29

and patient satisfaction, but had no beneficial effect on

morbidity. Given the growing number of leaflets andbooklets made available to GPs for their patients, this findingis important.There may be several explanations for the difference

between our findings and those of some other studies.7-9 Ourfollow-up period of 12 months was longer than that used insome investigations7,8 and some significant short-termreductions in morbidity may have gone undetected.

However, we wished to test for longer term benefits.There may have been a higher proportion of patients with

mild asthma in our study than in other studies, as well asmany who had had asthma for a considerable time. Such

patients may feel less motivated to change their self

management than do more severe or newly diagnosedasthmatics. The trial was well controlled and of reasonablestatistical power. Our ability to assess all groups fully beforeand after intervention helped to minimise possible biasintroduced by the higher drop-out rate in the interventiongroups compared with the control group. Furthermore,although drop-outs viewed their asthma as less troublesome,they were no different, in terms of their morbidity levels,from those completing the study.Reliance on patient recall in the assessment of morbidity

may be criticised, but was validated in our preliminary studyin which we found that morbidity reported by the patientscorrelated well with the GP assessment.14 In addition,Speight et al compared parent-assessed time lost from schoolwith school records and found that parents did not

overestimate absence due to asthma. The addition ofobjective measurements such as peak-expiratory-flowreadings would have been difficult. Single or intermittentreadings are of little value in describing long-term morbidity.The long-term use of peak-flow diaries would certainly haveinfluenced the educational intervention and might have hadan adverse effect on compliance.Our educational programmes were designed to be used

easily by GPs but took little account of the great variation inpersonality and attitudes amongst asthmatic patientsY Weconcentrated on improving knowledge alone, and in thisrespect we may not have been sufficiently comprehensive.Studies that have shown improvements in morbidity haveconcentrated more on behavioural aspects than on increasingknowledge, in their attempts to modify self management.’-9They have generally employed professional or speciallytrained staff and maintained more frequent or long-termcontact with patients. One evaluation of a self-administeredbehavioural intervention on paediatric asthma showedsimilar results to our own; patient knowledge and satisfactionwere improved, but few reductions in morbidity werefound.18 g

We must emphasise that the findings of this study were notentirely negative. Improved knowledge and patientsatisfaction were accompanied by a reduction in emergencyattendance at hospital in both intervention groups. Thusmorbidity can be reduced with improved patient knowledge.The tragic and avoidable death of 1 patient in this study

underlines the importance of improving our communicationswith asthma patients. Further studies designed to improveour understanding of self management are essential if we areto plan practical and effective forms of patient education.We thank the Chief Scientist’s Office of the Department of Health and

Social Security, and the Chest, Heart and Stroke Association forencouragement and financial support. Dr Ian Gregg, Dr Martin Bland, MrsSwatee Patel, Dr Robert East, Mr Tim Radford, Dr Michael D’Souza, andMiss Marian Tooley gave help and advice. We also thank the following GPs

who recruited patients to the study and participated in the maximumintervention phase: Drs Sim, Smyth, Goddard, Bettridge, Arthur,Chegwidden, Combes, Fisher, Stott, Brooks, Piper, Burton, Trevan, Stockley,Coole, Floyd, Scarisbrick, White, Boxer, D’Souza, Kane, Roberts, Topp,Avison, Baum, Bowskill, Clements, Crowley, Lister, Gomez, Lyons, andOttley.

Correspondence should be addressed to S. H., The Canbury MedicalCentre, 1 Elm Road, Kingston upon Thames KT2 6HR.

REFERENCES

1 Avery CH, March J, Brook RH. An assessment of the adequacy of self care by adultasthmatics. J Commun Health 1980; 5 (3): 167-80.

2 British Thoracic Association Death from asthma in two regions of England. Br Med J1982; 285: 1570.

3 Cochrane GM, Clark TJH. A survey of asthma mortality in patients between ages 35and 64 in the Greater London hospitals m 1971. Thorax 1975; 30: 300-05

4 Arnold AG, Lane DJ, Zapata E The speed of onset and severity of acute severe asthma.Br J Dis Chest 1982; 76: 157-63.

5. Speight ANP, Lee DA, Hey EN. Underdiagnosis and undertreatment of asthma inchildhood. Br Med J 1983; 286: 1253-56.

6. Anderson HR, Bailey PA, Cooper JS, Palmer JC. Influence of morbidity, illness label,and social, family and health service factors on drug treatment for asthma Lancet1981; ii: 1030-32.

7. Avery CH, Green LW, Krieder S. Reducing emergency visits of asthmatics: anexperiment in patient education. Presented as testimony at hearings of thePresident’s Committee on Health Education, Pittsburgh, 1972.

8 Maiman L, Green LW, Gibson G, MacKenzie EJ. Education for self treatment byadult asthmatics. JAMA 1979; 241 (18): 1919-22

9. Fireman P, Friday GA, Gira C, Vierthaler WA, Michaels L Teaching self

management skills to asthmatic children and their parents in an ambulatory caresetting. Pediatrics 1981; 68 (3): 341-48.

10. Creer TL, Backiel M, Ullman S, Leung P. Living with asthma NIH Publication84-2364. Bethesda MD: National Heart Lung and Blood Institute, 1985.

1 1 Hindi-Alexander MC, Cropp GJA. Evaluation of a family asthma program. J AllergyClin Immunol 1984; 74: 505-10.

12 Weiss JH. "Superstuff". Self management educational programmes for childhoodasthma, vol II, manuscripts. Bethesda MD: National Institute of Allergy andInfectious Diseases, 1981: 273-93.

13. Clark NM, Feldman CH, Freudenberg N, Millman EJ, Wasilewski Y, Valle I.

Developing education for children through study of self-management behavior.Health Educ Quart 1980; 4: 278-96.

14. Hilton S, Sibbald B, Anderson HR, Freeling P. Evaluating health education inasthma-developing the methodology preliminary communication. J R Soc Med1982; 75: 625-31.

15 Hilton S. Understanding your asthma. London: Asthma Society and Friends of theAsthma Research Council, 1981.

16 Baker RJ, Nelder JA. The GLIM System. Release 3. Oxford: Numerical AlgorithmsGroup, 1976.

17 Lask A. Asthma: attitude and milieu London: Tavistock Publications, 1966.18. Rakos RF, Grodek MV, Mack KK. The impact of a self administered behavioural

intervention program on paediatric asthma. J Psychosom Res 1985; 29: 101-08.

Dogma Disputed

WHAT HAPPENS TO WILD ANIMALS WITHBROKEN BONES?

CHRISTOPHER BULSTRODE JOHN KINGBRIAN ROPER

London Hospital, London E1 1BB

Summary Orthopaedic teaching suggests that long-bone fractures in wild animals are not

uncommon and that they can heal naturally. This paperinvestigates this statement. The unsystematic collection ofspecimens for museums has perpetuated the idea that thesefractures are not uncommon. Many fractures in adultskeletons seem to have occurred while the animal was still

young. A review of the original skeletons in two museumsdoes not support the view that major long-bone fractures inadult wild animals heal well. Contemporary observations onprimates in the wild over long periods show that fractures oflong bones in adult wild primates are rare and usually fatal,while falls which might be associated with juvenile fracturesare much more common and may well be the source of the

many well-healed fractures found in museum collections.

30

INTRODUCTION

"It is commonly supposed that, in order to unite, a fracturemust be immobilised. This cannot be so since, with fewexceptions, fractures unite whether they are splinted or not;indeed, without a built-in mechanism for union, land animalscould scarcely have evolved. "—A. G. APLEY, in Apley’s Systemof Orthopaedics and Fractures (1982).

THIS statement appears in many forms in orthopaedic texts.The underlying thinking is that long-bone fractures are notuncommon in adult wild animals and that they can healnaturally. Thus orthopaedic surgeons should bear this inmind before interfering with a "natural process". We havetraced the origin of the statement and re-examined theoriginal material, combining this with information nowavailable from long-term observations of animals in the wild.The results suggest that long-bone fractures in adult wildanimals are rare and are often fatal.

Writings early this century laid great emphasis on

darwinian natural selection. It was thought that any diseasedor injured animal would be killed. Animals shot for sportwere commonly found to be in good health and were taken tobe the survivors of this selection. However, as early as 19042the first paper appeared which suggested that the situationwas not so simple. In 1911 Duckworth3 reported on theskeletons of 14 adult orang-utangs which had been shot. 4 hadevidence of healed fractures. He concluded that fractureswere common in adult wild primates and that they usuallyhealed with little deformity. This evidence was extended bySchultz who reviewed museum specimens of eight primatespecies and found fractures in 12-34%, depending on thespecies.4 In a detailed study of 118 shot specimens of gibbon,an acrobatic ape which spends its life high in the canopy oftropical rain forest, Schultz found sixty-five fractures in 42animals: these included nineteen fractures of the humerus,radius, or ulna and twenty fractures of femur, tibia, or fibula.5 5

When he compared the lengths of 13 healed long bones withthe normal side in wild gibbons he noted a mean shortening ofonly 4 - 5% (range - 0 - 5% to 14 - 4%).

REVIEW OF DUCKWORTH AND SCHULTZ COLLECTIONS

We have examined the Duckworth collection of orang-utang skeletons in Cambridge and the Schultz collection ofgibbon skeletons in Zurich. Evidence of healed fractures of allbut long bones have been excluded from this analysis topermit comparison with other studies.6 The presence ofhealed fractures was noted, and the degree of angulation,length of overlap, and total length change of the healed anduninjured contralateral bone were compared.

All the healed fractures were in bones with closed epiphyses but ifthe fractured bone was longer than its partner we assumed thatepiphyseal overgrowth had occurred7 and that an animal injuredwhile young had survived to adulthood before being shot for study.If the fracture was in the epiphyseal zone and there was gross growthdisturbance with shortening and angulation the fracture wasassumed to have occurred in a juvenile skeleton which had sufferedepiphyseal damage.8

If one or more fractures in a skeleton with multiple fractures hadthese features it was assumed that all the fractures had occurred atthe same accident and were juvenile fractures. The justification forthis assumption comes from our analysis of the incidence ofmultiple fractures. We compared the theoretical distribution

expected if each fracture had occurred in a separate incident withthe observed distribution of the 16 fractures in the 56 availableanimals of the Schultz collection. The two distributions are

significantly different (Kolmogorov-Smirnov non-parametric onesample test, p<0 - 01) (table i).

TABLE I-DATA TO CALCULATE PROBABILITY OF MULTIPLE

FRACTURES HAVING OCCURRED INDIVIDUALLY

T

11 of the 14 skeletons in the Schultz collection with healedfractures sustained the injuries when they were juvenile. Inthe other 3 the timing of the injury is uncertain (table II).Both Schultz4 and Bramblett9 state that the number of

fractures in skeletons increases with age. However, our studyof the Schultz collection does not support this conclusion andexclusion of phalangeal and rib fractures (which are liable tomisdiagnosis) removes this trend from Bramblett’s data. Iffractures happened at a constant rate throughout life healedfractures would accumulate in older animals, a possibilitythat can be tested statistically (table III). Accumulation seemsmost unlikely, while the hypothesis that most fractures occurin juveniles fits the data very well.The study of shot specimens could introduce distortions

simply because some animals may be more easily collectedthan others. This difficulty, first raised by Randall,1O wasrefuted by Schultz 1 1 who argued that animals which had beeninjured previously would be more alert and quicker to escapethan those which had not been injured previously. However,Buikstra’s study6 of healed fractures in a museum collectionof skeletons and in skeletons of a complete population ofmacaques that had had to be destroyed for conservationsuggested that the collection of specimens for museums couldseriously distort the incidence of conditions, casting furtherdoubt on the validity of conclusions drawn from museumspecimens.TABLE II-OBSERVATIONS ON SCHULTZ COLLECTION OF 56 ADULT

GIBBON SKELETONS

*In some skeletons other fractures (eg, ribs, clavicle) were also noted.tOther humerus missing. yin acetabular size.R=radius, U=ulna, E= elbow, H=hip, T=tibia, F=fibula.

TABLE III-ANALYSIS OF BRAMBLETT’S DATA ON BABOON SKELETONS

z* Probability of accumulation being correct hypothesis <5% probability ofjuvenile fracture being correct hypothesis >70%

31

TABLE IV-INCIDENCE OF FALLS (AND DEATHS) IN TWO STUDIES OF

THE RED COLOBUS

OBSERVATIONS IN THE WILD

To bypass this difficulty we turned our attention to thenatural history of long-bone fractures as seen by observers ofwild primates. We gathered data from eleven researchworkers who have led teams studying primates in the wild forlong periods. Only 3 adult animals were observed to sustainmajor long-bone fractures. All 3 died soon afterwards; 1 diedfrom injuries and 2 were killed by predators. It is not easy toestimate how many animal-years of observation these recordsrepresent but a conservative estimate is 3000, giving an adultfracture (and mortality) incidence of 1 per 1000 animal-years.The incidence of fracture and mortality in juveniles andinfants is 1 per 10 animal-years in the red colobus, the onlyspecies for which accurate data are available. In arborealspecies such as the colobus the commonest cause of injuryseems to be falls 12,13 and these are 11 times more common inyoung animals than adults so the higher mortality in infants isin part due to the higher incidence of accidents and not just totheir lower chances of survival (table IV).

DISCUSSION

Museum specimens may not accurately represent thepattern of long-bone fractures in the wild. Fieldworkers maymiss some minor fractures and ones in juveniles but are notlikely to miss a major fracture. Juvenile bones are less brittleand heal more vigorously than adult bones and youngprimates supported and protected by their parents probablystand a better chance of surviving in the wild than does anadult, without such support, who sustains a similar injury. Asubstantial proportion of the healed fractures seen in museumcollections probably happened in juveniles, and Schultz’observation that the incidence of fractures increased with agemay be an artifact of the way in which specimens werecollected.Almost all fractures in the long bones of man today are the

result of high-energy impact in, for example motor vehicleaccidents or sport, or the osteoporosis of senility. We havelooked at the records of an accident-and-emergencydepartment, searching for fractures in patients over 18 butunder 50 that had not involved any of the "benefits" ofcivilisation and that could be said to be "wild" fractures. Theincidence was about 1 such fracture per 1000 man-years, a

figure similar to that observed in primates.It seems to be difficult to say what happens to wild primates

which break their bones. Fractures in juveniles are quitecommon in man and in wild primates but the incidence ofmajor adult long-bone fracture is more difficult to estimate.Major fractures are probably very rare and, in non-humanprimates, usually fatal.Orthopaedic surgeons have thought for many years that

long bones will heal naturally in the wild and that they shouldnot be overzealous in their treatment lest they prejudice anaturally successful healing process. The data on which thissupposition is based are open to alternative interpretation.

BX’e thank the following for letting us have their field experience: Dr JGoodall, Dr T. Struhsaker, Dr G Schaller, Dr K. Homewood, ProfR. Martin,Dr S Strum, Dr D Western, Dr S. Cobb, Dr P Hamilton, Dr C. Hillman, and

Dr J. Lewis. We also thank the Anthropology Museum, Cambridge, and Dr P.Schmidt, curator of the Anthropology Museum, Zurich University, for accessto museum specimens.

Correspondence to C. B.

REFERENCES

1. Pearl R. Evolution and mortality. Quart Rev Biol 1928, 3: 271.2 Duckworth WLH. Os fractures des orang-utangs. Studies from the anthropological

Laboratory Anatomy School, Cambridge, 1904: 51-53.3. Duckworth WLH. On the natural repair of fractures as seen in the skeletons of

anthropoid apes. J Anat Physiol 1912; 46: 81-85.4 Schultz AH The occurrence and frequency of pathological and teratological conditions

and of twinning among non-human primates. Primatologia 1956, 1: 965-1014.5 Schultz AH Notes on diseases and healed fractures in wild apes. Bull Hist Med 1939; 7:

571-82

6 Buikstra JE. Healed fractures in Macaca mulatta: Age sex and symmetry. Folia Primatol1975; 23: 140-48.

7. Mercer Rang. Childrens orthopedics. Philadelphia: JB Lippincott, 1974: S.8. Salter RB, Harris WR. Injuries involving the epiphyseal plate. J Bone Joint Surg 1956;

38A: 10779 Bramblett CA. Pathology in the Darajani baboon. Am J Phys Anthropol 1976; 26:

331-40

10. Randall FD The skeletal and dental development and variability of the gorilla. HumanBiol 1944; 16: 23-76

11. Schultz AH. Age changes and variability in gibbons. Am J Phys Anthropol 1944; 2:1-124.

12. Marsh C Ecology and social organisation of the Tana River colobus. Ph D thesis,University of Bristol. 1976

13 Struhsaker T. The red colobus monkey. Chicago. University of Chicago Press, 1975

Fallacies

VARICOSE VEINS ARE CAUSED BY DEFECTIVEVALVES IN THE VEINS

IT is perhaps unfair to ascribe the theories of varicose veinsto William Harvey. True, he did say: "But the valves aresolely made and instituted lest the blood should pass from thegreater into the lesser veins, and either rupture them or causethem to become varicose ...". He was explaining the divinedesign which prevented varices, not explaining the cause ofthem. He goes on to describe his experiences of dissection andhow it showed that veins were always equipped with valves sothat, even when a vein was locally bereft, there were otherconnecting veins so provided. He also relates the difficulty ofpassing a probe away from the heart and leaves us with afurther observation: "and although in some places the valves,by not acting with such perfect accuracy, or where there is buta single valve, do not seem totally to prevent the passage ofblood from the centre, still the greater number of them

plainly do so: and then where things appear contrived morenegligently, this is compensated either by the more frequentoccurrence of the succeeding valves or in some other

way ...". Harvey thus did not suggest that varicose veinswould occur from valve defects, but showed that the divinelycreated plan for the circulation which he was describing alsoserved to prevent varicose veins.The first notable study of valves in varices of which I am

aware is that of Sir Benjamin Brodie, who not only describedthe bone abscess and breast tumour bearing his name but alsoinvestigated the circulation. In May, 1807 he sent to Dr WmCharles Wells, who subsequently reported them, two cases of"rheumatic excrescence on the heart valves". No doubt it waswhile pursuing this line of thought that he was prompted tostudy the more peripheral circulation in the veins. The test hedescribed, which in attenuated form is now referred to asTrendelenburg’s test, showed that in severe varicose veinsthe valves were incompetent and allowed reverse flow. Thisappears to have been used as proof of the theory that varicoseveins are due to faulty valves ever since.

If, however, it is the valves that are at fault, why do somepeople have bad varicose veins without faulty valves. Why