working feverishly, butachieving nothing, towards their goal of totalabstinence and the abolition of all smoking, thisenormous change in smoking habits occurred more orless spontaneously without any formal official effort.The reasons behind this switch to filters is not

altogether clear. It began before there was heavypublicity regarding the health hazards of smokingand it was not accelerated at the time of the first

report of the Royal College of Physicians in 1962.Though some awareness existed that filter-tippedcigarettes are safer, the majority gave cleanliness,better flavour, and the lower price as their chiefreasons for switching.2 But switching to filter-tippedcigarettes is not the only change that smokers havemade. There has also been a move towards " milder "

brands.SWITCH TO LOW-TAR AND LOW-NICOTINE

CIGARETTES

In September, 1971, the Consumers Association

published a " league table " showing the tar and nico-tine yields of popular brands of cigarettes.16 This wasfollowed by massive increases (360 % in six months) 17in the sales of ’ Silk Cut’ cigarettes which were listedas having the lowest tar and nicotine yields. Thisswing to milder cigarettes was a spontaneous response

on the part of the smoking public to simple informa-tion without exhortation. The information suggesteda course of action which was within the individual’scapacity to implement. By this simple action of

balanced, unbiased presentation and publication of

straightforward facts the Consumers Associationachieved at a single stroke a greater change in smokingbehaviour than the £200,000 plus a year spent by theHealth Education Council on sporadic television com-mercials and ineffectual hoardings.The manufacturers wasted no time in attempting

to exploit this demand for what was perceived as asafer cigarette. By April 11, 1973, when the Govern-ment published an official league table for 101 brandsof cigarettes sold in Britain,i8 there were no less thanten brands with nicotine and tar yields lower thanthe brand which had headed the Consumers Associa-tion list just eighteen months earlier. However, themanufacturers’ zeal misfired somewhat. Many of thenew extra-mild brands were tried but then rejectedby the public. Whether this was because the nicotinelevels were too low or because the draw resistancethrough the tightly packed filters was too high, isprobably so far known only within the trade.

TOWARDS A REALISTIC GOAL

The traditional health-education approach to

smoking control has been an " anti-smokingapproach " with the ultimate goal orientated towardsabstinence and the abolition of smoking. Over the pastfifteen years there has been virtually no progress in thisdirection, and unless the direction is changed thereis unlikely to be much more progress in the future.Rather than consideration of alternative and morerealistic goals, the response to past failures has beento call for more money and harsher restrictivemeasures. But even if the Government could be

persuaded to ban all promotion and advertising oftobacco products and to provide the funds for a mas-sive intensification of anti-smoking propaganda, it isdoubtful whether much would be achieved by whatamounts to flogging a dead horse harder.

It seems that insufficient recognition has been givento the nature of cigarette smoking as a dependencedisorder and the degree to which most smokers aredependent on the drug effect of nicotine. The lack ofresponse to health education in the past does not

mean that smoking habits are refractory to health edu-cation as such, but rather that the demands of healtheducation have been too difficult for the averagesmoker to achieve. It is not so much the motivationas the ability to stop which is lacking. The switch tofilters and the willingness of smokers with little

prompting to switch to or at least have a go at milderbrands of cigarette suggests that smoking habits, eventhough they are not readily abolished, may still be

changed. To attempt to control smoking by abolish-ing it may be as unrealistic as it would be to try tocontrol alcoholism by prohibiting all alcohol drink-

ing. Instead of aiming at abstinence and the abolitionof smoking, health education should perhaps adopta more realistic goal. Rather than anti-smoking, theaim should be towards achieving acceptably safe,light to moderate, controlled smoking. With this morefeasible goal, success is not only possible but probable,

257

APPROACHES TO SAFER SMOKING

The second report of the Royal College of Physi-cians (RC.P.) 19 rightly emphasised that from the

health point of view the safest thing to do was to

avoid smoking altogether. However, they recognisedthat it was beyond the capacity of many smokers toachieve this, and suggested alternative ways of

reducing the hazards for those who continued

smoking. The first and preferable approach advocatedwas to switch to cigars or a pipe. But this advice is

incomplete. Unlike most " primary " pipe and cigarsmokers (i.e., those who have never been regularcigarette smokers), heavy cigarette smokers often con-tinue to inhale when they switch to cigars or a pipe.This " secondary " type of pipe and cigar smokinggives rise to blood carboxyhaemoglobin (COHb) levelsas high, and presumably as dangerous, as occurs

with cigarette smoking.20,21The second approach advocated by the R.C.P.

report for those unable to give up cigarettes was setout as six guidelines to less hazardous cigarettesmoking: smoke fewer cigarettes, inhale less, smokeless of each cigarette, take fewer puffs from eachcigarette, take the cigarette out of the mouth betweenpuffs, and smoke brands with low nicotine and tarcontent. The two main principles behind these guide-lines are clear; to inhale as little smoke as possible andto ensure that the smoke which is inhaled is of thelowest possible harmfulness. However, in restrictingtheir interest to tar and nicotine content the R.C.P.

guidelines have overlooked a major source of harm-fulness in tobacco smoke, namely carbon monoxide(CO). While the tar is the chief source of carcinogens,the CO has been heavily implicated as a cause of

arteriosclerosis, ischarmic heart-disease, and fetal

damage.22-25 Brands of cigarette vary considerably inCO yield.26 s Assessment of a cigarette’s degree ofhazard is therefore incomplete without informationabout its CO yield. This makes it imperative that COyield be added to official publications of tar andnicotine yield.27,28The six R.C.P. guidelines have another major short-

coming. To avoid smoking the proximal part of acigarette does, indeed, lower the harmfulness of thesmoke taken in, as does smoking a cigarette with alow nicotine and tar content. But, due to its role as adeterminant of smoking behaviour (see above), lower-ing the nicotine content of a cigarette reduces theharmfulness of its smoke only at a cost of increasingthe amount of smoke which is likely to be inhaled.With smokers who do not inhale it matters littlewhether the nicotine, tar, and CO yields of their

cigarettes are high or low, but for smokers who

require a nicotine effect-and most smokers do-weknow that when the nicotine yield is reduced, theytake more and bigger puffs and smoke more cigarettes,which means that they take in more tar and CO perunit of nicotine. If, on the other hand, the nicotineyield is high they puff and smoke less, so that thesafest cigarette is likely to be the one with a low taryield and a low CO yield but a high, rather than low,nicotine yield. Such a cigarette would minimise theamount of tar and CO it is necessary to inhale to

obtain a given amount of nicotine.

With selective and ventilated filters it is likely thatthe manufacturers will soon be able to virtuallyeliminate tar, CO, and other harmful constitutents oftobacco smoke. Since the absorption of nicotine isthe main reason for smoking, as long as sufficientnicotine is present the removal of all other constituentswould be tolerated by smokers. The removal of nico-tine, however, would not be acceptable. The key tosafer smoking rests with the harmfulness of nicotine.This is still largely unknown. If it proves to be rela-

tively harmless the goal of safer smoking will then beeasy to achieve, for with levels of tar, CO and otherharmful constituents reduced to a minimum it wouldstill be acceptably safe to smoke fairly heavily and itwould not be necessary to curb consumption, andnicotine intake, to an extent that is too difficult.

But if, as seems more likely, persistent high nicotineintake is found to be deleterious to health, the goalof acceptably safe smoking would also require that itbe light to moderate and controlled. This would bemore difficult to achieve but still quite possible. Itwould mean the virtual elimination of cigarettesmoking in favour of non-inhaled smoking of pipesand medium to large cigars. As discussed above, mostpeople are simply unable to inhale cigarettes withoutbecoming dependent on them. Only with the slowerbuccal absorption of nicotine from non-inhaled pipeand cigar smoke, would the majority of the smokingpopulation stand much chance of avoiding dependenceand controlling consumption at a light to moderatelevel.

Future progress in the identification of those at

especially high risk of lung cancer 29 and the cardiacconsequences of smoking 30 will further refine our

notions of acceptably safe smoking.CONCLUSION

With the combined effect of health education

coupled by selective taxation to the powerful price dis-incentive,31 it should be possible gradually to phaseout dangerous cigarette smoking in favour of

acceptably safe, light to moderate, controlled, non-inhaled smoking of pipes or medium to large-sizedcigars. Instead of the traditional goal of abstinenceand the abolition of smoking, a programme aimedat this more realistic goal need no longer be doomedto fail. What is being suggested is that a smoking-control strategy would be more likely to succeed ifit abandoned the prohibitionist position which seeksto turn us all into the tobacco equivalent of teetotallersand aimed instead to help us to use tobacco as we arenow able to use alcohol.

I thank Clare Wilson and Prof. Edward Lichtenstein fortheir helpful comments, Barbara Stevens for secretarial help,and the Medical Research Council and the Department ofHealth and Social Security for financial support.

REFERENCES

1. Russell, M. A. H. Br. J. Addict. 1971, 66, 157.2. McKennell, A. C., Thomas, R. K. Adults and Adolescents’

Smoking Habits and Attitudes. H.M. Stationery Office, 1967.3. Russell, M. A. H. Br. J. med. Psychol. 1971, 44, 1.4. Armitage, A. K., Hall, G. H., Morrison, C. F. Nature, 1968, 217,

331.5. Finnegan, J. K., Larson, P. S., Haag, H. B. Science, 1945, 102, 94.6. Knapp, P. H., Bliss, C. M., Wells, H. Am. J. Psychiat. 1963, 119,

966.7. Johnston, L. M. Lancet, 1942, ii, 742.

258

8. Ashton, H., Watson, D. W. Br. med. J. 1970, ii, 679.9. Frith, C. D. Psychopharmacologia, 1971, 19, 188.

10. Russell, M. A. H., Wilson, C., Patel, U. A., Cole, P. V., Feyerabend,C. Br. med. J. 1973, iv, 512.

11. Lucchesi, B. R., Shuster, C. R., Emley, G. S. Clin. Pharmac. Ther.1967, 8, 789.

12. Deneau, G. A., Inoki, R. Ann. N. Y. Acad. Sci. 1967, 142, 277.13. Clark, M. S. G. Br. J. Pharmac. 1969, 35, 367.14. Armitage, A. K. in Smoking Behaviour: Motives and Incentives

(edited by W. E. Dunn); p. 83. Washington, D.C., 1973.15. Todd, G. F. (editor). Statistics of Smoking in the United Kingdom;

p. 14. Tobacco Research Council, 1972.16. Consumers Association Which ?, September, 1971, p. 280.17. Gallaher Ltd., London. Personal communication.18. Lancet, 1973, i, 874.19. Royal College of Physicians. Smoking and Health Now. London,

1971.20. Cowie, J., Sillet, R. W., Ball, K. P. Lancet, 1973, i, 1033.21. Castleden, C. M., Cole, P. V. ibid. 1973, ii, 21.22. Surgeon General. The Health Consequences of Smoking. U.S.

Department of Health, Education and Welfare, 1972.23. Astrup, P. Br. med. J. 1972, iv, 447.24. Astrup, P., Trolle, D., Olsen, H. M., Kjeldsen, K. Lancet, 1972, ii,

1220.25. Wald, N., Howard, S., Smith, P. G., Kjeldsen, K. Br. med. J. 1973,

i, 761.26. Russell, M. A. H., Wilson, C., Cole, P. V., Idle, M., Feyerabend, C.

Lancet, 1973, ii, 687.27. Russell, M. A. H. ibid. p. 973.28. Russell, M. A. H. ibid. p. 1029.29. Kellermann, G., Shaw, C. R., Luyten-Kellermann, M. New Engl.

J. Med. 1973, 289, 934.30. Turner, R., Ball, K. Lancet, 1973, ii, 1137.31. Russell, M. A. H. Br. J. prev. soc. Med. 1973, 27, 1

Occasional Survey

SOURCE OF NON-LETHAL PULMONARYEMBOLI

N. L. BROWSE M. LEA THOMAS

Departments of Surgery and Radiology, St. Thomas’Hospital, London SE1

Summary The site of origin of deep-veinthrombosis and pulmonary emboli has

been assessed in a study of 320 phlebograms con-taining thrombus, and 201 patients with non-lethalpulmonary embolism. The calf has been found tobe the commonest site of deep-vein thrombosis, but40% of the thrombi in the ilio-femoral segmentappear to have arisen in these veins independent ofany calf thrombosis. The pulmonary emboli arosefrom all sites in a proportion similar to the incidenceof thrombosis in these sites.

INTRODUCTION

IN the past few years there has been much dis-cussion by clinicians about the site of origin of

peripheral venous thrombosis, the direction in whichthrombus propagates, and which varieties most oftenbecome pulmonary emboli. The main argument isabout the frequency of primary femoral-vein throm-bosis. Some believe that almost all femoral-veinthrombus is secondary to the downstream propagat-tion of calf-vein thrombus, and others that most ilio-femoral thrombi begin in the valve cusps of the ilio-femoral veins independent of the calf. The morbidanatomists have repeatedly stated that thrombi arisein multiple sites, and that the thrombi large enoughto be lethal come from the iliac and femoral veins.To throw some light on this problem, we decided

to review all the phlebograms which we have per-

formed on patients with deep-vein thrombus or pul-monary embolism during the years 1969-73 to assessthe incidence of the sites of thrombosis, and to

ascertain the source of the emboli.

METHODS

The phlebograms were performed by the techniquesof ascending peripheral, per-femoral, and intraosseous

phlebography, described by Lea Thomas.1 In only 7%of patients was it necessary to supplement the ascendingphlebogram with the other techniques. The criteria forthe diagnosis of thrombosis were those described by DeWeese and Rogoff 2 and Lea Thomas et al.3The films were assessed jointly to decide the site of the

thrombosis.. Calf thrombosis was defined as thrombus confined tothe veins below the commencement of the main poplitealvein (the confluence of the vena comites of the tibialarteries) and/or in the muscle veins.

Thigh thrombosis was defined as thrombus betweenthe beginning of the popliteal vein and the entry of theprofunda vein, including thrombus within the profundavein.

Pelvic thrombosis was defined as thrombus in the veinsabove the entry of the profunda veins, including the venacava and the internal iliac veins.As well as defining the site of thrombosis, a note was

made whether thrombus in one site was connected to

thrombus in another site or whether it appeared to be

independent.The diagnosis of pulmonary embolism was based on the

clinical judgment of the clinicians in charge of the patient.In all cases this was based on the accepted clinical featuresof pulmonary embolism, but in a considerable proportionthe diagnosis was supported by an abnormal lung-scan.

RESULTS

Site of Peripheral Thrombosis

During 1969-73 thrombus was seen in the phlebo-grams of 320. patients. 210 patients had unilateral

thrombosis, and 110 had bilateral thrombosis, givinga total of 430 legs for study. In those with bilateralthrombosis the site of thrombosis was symmetricalin 64 and asymetrical in 46. The site of thethrombosis in these 430 legs is shown in table i-the horizontal lines joining the Xs indicate that thethrombosis was continuous between the two sites.

It can be seen that the commonest variety ofthrombosis was thrombus confined to the calf (42%of cases) followed by thrombus in the calf continuous

TABLE I-SITE OF DEEP-VEIN THROMBOSIS IN 430 LEGS