S O U T H  A F R IC A N  J O U R N A L  O FSPORTS MEDICINE
SPORTGENEESKUNDE
JOURNAL OF THE S.A. SPORTS MEDICINE ASSOCIATION 

TYDSKRIF VAN DIE S.A. SPORTGENEESKUNDE-VERENIGING

V O L U M E 5 N U M B E R 2 M A Y  1990

Editor in C hief: D rC  Noble M B  BCh. 

FCS(SA)

Associate Editors: ProfTSnakes, M B  CliB, 

\1D

D> Dati’ii'iun Velden M B  ChB tSit’ll) M  Prax 

Medl Pretoria)

Advisory Board:

Medicine:

Dr I  Cohen M B  C hB , D . Obst. R C O G  

Orthopaedic traumaiologv:

O r P Fire) BS c (Eng). M B  BCh? Wits). M 

Med(Onho) 'Wits)

Bug E  Hugo M B  C hB , MMcd<Chir> 

Orihopaedics:

D r J C  Usdin M B  B C h, F R C S  (Edin) 

Cardiology:

Col D P  My burgh SM  M B  ChB FA CC 

Physical Educaiion:

Prof Hannes Botha D  Phil (Phys Ed) 

Gynaecology:

Dr Jack Adno M B  BCh (Wits), M D  (Med) , 

Dip O  (s’ G  (Wits)

S A S G V
S A S M A

CONTENTS

Editorial Comment
C ausation of injury ................................................... 3

Preventative Sports Medicine
A ltitude fails to increase susceptibility 
o f ultram arathon runners to post-race upper 
respiratory tract infections ...................................... 4

Rugby Injuries
R ugby injuries of the cervical spine and
spinal cord —  has the situation im proved? ........... 9

Sport Injuries
A survey of all sport injuries ..................................... 16

Sports Medicine
Physical exam ination of the ankle and the foot ...... 20

P U B L IS H E D  BY T H E  S O U T H  A F R IC A N  SPO RT S M E D IC IN E

A SS O C IA T IO N

H A T F IE L D  F O R U M  W EST

1067 A R C A D IA  ST R E E T

H A T F IE L D

P R E T O R IA . 0083

P ic tu re> courtesy o f P h o to file /Im a g e  B a n k

The journal of the SA S p o m  Medicine Association is published bv Medpharm Publicauons. 3rd Floor 

N’oodhulpliga Centre. 204B H F  Verwoerd Drive, Randburg2194 Tel (011; 787-4981/9 The views expressed 

in this pubhcauon are those o( ihe authors and not necessarilv those of the publishers

P r im e d  b v  T h e  N a t a l W itn ess P r im in g  hi id P u b lish in g  C o m p a n y  (P i v) Ltd

SPORTGENEESKUNDE VOL 5. NR 1

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E D IT O R IA L

CAUSATION OF INJURY

One of the major roles a sports medicine doctor plays is 

advising on prevention of injury. To understand how in­

jury can be prevented one must understand how injury is 

caused.

Except for the overuse injuries which to a large extent 

occur in endurance sports most injuries are due to over­

loading of a body part. This may be due to intrinsic fac­

tors e.g. contraction or stretching of a muscle beyond 

which that muscle cannot adapt.

The second factor is extrinsic which means that an ex­

ternal force is applied to a body part which cannot with­

stand it. Tearing of knee ligaments following a rugby 

tackle is a good example of this.

The overloading may be singular or repetitive, in the 

latter giving rise to chronic injuries such as tennis elbow.

Thus there are two basic factors in the causation of in­

jury

•  the force;

•  the adaptability of the body to resist the force.

Let us consider the second factor first.

A large number of variables are associated with ones abil­

ity to adapt to force.

Age

In youth the epiphyses are more liable to intrinsic over­

loading than any other part of the muscle-skeletal system. 

Severe disease of the heel (9-12 years), Osgood-Schlatter 

disease of the upper tibial tuberosity, (13-15 years) and 

apophyseal avulsion injuries of the pelvis (16-18 years) 

are common growth injuries.

From 18 years to 30 years the epiphyses are usually 

fused and muscle tears are more common. After 30 years 

of age injuries to tendons are more common as these be­

come progressively weaker with ageing.

Extrinsic forces are much more variable injuries occur­

ring to all tissues depending on the site of application. 

Muscles tend to protect other tissues. In adolescence 

muscles are relatively weak and protection of the spine 

may be inadequate resulting in spinal injuries.

In older athletes there is progressive deterioration of 

tissue with a loss of tissue elasticity. Over loading forces 

are more likely to result in injury to weakened tissue.

Ligamentous Laxity

This is somewhat controversial but it would appear that 

people with lax ligaments are more likely to injure liga­

ments resulting in dislocations. Palettar subluxation and 

dislocations are typical examples of this where minimal 

violence may cause injury.

Fitness

Good fitness implies that the sportsman has adapted to 

the stresses that the specific forces have placed on his 

body. Fitness is specific; a long distance runner will re­

quire muscle endurance and a weight-lifter muscle 

strength. To obtain fitness progressive loading is manda­

tory. Failure of adaptation occurs when the training pro­

gramme has been too rapid. If the forces are too great no 

amount of fitness will prevent injury.

Warm up

An adequate warm-up means that the tissues have not 

been put into the functional mode i.e. sudden overload­

ing is liable to cause injury. At least one degree increase in 

body temperature and a full range of joint movements are 

the m inim um  requirements.

Technique

Incorrect technique causes overloading and is a major 

source of injury.

Force

If the force exceeds the maximum loading a tissue can tol­

erate tearing will occur no matter how great the fitness of 

the athlete.

Thus in a sport like rugby a tackle of excessive force 

will cause injury. If the tackle is high or late, injury is 

more likely to occur. Excessive forces in rugby may occur 

in a number of situations. The scrum, especially the loose 

scrum, and the tackle are the two danger areas.

In conclusion before one can offer advice on prevention 

of injuries it is essential to understand all the factors 

which cause injury.

Dr. Clive Noble M BB Ch, FCS(SA)

Editor-in-chief

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SPORTSGENEESKUNDE VOL. 5 NR. 2

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P R E V E N T A T IV E  S P O R T S  M E D IC IN E

ALTITUDE FAILS TO INCREASE 
SUSCEPTIBILITY OF ULTRAMARATHON 

RUNNERS TO POST-RACE UPPER 
RESPIRATORY TRACT INFECTIONS

Distance runners are more pre-disposed to URT 
infections than non-runners

E M  P eters

INTRODUCTION

Reduced host resistance to infection fol­

lowing participation in an ultramara­

thon event, has been attributed to dam­

age to the local mucosal membranes of 

the upper respiratory tract (URT). 

Physical properties of the mucous mem­

branes have been reported to change 

and to result in impaired lymphocyte, 

neutrophil and macrophage function 

(Solomon and Armkraut, 1981).

It was hypothesized that the amount 

of damage to the mucous membranes 

should be greater at altitude due to:

•  the reduced relative humidity and 

greater “dryness” of the air inhaled 

by runners; and

•  the increased pulmonary ventilation 

at a given running speed.

This study compared the percentage 

incidence of U RT infections following a 

56 km ultramarathon run in Pretoria

Edith M  Peters
M Sc(M ed) in Sport Science, U C T
Division o f Physical Education 
West Campus
University o f the Witwatersrand
P O  Wits
2050

(reported relative humidity: 52%; alti­

tude ±160m) to the incidence obtained 

amongst runners who had completed a 

56 km at sea level (reported relative 

humidity: 79%) in Cape Town (Peters 

and Bateman, 1983).

METHOD

The officially recorded maximum and 

m inim um  temperature and relative hu­

midity readings in Cape Town on 10 

April 1982 were obtained from the 

weather bureau in Pretoria.

Questionnaires were completed by 

±130 entrants for the Milo Korkie 

Ultramarathon, a 56 km race from 

Pretoria (±1600 m above sea level) to 

Johannesburg (1800 m above sea level) 

during the seven days prior to the race. 

Information requested included run­

ning history, state of health and training 

record prior to participation in the race. 

Each athlete nominated a control of 

similar age and with whom they resided 

or were in frequent contact before the 

race.

Two weeks after the race, 116 runners 

were questioned with regard to U RT  

symptoms experienced during the post­

race period and their running perform­

ance in the 56 km race. The incidence of 

symptoms among the control group 

during this period was also recorded.

Data with regard to environmental 

conditions on the day of the race were 

obtained from the Weather Bureau in

Pretoria (Table 1).

Statistical analysis of the results in­

cluded the use of chi-square analysis 

and calculation of co-efficients of corre­

lation.

RESULTS

O f the 117 subjects who were ques­

tioned, 106 (90,6%) were male and 11 

(9,5%) were female. Five (4,3%) of the 

subjects were less than 25 years old; 84 

(72,4%) were aged between 25 and 40 

years and 28 (23,9%) were over the age 

of 40.

Thirty-one (28,7%) of the 108 sub­

jects who completed the race reported 

non-allergy derived U RT  symptoms 

during the two weeks following the race 

as compared to 14 (12,9%) among the 

control group. This is a significantly 

higher percentage incidence (x2=22,8; 

p<0,005). Only seven (23%) of the 

symptomatic runners were matched 

with symptomatic controls. Seven of 

the runners remained symptom-free de­

spite being in contact with a symptoma­

tic control.

The greatest majority (57%) of the to­

tal sample of runners who completed 

the race (n=108) had completed less 

than 85 km.wk-1 in training. Thirty-five 

percent of this subsample who had com­

pleted less than 85 k m .w k 1 became 

symptomatic. Only eight percent of the 

symptomatic group (n=108) had 

completed more than 120 km .wk'1 in

4 ---------------------------------------------------------------------------------------------------
SPORTS M E D IC IN E  VOL. 5 NO. 2

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P R E V E N T A T IV E  S P O R T S  M E D IC IN E

Table 1: Environmental Conditions at the time of 56 km races in Cape Town 
(sea level) and Pretoria (moderate altitude)

Venues of Relative Maximum Minimum Mean

56 km races Humidity Temp. Temp. Temp.

Pretoria 52% 25°C 14,8°C 20°C

Cape Town 87% 24°C 14,0°C 16°C

Table 2: Incidence of U R T  symptoms amongst runners and 
their matched controls (n =  108)

Asymptomatic Symptomatic
Control Control

Symptomatic Runners 24 7

Asymptomatic Runners 68 7

Table 3: Time taken to complete the race in symptomatic and asymptomatic 

groups

Time taken to 
complete race <4h30 4h30-5h00 5h00-5h30 5h30-6h00 >6h00

Symptomatic

subjects 7 10 6 6 2

Asymptomatic

subjects 15 18 22 18 2

Percentage

Symptomatic 31,8 35,6 21,4 25 50

n 22 28 28 24 4

Table 4: Nature and Duration of symptoms (n=46)

c ld a y 13 days 4- 7 days > 7  days Total

-R unning nose 2 5 2 6 15

- Sneezing - 3 - 4 7

- Sinusitis 2 1 - 1 4

Nasal 4 9 2 11 26

Sore throat - 9 2 3 14

Cough - 1 1 2 4

Fever — — 2 2

Total number
of symptoms 4 19 5 18 46

training.
Only 12 of the 108 who finished the 

race, did not compete at maximal effort, 

indicating dissatisfaction with the times 

in which they completed the race. O f 

the 31 runners who completed the race 

and developed U RT  symptoms there­

after, 29 (94%) indicated that they were 

satisfied with their performance in the 

event.

The greatest number of symptomatic 

runners (n=10) finished the race be­

tween 4h30 and 5 hours. However, of 

the total subsample which finished the 

race in less than 5 hours (n=50) 34 per­

cent (17) were symptomatic (Table 2). 

W ith increasing time taken to complete 

the race, the percentage symptomatic 

decreased to a 24 percent incidence 

amongst the group completing the 56 

km between 5h30 and 6 hours. It in­

creased again in the sample taking more 

than 6 hours to complete the race 

(n=28).

The most prevalent symptoms after 

the race were nasal (57%) followed by 

sore throats (30%). Thirty-nine percent 

of the symptoms lasted for more than 

seven days and only two reported fever 

accompanying the U RT  symptoms. 

Four (9%) of the symptoms reported 

were trivial lasting less than one day. 

Eleven (33,3%) of the symptomatic sub­

jects treated their symptoms with vari­

ous cold cures and/or anti-pyretics, 

whereas one subject reported taking 

anti-biotics.

In an attempt to include only patients 

who presented with symptoms of an in­

fective origin, persons with a recent his­

tory of allergic rhinitis (n=5) were ex­

cluded. As sinusitis is usually infective 

in origin, this was included in the nasal 

symptoms category and was not isolated 

as a separate category. Lower respira­

tory tract conditions (e.g. bronchial, 

tracheal) were not included in this sur­

vey.

DISCUSSION

This epidemiological study confirms 

previous findings of a significantly 

higher incidence of U RT  infections 

amongst runners than their matched 

controls following participation in an

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P R E V E N T A T IV E  S P O R T S  M E D IC IN E

ultradistance marathon event (Peters 

and Bateman, 1983; Douglas and Han­

son, 1978). The higher incidence of 

U R T  symptoms amongst runners fol­

lowing participation in ultradistance 

running events has been attributed to:

•  the impairment of host resistance to 

infection resulting from the pro­

longed stress; and/or

•  local damage to the mucosal surfaces 

resulting from their drying and cool­

ing during mouthbreathing (Peters 

and Bateman, 1983).

In this study, the exposure to moder­

ate altitude with the concomitant in­

crease in pulmonary ventilation, higher 

■ mean temperature and greater dryness 

of the air (Table 1) did not result in an 

increased incidence of U R T  infections 

among a sample of runners who com­

pleted a 56 km race when compared to 

the incidence among a similar sample 

who ran a race of the same length at sea 

level. These results thus appear to indi­

cate greater contribution of impaired 

systemic immune mechanisms than re­

duced local mucosal function to the re­

duced resistance to infection experi­

enced by the athletes.

It is well documented that the physio­

logical and biomechanical stress of exer­

cise results in elevated blood catechola­

mine and corticosteroid levels, which, 

in turn, influence immuno-competence. 

Adrenaline concentrations in the blood 

have been reported to rise as much as 8 

times during prolonged exercise (Galbo 

el al, 1977) thereby possessing substan­
tial potential to modulate immune func­

tion. Elevated adrenaline levels are 

known to reduce the number and func­

tion of circulating lymphocytes, result­

ing in both lymphocytosis and neutro­

philia (Gary el al, 1983). Suppression of 
immune function has also been reported 

following elevation of blood cortisol 

levels (Solomon and Armkraut, 1981) 

and manifests with:

n = 1 41

N u m b e r of 
s u b je c ts

n = 1 41

n = 1 08
S y m p t o m a t ic  a l 
a lt it u d e  ( 1800m )

| S y m t o m a i t c  a t 
s e a  le v e l

R u n n e rs  C o n tro ls  (non ru n n e rs )
F ig u r e  1. A  c o m p a ris o n  of the  in c id e n c e  of U R T  s y m p to m s  a m o n g s t ru n n e rs  a nd  c o n tro ls  
at m o d e ra te  a ltitu d e f 1 8 0 0 m ) a nd  sea level.

n =60

45

40

35
05 

O 
CD

S ' 30
O)
"o
S 25 n  
E3
2  20

10

n=37

a s y m p to m a tic

s ym p to m a tic

<85

n=9

1 1 1  f l
p < 0 . 0 0 5

86-120 >120

F ig u re
T rain ing  D ista n c e  (k m .w k '1)

2: U R T  s ym p to m s  and tra in in g  d is ta n c e  p rio r to c o m p e tin g

•  selective depletion of T lymphocytes 

and reduced T cell cytotoxicity (Mc­

Carthy and Dale, 1988);

•  macrophage receptor is the blockage 

andchemotaxis (Lewicki et al, 1987);

•  reduced distribution and activity of 

natural killer (NK) cells. (MacKin­

non, 1989).

Eskola ei al (1976) have reported re­
duced lymphocytosis at the end of 

marathon races while Edwards et al

(1984) reported significant changes in 

the B cell/T cell lymphocyte ratio. Re­

cently, research workers have been able 

to discriminate changes in the subsets of 

T lymphocyte compartment showing a 

reduction in the helper to suppressor 

ratio following exercise (Berk et al,
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SPORTS M E D IC IN E  VOL. 5 NO. 2

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PR E V E N T A T IV E  s p o r t s  m e d i c i n e

N a tu re  o f s y m p to m s  

| [ N a s a l 

j 2  S o re  th ro a t 

| H  C o u g h  

N d  F e v e r

D u ra tio n  o f s y m p to m s

F ig u r e  3: N a tu re  a n d  d u r a tio n  o f S y m p to m s

C O L D  A IR D R Y  A IR

H Y P E R V E N T IL A T IO N  

M O U T H  B R E A T H IN G

D rying  nf m n c n s a l s e c re tio n s

• |  e ffe c tiv e n e s s  o f m u c o c ilia r y  c le a r a n c e  m e c h a n is m
in n o s e  a n d  b ro n c h ii

• |  q u a lity  + e f fe c tiv e n e s s  o f s e c re te d  

a n ti- b o d ie s  (Ig A 's )

e n z y m e s ( ly s o z y m e s ,la c to fe r in , p e ro x id a s e  

-  in tr a - b r o n c h ia l m a c r o p h a g e s

F ig u re  4 ' L o c a l d a m a g e  re s u ltin g  in im p a ir m e n t o f im m u n e  fu n c tio n .

1985). Further, neutrophilia (Petrova et 
a l, 1983) eosinophilia and eosinpenia 
(Keast et al, 1988) have been recorded 
following exercise.

A recent study by Lewicki et al (1987) 
suggests that non-specific immunity 

may be the greatest contributor to in­

creased susceptibility of suppression of 

resistance to infection. This is sup­

ported by the studies of Tomasi el al
(1982) tested eight nationally ranked 

Nordic skiers before and after comple­

tion of a 50 km race. When compared to 

a control group, lower levels of salivary

IgA were found in the skiers before the 

race and antibody levels dropped even 

lower during the race. Petrova el al
(1983) produced evidence of reduction 

of both serum and secretory immuno- 

globin which was related to increasing 

intensity of exercise workload.

Smith et al (1988) have described that 
with greater oxygen turn-over during 

exercise, greater production of oxygen 

derived free radicals can play a substan­

tial role in depressing immune function.

It is therefore possible that the athlete 

who is deficient in the anti-oxidant vita­

mins (C, E and A) may have a greater 

susceptibility to infection than the run­

ner who possesses more positive vita­

min status. This is a factor which we are 

at present investigating and which may 

well have increased the results of this 

and previous epidermiological surveys.

This study showed that the less 

trained runners, i.e. runners who have 

completed less than 84 km .w k'1, had the 

highest incidence of infection. It is poss­

ible that the combination of little train­

ing with less oxygen radicals available to 

activate the neutrophils (less respiratory 

burst) and the greater degree of acute 

stress experienced by the unadapted or­

ganism with greater impairment of host 

resistance to infection, may have con­

tributed to this result. It was not poss­

ible to address the “overtraining” 

phenomenon as so few of our sample 

had been completing more than 160 

km.wk'1 in training and no record was 

kept of the intensity of the training.

As found in our previous study, there 

was a high incidence of infection 

(± 32%) 'amongst the faster athletes. 

Those athletes who completed the race 

in less than 5 hours had encountered a 

greater stress situation than the slower 

athletes. On the other end of the spec­

trum, the athletes who were on the road 

for more than 6 hours, also showed a 

greater incidence of infection. It ap­

pears that prolonging the stress situ­

ation may also result in greater impair­

ment of host resistance to infection.

Three factors thus point to decreased 

general host resistance to infection and 

not local mucosal being the primary 

cause of the increased incidence among 

ultra-distance runners. Firstly, despite 

the environmental conditions being 

more conductive to local mucosal dam-

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SPORTSGENEESKUNDE VOL. 5 NR. 2

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P R E V E N T A T IV E  S P O R T S  M E D IC IN E

age than in our previous study, this was 

not reflected by a greater incidence of 

infection. Secondly, the greater stress 

experienced by the less trained athletes 

correlated with a higher incidence of in­

fection and thirdly, the fact that in both 

studies, it has been in the faster group of 

athletes who also experienced greater 

impairment of their immune response at 

systemic level, that the greater incidence 

of infections was recorded.

It is however, incumbent upon re­

searchers to continue with biochemical 

investigation into the exact mechanisms 

underlying this apparent reduced resist­

ance to infections following prolonged 

exercise.

A ckn ow ledgem en t: The fourth year 
Biokinetics students (1989) o f the D iv ­
ision o f Physical Education at the Uni­
versity o f the Witwatersrand, are 
thanked fo r their assistance in collecting 
the data obtained fo r this publication.

R E F E R E N C E S

1. Berk LS, Tan SA, N iem an D C , Eby W C : 

The suppressive effect o f siress from acuie 

exhaustive exercise on T  lymphocyte helper/ 

suppressor cell ratio in athletes and non­

athletes. Abstract. Medicine and Science in 

Sports and Exercise, 17: 706(1985).

2. Crary B, Hauser SL , Borysenko M , K utz I, 

Hoban C: Epinephine-induced changes in 

the distribution of lymphocyte subsets in the 

peripheral blood o f hum ans. Journal of Im ­

munology, 131: 1178-1181,(1983).

3. Douglas D J and Hanson PJ: Upper respira­

tory infections in the conditioned athlete. 

Medicines and Science in Spons and Exer­

cise, 10: 55(1978).

4. Edwards A J, Bacon R H , Elms C A , Veradi 

R , Felder M : Changes in the populations of 

lymphoid cells in humarr peripheral blood 

following physical exercise. Clinical and Ex­

perimental Immunology, 58: 420-427 
(1984).

5. Eskola J, Ruuskanen 0 ,  Soppi E, Viljanen 

M K , Jarvinen M : Effect of sport stress on 

lymphocyte transformation and anti-body 

formation. Clinical and Experimental Im­

munology, 3: 339-345 (1978).

6. Galbo H , Christensen N J, Horbst JJ: 

Glucose-induced decrease in glycogon and 

epinephrine responses to exercise in man. 

Journal of Applied Physiology, 42: 525-530 
(1977).

7. Keast D , Cameron K . and Morton A R: 

Exercise and the im m une response. Sports 
Medicine, 5: 248-267(1988).

8. Lewicki R , Tchorzewski H , Denys A , 

Golinska A: Effects of physical exercise on 

some parameters o f im m unity in con­

ditioned sportsmen. International Journal 

of Sports Medicine, 8: 309-314 (1987).

9. M acK innon LT: Exercise and natural killer 

cells. W hat is the relationship? Sports 
Medicine, 7:141-149(1989).

10. M cCarthy D A  and Dale M M : The Leuco- 

cytosis of exercise. A review and model. 

Sports Medicine, 6: 333-363 (1988).

11. Nicholl PJ, W illiam s BT: Medical problems 

before and after a popular marathon. British 

Medical Journal, 285, (1982).

12. Peters E M , Bateman ED : Ultramarathon 

running and upper respiratory tract infec­

tions, 5/4 Medical Journal, 64: 1 582-584, 
(October 1983).

13. Solomon G F , Armkraut AA: Psycho- 

neuro-endocrinological effects in im m une 

response, Annual Review Microbiology, 35: 
178-179,(1981).

14. Smith JA , Telford R D , Hahn A G , Mason 

IB , Weideman M J: Training, Oxygen radi­

cals and the im m une response, Excel, 4: 3-6, 
(1988).

15. Tomasi T B, Trudeau FB, Czerwinski D , 

Erredge S: Im m une parameters in athletes 

before and after strenuous exercise. Journal 

of Clinical Immunology, 2: 173-178 (1982).

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r u g b y  i n j u r i e s

RUGBY INJURIES OF THE CERVICAL SPINE AND SPINAL CORD- 
HAS THE SITUATION IMPROVED?

AT S ch er

ABSTRACT

Paralysis due to injury of the cervical spinal cord in rugby players, is a subject of great concern. Since the 
publication of previous reports on these injuries, considerable attention has been paid to amending the 
rules governing rugby and improving the standard of refereeing. In an attempt to assess whether these 
measures have reduced the incidence of injury or altered the type of injury sustained, an analysis of 
injured rugby players admitted to the Spinal Cord Injury Centre at Conradie Hospital during the period 

1981 to 1987 has been made. Results of this study indicate that there has been no decrease in the 
incidence of these serious injuries. The scrum and tackle remain the most important cause of injury. 
Flexion violence applied to the head and neck is still the major injuring force. Foul play, in particular the 
high tackle remains an important and avoidable cause of injury. A new finding is the identification of a 
group of rugby players who have sustained temporary paralysis without evidence of orthopaedic injury.

INTRODUCTION

In 2 previous papers1,2 I have reported 

on patients admitted to the Spinal Cord 

Injury Centre at Conradie Hospital in 

Cape Town who have sustained para­

lysis due to rugby injuries to the cervical 

spinal cord. These reports dealt with a 

total of 50 players admitted during the 

period 1964 to 1980. In a series of 

papers, I identified the important 

phases of the game responsible for the 

majority of injuries, specifically the 

tight scrum,1 the tackle,3 rucks and 

mauls.4

A T  Scher M B C h B D M R D
Department o f Radiology
Tygerberg Hospital and University o f
Stellenbosch
P O  B ox 63
T Y G E R B E R G
7505

----------------------------------------------------------------------------------------------------------------- 9
SPORTSGENEESKUNDE VOL. 5 NR. 2

Since the first paper,1 published in 

1976 there has been much discussion as 

regards reducing the incidence of these 

serious injuries and various changes to 

the rules have been introduced.

In an attempt to ascertain whether 

there has been a decrease in the inci­

dence of, or change in the mechanism 

of, these injuries following on changes 

in the rules, an analysis of rugby players 

admitted to the Spinal Cord Injury 

Centre with injuries of the cervical spi­

nal cord during the 7 year period 1981 

to 1987 has been made.

Method and materials

The case histories and radiographs of all 

patients admitted during the period 

1981 to 1987 with spinal cord injury due 

to rugby, have been analyzed. Specific 

attention has been paid to the circum­

stances of injury, orthopaedic injuries as 

reflected on X-ray and the neurological 

deficit present on clinical examination. 

The cases were subdivided into groups 

according to the phase of the game dur­

ing which the injuries were sustained. 

These cases were further subdivided 

into groups using the admission 

radiographs of the cervical spine as indi­

cators of the mechanism of injury.

Results

A total of 38 players with cervical spinal 

cord injury either permanent or tem­

porary, have been identified.

Age of patients

The age distribution is shown in Table 

I. Nine (24%) of the players were 17 

years of age or under at the time of in­

jury.

Orthopaedic levels of injury

Table 2 shows the distribution of the 

levels of injury. Noteable is the high 

percentage (32%) of players who sustain 

injury at the C4/C5 level. Two players 

injured at the C2 level and 10 players

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R U G B Y  IN J U R IE S

Table 1: Age distribution

Age No. of 
players

Age No. of 
players

14 1 15 1
16 3 17 4
18 — 19 3
20 — 21 1
22 4 23 5
24 3 25 2
26 1 27 2
28 1 29 1
30 1 31 3
32 — 33 -
34 — 35 —
36 r ~ 37 —
38 — 39 1
40 — 41
42 IP

Total: 38

Table 2: Orthopaedic levels of injury

Level Number Level Number

C2 2 C2/3 _
C3 C3/4 1
C4 1 C4/5 12
C5 2 C5/6 5
C6 3 C6/7 2
C7 - C7/T1 -

No. Orthopaedic injury: 10

Table 3: Phases of the game in which 
injury occurred

No. %

Scrums 15 39%
Tackles: (A) Tackier

3 i 42%
(B) Tackled 13 j

Rucks/mauls 4 10%
Collision 1 2,6%
Unknown 2 5%

Table 4: Degree of paralysis due to 
injury in different phases of the game

Incomplete Complete

Scrum 9 6

Tackle 12 4
Ruck 3 1
Other 1 1

Collision - 1

showed no evidence of orthopaedic in­

jury on X-ray examination. This is in 

contrast to the large series reported by 

Silver5 in which no high cervical spinal 

injuries were found nor any case re­

ported without evidence of injury on 

X-ray.

Phases of the game in which injury 
occurred (Table 3)

The majority of injuries were sustained 

either in the scrum (39%) or during 

tackles (42%). This is in keeping with 

the findings in previous analysis.1,2

Degree of paralysis due to injury in 
different phases of the game (Table 4)

It can be seen in Table 4 that the major­

ity of players (61%) sustained incom­

plete paralysis. 39% of players were 

completely paralysed. Notable is the 

high incidence of scrum injuries 

amongst this group.

Type of orthopaedic injuries sustained 
in different phases of the game (Table
5)
Reference to the table shows that there 

is a wide spectrum of orthopaedic inju­

ries. Notable is the high number of 

flexion-dislocations sustained conse­

quent upon collapse of the scrum.

Mechanism of injury as reflected on 
admission radiograph (Table 6)

Reference to the table shows that flexion 

was the most frequent important injury 

force. Twenty-five players (66%) sus­

tained their injuries as a result of pure 

flexion violence or a combination of 

flexion and rotation.

DISCUSSION

Comments on players injured in 
scrums

Fifteen (39%) players were injured in

scrums. This figure correlates well with 

the 40% incidence of scrum injuries 

noted in my previous analyses1,2 and 

also with international experience. 

Burry and Gowland6 reporting on a 

series of New Zealand rugby players 

with cervical spinal cord injuries, noted 

a 35% incidence of scrum injuries. W il­

liams and Mackibben7 in a similar analy­

sis in Wales reported a 44% incidence.

Thirteen of the 15 players were in­

jured as a result of collapse of the 

scrum. One player was injured by crash­

ing of the two packs of forwards with 

the injured player being caught un­

aware. Details of the position of all the 

players injured are not available, but the 

majority of scrum injuries involved 

players in the front row, either props or 

hookers. (Figure 1) As shown in pre­

vious studies,12 scrum injuries often re­

sult in severe neurological deficit. Six of 

the players sustained complete, perma­

nent quadriplegia. Analysis of the type 

of orthopaedic injury sustained in the 

scrum, Table 5, reveals that the majority 

of injuries were anterior dislocations, 

either bilateral or unilateral. This is in 

keeping with the findings in the pre­

vious study.1 The common mechanism 

of injury is flexion trauma as the major­

ity force with a rotational component in 

those cases with unilateral facet disloca­

tion. In cervical spinal cord injury due 

to causes other than rugby, the percent­

age of patients with bilateral locking of 

facets is much lower. In a series of 335 

unselected cervical spinal cord injuries, 

only 15,5% (52) cases of bilateral lock­

ing of facets were recorded.8 The mech­

anism of these injuries was for some 

time, controversial. Roaf,9 using 

cadaveric spines, was unable to produce 

dislocation unaccompanied by fracture 

by hyperflexion alone and found that 

some degree of rotation must also be 

present. This was not in keeping with 

clinical observations, in particular as re­

gards scrum injuries. Clear histories 

were obtainable from players in the 

front row who stated that as the scrum 

collapsed, their foreheads struck the 

ground and while the rest of the pack 

kept on pushing, their necks were pro­

gressively flexed and paralysis suddenly 

ensued. In 1978 Bauze and Ardran,10 in 

an experimental study showed that pure 

dislocation unaccompanied by fracture

1 0 ---------------------------------------------------------------------------------------------------
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R U G B Y  IN J U R IE S

Table 5: T ype of orthopaedic injury sustained in different phases of the game

B.L.F U.L.F. Subluxation
“Tear drop” 

Fracture
Compression

Fracture
Hangman’s
Fracture

No Orthopaedic 
Injury

Scrum 7 3 2 _ _ _ 5

Tackle _ 2 — 1 3 2 6

Ruck 1 2 1 — - — —

Other 2 - - 1 - - -

Table 6: Classification of cases in relation to mechanism of injury as reflected 
on radiological examination

Flexion Subluxation

Dislocation with bilateral locking

3

of facets 10

Wedge fracture 3

“Tear-drop” fracture 2

Flexion/rotation Unilateral locking of facets 7

Vertical compression “Burst” fracture -

Hyperextension Avulsion fracture of the vertebral body 

Fractures of the spinous processes and
-

laminae —

Posterior vertebral displacement -

Fracture dislocation

Haemorrhage into the retrotracheal soft
—

tissue

Hyperextension injury in the elderly

—

without radiographic evidence 1

Hangman’s fracture 2

No orthopaedic injury 10

could occur with flexion force. W ith the 

neck slightly flexed, and the vertex fixed 

on the ground, the normal cervical lor­

dosis is lost and the spine straightened. 

In this position, the force is transmitted 

down the long axis of the spine. When 

the force exceeds the energy-absorbing 

capacities of the involved structures, far 

less force is required to dislocate the 

vertebrae and dislocation can occur 

without fracture.

Comment on tackle injuries

Sixteen (42%) of players were injured 

during a tackle. Three players were in­

jured attempting to tackle an opponent, 

while the remaining 13 were tackled. 

Neurological deficit was less severe 

and only 4 players sustained complete 

paralysis. The spectrum of orthopaedic 

injury is shown in Table V and varies 

considerably from the orthopaedic inju­

ries due to scrumming. Noteable are the 

large group of players who showed no 

orthopaedic injury on X-ray and also 

the two players with high (C2) fractures. 

The wider variation of orthopaedic in­

jury and lesser degrees of neurological 

deficit in tackle injuries as compared to 

scrums is in keeping with the more var­

ied mechanism. Nevertheless, reference 

to Table VI shows that flexion injuries

predominate. In these cases the element 

of restraint of the vertex is often absent 

and the amount of damage to the spinal 

cord often less severe. One player was 

injured as a result of a double tackle. 

(Figure 2) Six players were injured as a 

result of high tackles around the neck. 

The mechanism of injury in double 

tackles11 and high tackles12 has been ana­

lyzed in previous studies.

The overall percentage of injuries 

sustained in tackles has increased, 

which is in keeping with the findings of 

Silver.5 O f particular note and cause for 

concern, is the finding that 6 players 

were injured by a high tackle. In Silver’s 

series,5 only one is recorded as having 

been injured due to a high tackle. Silver 

also reported 4 players injured as a re­

sult of double tackles.

Comment on injuries sustained in 
rucks and mauls

Only 4 (10%) of the players were injured 

in these phases of the game. One player 

reported that he was injured while try­

ing to break loose, 2 players jumped on 

him and while he was lying on the 

ground trampled and kicked him. The 

other players appear to have been in­

jured by players falling on top of them 

while they were lying on the ground.

There is a surprising discrepancy be­

tween the figures found in the survey of 

Silver5 and ours in this respect. He re­

cords a marked increase in the number 

of players injured in these phases of the 

game. A similar finding has been made 

in the 20 year survey of cervical spinal 

injuries in Wales.7 The reason for this 

marked decrease in the percentage of 

players injured in rucks and mauls is not 

clear.

12 ---------------------------------------------------------------------------------------------------
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R U G B Y  IN J U R IE S

Figure 1: Anterior dislocation at the 
C4/C5 level with unilateral facet disloca­

tion. This player was a 14 year old 

hooker who sustained complete quadri-

plegia and died some weeks after injury.

Players with spinal cord injury without 
radiological evidence of orthopaedic 

injury

Five of these players were injured in 

tackles and the rest in collapsing 

scrums. Although spinal cord injury 

without evidence of orthopaedic injury 

X-ray is found commonly in patients 

admitted to spinal cord injury units, 

these are generally elderly patients with 

spondylosis. The observation of this 

large group of young rugby players suf­

fering this type of injury is new and has 

not been recorded in other surveys. A 

recent paper has however reported on 

similar findings in rugby players and is 

the subject of another paper in prepar­

ation.

CONCLUSION

During the period 1964 to 1980, 50 

rugby players with cervical spinal cord 

injury were admitted to the Spinal Cord

Figure 2: Typical double tackle with one player attempting to grasp 

of the tackled player.

Figure 3: Frustrated opponents applying force to the neck while trying to 

gain possession of the ball.

_________________________________________________________________________________________________________________________________________-  13
SPORTSGENEESKUNDE VOL. 5 NR. 2

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R U G B Y  IN J U R IE S

Injury Centre at Conradie Hospital,2 an 

average of 3 players a year. During the 

period under review in the present 

paper (1981 to 1987) 38 players were ad­

mitted, an average of 5,4 players a year. 

This indicates that despite increased 

public awareness of serious rugby spinal 

injuries and considerable amendments 

to the rules, the incidence of rugby spi­

nal cord injuries in the Cape Province 

has not decreased. Silver and G ill14 

comment on the gratifying decrease of 

serious cervical spinal cord injuries in 

rugby players in the United Kingdom, 

Wales and New Zealand, but note that 

the only country where there has not 

been a decrease in the incidence is South 

Africa.

As commented on in previous 

papers, 1,2 and also in reports from over­

seas,7 flexion remains the most import­

ant mechanism of injury (Figure 3). The 

two phases of the game where most 

serious injuries occur are again ident­

ified to be the scrum and the tackle. In 

the scrum, flexion usually combined

with restraint of the vertex or combined 

with rotation produces most injuries. 

The mechanism of injuries in tackles is 

more varied, but flexion violence again 

predominates.

Foul play was responsible for a signi­

ficant number of injuries. Apart from 

the single instance, where a player was 

injured by crashing of the scrum, a dis­

turbing number of players were injured 

by the high tackle. Despite previous 

comment on the danger of this illegal 

play,12 no decrease in these avoidable in­

juries appears to have taken place.

R E F E R E N C E S

1. Scher AT. Rugby injuries to ihe cervical spi­

nal cord. 5  A frM edJ 1977; 51: 473-475.
2. Scher AT. Rugby injuries of the spine and 

spinal cord. Clin Sports Med 1987; 6(1): 87- 
99,12.

3. Scher AT. The high rugby tackle - an avoi­

dable cause o f cervical spinal injury? 5  Afr 

medj 1978;53;1015-1018.
4. Scher AT. Rugby injuries to the cervical 

spine sustained during rucks and mauls. 5  

A frM edJ 1983;64: 592-595.

5. Silver JR . Injuries of the spine sustained in 

rugby. B rM e d J 1984; 288: 37-43.

6. Burry H C , Gowland H . Cervical injury in 

football - a New Zealand survey. Br J  

Sports Med 1981; 15: 56-60.

7. W illiam s P and M c K ib b in  B. Unstable cervi­

cal spine injuries in rugby - a 20-year review. 

Injury 1987; 18(5): 319-332.

8. Braakman R , Penning L. Injuries of the cer­

vical spine. Excerpta Medica. Amsterdam 

1971.

9. Roaf R. A study o f the mechanics o f spinal 

injuries. J  Bone J l  Surg 1960; 42B (4): 810- 
823.

10. Bauze R J, Ardan G M . Experimental pro­

duction o f forward dislocation in the hum an 

cervical spine. J  B o nejt Surg 1978; 60B (2): 
239-245.

11. Scher AT. The “double tackle” - another 

cause of serious cervical spinal injury in 

rugby players. 5  Afr Med J  1983; 64: 595- 

596.

12. Scher AT. The high rugby tackle - a con­

tinuing menace. 5  Afr Sports Med 1981; 11:

3.

13. Torg JS, Pavlov H , Genuario SE et al. 

Neurapraxia o f the cervical spinal cord with 

transient quadriplegia. J  Bone J l  Surg 1986; 
68 A (9): 1354-1370.

14. Silver J R , G ill S. Injuries o f the spine sus­

tained during rugby. Sports Med 1988; 5: 

328-334.

AER LINC US FgLnAVS TS

14
SPORTS M E D IC IN E  VOL. 5 NO. 2

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S P O R T  IN J U R IE S

A SURVEY OF ALL SPORT INJURIES
EXAMINED AT THE BUREAU FOR STUDENT HEALTH 

OF THE UNIVERSITY OF THE ORANGE FREE 
STATE DURING THE PERIOD 

JANUARY 1985 -  DECEMBER 1985
EA M  Prinsloo

AIM

The incidence of sport injuries was ex­

amined. The type of injury sustained in 

various sport events was examined. 

Special attention was given to rugby and 

athletic injuries. The study was done to 

determine the need for sport medicine 

education in South Africa.

M E T H O D S

The clinical records of the doctors and 

orthopedic surgeons were used. All per­

sons included in the study were sports­

men of the University of the Orange 

Free State who sustained injuries during 

the period January 1985 - December 

1985.

Attention was given to the type of 

sport, type of injury, level of compe­

tition, recurrent injuries, referral to or­

thopedic surgeons, sex of sportsmen 

and special investigations done.

R E S U L T S

(Table 1)

There was a total of 438 injuries; 5% of 

consultations in 1985.

There were 145 referrals to ortho­

pedic surgeons.

Table 1: Injuries in various sporting
events

Sport Number %

Rugby 246 56,2
Athletics 60 13,7
Hockey 23 5,3
Marathon 19 4,3
Netball 14 3,2
Soccer 12 2,7
Squash 9 2,0
Gymnastics 8 1,8
J udo/Boxing/Karate 8 1,8
Cricket 7 1,6
Jogging 7 1,6
Swimming/Diving 5 1,1
Volleyball 4 0,9
Tennis 4 0,9
Water-skiing 3 0,7
Weightlifting 3 0,7
Cycling 1 0,2
Biathlon 1 0,2
Parachuting 1 0,2
Rowing 1 0,2
Tug at the rope 1 0,2
Fencing 1 0,2

Total 438 100%

D r E A M  Prinsloo

R U G B Y  IN JU R IE S

(Graph 1)

193 Injuries were sustained during hos­

tel league: 25 at Club level, 25 at Provin­

cial level, 1 Springbok player.

The high incidence at hostel level 

may be due to different factors. More 

players participate at this level. The 

players are usually not very fit. Players 

play in unusual positions. The motive 

to win is very high in hostel league.

a>
■O® 3 M _

5 8 8 gf l  w  o  ^  c  ™

Graph 1: Rugby injuries

60

Graph 2:
(Rugby)

Injuries per month

1 6 ---------------------------------------------------------------------------------------------------
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S P O R T  IN J U R IE S

Causes of injuries

Graph 2 indicates the number of inju­

ries per month. 24% (58/246) were re­

current injuries. Rugby players tend to 

play with injuries.

The doctor should put the health of 

his patient first and stand up to coaches 

who want to force injured players to 

play.

The player, team doctor and coach 

should work together as a team. They 

should have confidence in the doctor 

and he has to show enough interest and 

knowledge of the game.

Knee injuries

(Graph 3)

24% (59/246) were knee injuries.

posterior cruciate 
ligament

medial kapsular 
ligament

tear posterior 
oblique ligament 
partial tear

medial collateral 
ligamenl

Examination 
See Figures 1-7.

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Posterior view right knee

Figure 1:1+ Medial instability 

Knee in full extension

Posterior view right knee

Figure 2:3+ Medial instability 

Knee in full extension 

Tear anterior and posterior

Graph 3: Knee injuries

Medial view right knee

Figure 3:1 + Medial instability 

Knee 30 flexion

tear medial 
kapsular ligament

tear anterior 
cruciate 
ligament

tear posterior 
oblique ligament

tear medial 
collateral 
ligament

Medial view right knee

Figure 4:3+ Medial instability 

Knee 30 flexion

tear medial
collateral
ligament

tear medial
kapsular
ligament

tear anterior 
cruciate ligament 
(not shown)

tear posterior 
oblique ligament

SPORTSGENEESKUNDE VOL. 5 NR. 2

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S P O R T  IN J U R IE S

Referrals
42 knee injuries were referred to ortho­

pedic surgeons. 27 patients were oper­

ated upon.

10 medial menisectomy

5 lateral menisectomy

7 anterior cruciate reconstruction 

1 lateral collateral tear

1 iliotibial band

2 arthroscopy for loose fragment - 

knee

Post-operative physiotherapy plays an 

important part in treatment.

Ankle injuries

39 ankle injuries 

32 lateral ligament injuries 

9 medial ligament injuries 

2 lateral malleolar fractures

Treatment
Most grade II + injuries are put in plas­

ter of pans. Physiotherapeutic rehabili­

tation after removal of plaster of paris.

Gravity sign

Figure 7: Posterior cruciate ligament 
tear (Posterior instability)

popliteustendon

iliotibial band

arcuate ligament

partial tear 
lateral collateral 
ligament

tom lateral
capsular
structure

Posterior view right knee

Figure 5: Lateral instability with knee in 
full extension (2+)

Figure 6
Lateral view right knee
(1 + instability knee 30 flexion)

Lateral view right knee
(3 + instability)

18
SPORTS M E D IC IN E  VOL. 5 NO. 2

tear arcuate 
ligament

tear popliteal 
ligament

tear lateral 
collateral ligament

tear lateral 
capsular ligament

popliteustendon

tearpopliteus
tendon

tear lateral 
collateral ligament

tear arcuate 
ligament

tear lateral 
capsule

tear iliotibial 
band

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S P O R T  IN J U R IE S

Table 2: Marathon injuries

Injury N um ber %

Stress fracture 6 31,6

Iliotibial band 5 26,3

Achillestendonitis 4 21,0

“Shins” 2 10,5

Sports anemia 1 5,3

Chondromalasia 1 5,3

Total 19 100%

Table 3: Type of athletic injury

Injury No. %

Hamstring 14 23,3

Knee 11 18,3

chondromalasie (5)
bursa (3)
osteochondritis dissecans (1)
anterior cruciate ligament (1)
tibiofibular ligament (1)

“Shins” 6 10,0

Iliotibial band 4 6,7

Adductor Hip 4 6,7

Ankle 4 6,'/
ligament (3)
osteofyte (U

Back 3 5,0

Foot 3 5,0

Stress fracture 3 5,0

Quadriceps 2 3,3

Calf 2 3,3

Hand/elbow 2 3,3

Achillestendonitis 1 1,7
Compartment syndrome 1 1,7

Total 60 100%

Table4: Injuries in various items

Item Number %

Middle/Longdistance 22 36,7

Longjump 12 20,0

Sprints 12 20,0

Javelin 6 10,0

High jump 4 6,7

Steeplechase 2 3,3

Hurdles 1 1,7

Shotput 1 1,7

Table 5: Injuries in track events

Item Injury Number

Sprints Hamstring 6
Quadriceps 2
Knee/bursa 2

Back 1

“Shins” 1

Middle/Long Hamstring 4

distance Iliotibial band 4

Knee 4

“Shins” 3
Stress fracture 2

Calf 1

Back 1
Compartment
sindrome

1

Ankle ligament 1

Gout 1

Steeplechase Chondromalasia 1

Adductor hip 1

Shoulder injury

Total of 33 injuries:

15 acromioclavicular ligament tears

5 sternoclavicular injuries

6 rotator cuff injuries 

5 anterior dislocations

2 capsular injuries

Neck injuries

Only 9 injuries:

8 soft tissue 

1 cervical disk

ATHLETIC INJURIES

Analysis
60 athletic injuries

19 marathon injuries (SeeTable 2)

Anatomical analysis See Table 3.
Type o f injury in various items 
See Table 4, 5 and 6.

Stress fractures Tibiotalor pinching.

CONCLUSION

There is much room for research into 

sport injuries and there is a need for 

post-graduate education in sport 

medicine in South Africa.

There should be better co-operation 

between sportman, coach and team 

physician.

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S P O R T S  M E D IC IN E

PHYSICAL EXAMINATION OF THE 
ANKLE AND FOOT

R F  S p en cer

INTRODUCTION

Adequate physical examination of any 

part of the musculoskeletal system 

should be preceded, whenever possible, 

by comprehensive history and general 

examination. One must bear in mind 

that pain is often caused by compensa­

tory stresses in response to malaligne- 

ment.1 It is therefore essential, when as­

sessing an ankle or foot problem, to 

exclude the possibility of pathology in 

the spine, hip or knee.

Routine physical examination should 

follow traditional guidelines. These can 

be summarised under the following 

headings:

•  Look

•  Feel

•  Move

•  Test stability

The process of looking should com­

mence as early as possible and should 

embrace all aspects of the athlete’s gen­

eral demeanour and gait. It should then 

focus on the limb in question and assess 

discrepancies of contour, difference in 

girth when comparing left and right, 

and the posture when standing observed 

from both front and back. At this stage 

it may be appropriate to ask the patient

R F  Spencer F R C S , F C S  (SA ) Orth
Senior Lecturer in Orthopaedic Surgery 
U niversity o f N a ta l M  edical School 
P O  B ox 17039 
Congella4013 
N atal, South Africa.

to stand on tiptoe to assess possible 

problems in the tendo-Achilles mech­

anism.

One should then proceed to look at 

the particular area in question, paying 

attention to previous scars, sinuses and 

areas of erythema or bruising. Palpation 

can then be carried out for differences in 

skin temperature, areas of tenderness, 

and prominent bony landmarks. D ur­

ing the palpation process the foot may 

be gently moved both passively and ac­

tively to assess crepitus within the ten­

don sheaths and joints. Particular atten­

tion should then be paid to localized 

areas of tenderness. Movements should 

be assessed both actively and passively. 

Active movements should be assessed 

first in order to delineate the range of 

relatively painfree movement. Passive 

movements may then be carried out to 

assess the range more fully. Once again, 

crepitus both in the joints and tendon 

sheaths should be noted. Finally, stabil­

ity may be tested. It is important when 

assessing the medial and lateral ligamen­

tous structures of the ankle to hold the 

heel and not the forefoot when doing 

this. Varus and valgus stresses can be 

applied to assess any possible instability. 

At this stage special investigation appro­

priate to the diagnosis may be required.

TENDO ACHILLES PATHOLOGY

The patient with an Achilles tendon 

problem may have difficulty standing 

on tiptoe and contracting the calf mus­

cles. More than one pathology may be 

present in this region2. The mesotenon 

may be diffusely inflamed and tender

and give rise to clearly visible swelling 

in the region when viewed from behind 

and compared with the other side. This 

condition is referred to as Achilles peri- 

tendonitis.

At the same time, or in isolation, 

either of the bursae in the region may be 

inflamed. There is a bursa deep to the 

Achilles tendon and one superficial to 

it. The latter may become inflamed as a 

result of wearing tight running shoes. 

Focal areas of mucoid degeneration or 

partial rupture of the tendo-Achilles 

may be assessed by palpation. Where a 

complete rupture has occurred the 

patient will commonly complain of a 

sudden pain in the region not unlike the 

feeling of having been kicked in the 

back of the heel. The most useful test 

for assessing this situation is the 

Thompson’s (or Simmonds’) test. This 

is best performed with the patient prone 

with the feet overhanging the end of the 

examination couch. It may immediately 

become obvious that there is a gap in 

the tendinous mechanism. The foot on 

the affected side does not naturally 

assume a slight equinus position. The 

diagnosis is confirmed by squeezing the 

calf muscles on both sides. On the af­

fected side the foot will not move into a 

position of plantar flexion, whereas it 

will do so on the unaffected side. It is 

pertinent to note that the patient may be 

able to actively plantar flex the foot in 

the presence of a complete rupture of 

the tendon.

Other tendons in the region of the 

ankle joint may become affected by in­

flammatory processes and tenosynovi­

tis. Similarly, the peroneal tendons may 

be subject to subluxation and disloca­

tion.

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S P O R T S  M E D IC IN E

SEVER S DISEASE

This condition frequently affects young 

and adolescent athletic individuals, and 

gives rise to pain and local tenderness in 

the region of the insertion of the tendo- 

Achilles into the calcaneus. The con­

dition may be a traction apophysitis of 

the tendon insertion. The radiological 

features include flattening and sclerosis 

of the posterior calcaneal apophysis.

NERVE ENTRAPMENT 
SYNDROMES

Two nerve entrapment syndromes may 

become troublesome to the athlete. The 

superficial peroneal nerve emerges from 

the deep fascia on the anterolateral 

aspect of the leg. It may become 

constricted when it passes through the 

fascia giving rise to pain on the dorso­

lateral aspect of the foot and over it’s 

site of emergence. Similarly, the poste­

rior tibial nerve may be constricted 

within the flexor retinaculum on the 

posteromedial aspect of the ankle. This 

gives rise to pain and paraesthesiae on 

the plantar and medial aspects of the 

foot. Palpation may reveal tenderness 

and sometimes a positive Tinel sign 

over the area of constriction.

The diagnosis may be confirmed by 

inflating a blood pressure cuff over the 

calf to a pressure between the systolic 

and diastolic levels for a minute or so, 

thus providing the onset of typical 

symptoms.

FRACTURES AND SPRAINS OF 
THE ANKLE

The typical fractures and fracture dislo­

cations around the ankle joint are exten­

sively covered in standard text books. 

The clinical findings are usually quite 

characteristic with extensive ecchy- 

moses, crepitus and severe bony tender­

ness in the region. Attention must be 

paid to the neurovascular status of the 

foot.

Sprains may involve either the medial 

or lateral structures at the ankle joint. 

The internal or medial type of strain is

less common and involves the super­

ficial part of the deltoid ligament. This 

is most easily assessed by examining the 

patient from behind and comparing the 

two sides, a clear swelling being visible 

over and inferior to the medial malleo­

lus on the affected side. On the lateral 

side, the ligament is divided into three 

parts; the anterior and posterior talo­

fibular and the calcaneofibular liga­

ments. Frequently, only the anterior 

talo-fibular ligament is damaged giving 

rise to the common “sprained ankle”. In 

this condition swelling over and antero­

lateral to the lateral mallolus is visible 

and pain is elicited by inverting the foot.

However in more severe injuries all 

three bands may be ruptured giving rise 

to possible instability. An injury of this 

kind is thought by many to be an indi­

cation for surgical treatment. The diag­

nosis is best made by taking stress views 

in both the AP and lateral projections.

The AP stress view is obtained by ap­

plying a varus strain to the heel while 

taking the film. Instability is demon­

strated by an opening of the lateral as­

pect of the ankle mortice. (Figure 1).

lateral medial

Figure 1: Diagram of AP varus stress Xray showing lateral instability and 
talar tilt.

Figure 2: Diagram of lateral “anterior drawer”. Xray showing anterior 
subluxation of the talus.

anterior posterior

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S P O R T S  M E D IC IN E

The lateral view, or so called anterior 

drawer test, is best obtained by placing 

the patient’s heel on a sandbag and 

pushing downwards on the tibia. If in­

stability exists, the tallus can be seen to 

subluxate forward in the ankle mortise. 

(Figure 2). Some Surgeons believe that 

the AP views should be augmented us­

ing an arthrogram, which will show dye 

leaking extensively into the lateral soft 

tissues.

It should be remembered that follow­

ing rupture of the lateral ligamentous 

structures, whether these have been 

managed by operative or non-operative 

means, the normal proprioceptive 

structures within the ligament have 

been damaged. Therefore, although no 

residual instability may be demon­

strable clinically, the patient may com­

plain of a feeling of instability on the 

lateral side. This condition is referred to 

as “stable instability”.

OTHER CONDITIONS GIVING 
RISE TO INSTABILITY

Loose bodies within the ankle joint are 

occasionally a cause of instability. These 

may arise from anterior traction spurs 

in the so called “Footballer’s Ankle”, or 

from osteochondritic fragments which 

have become detached. The most com­

mon cause of the latter is the condition 

of osteochondritis dissecans, which fre­

quently affects the superior weight bear­

ing surface of the talus. Another lesser 

known condition is the so called menis- 

coid lesion. This consists of a synovial 

and fibrous frond of tissue which grows 

into the ankle mortice as a result of re­

peated trauma to the area.

It may impinge between the weight 

bearing surfaces and give rise to symp­

toms.

DEGENERATIVE DISORDERS

“Footballer’s Ankle” may affect the 

younger patient, giving rise to traction 

spurs from the capsule and decreased 

joint space with sclerosis, stiffness and 

pain. In older athletes, post traumatic 

osteoarthritis becomes a factor to con­

sider. The patient will complain of 

mechanical pain, clinical examination

may reveal diffuse synovial swelling, 

tender osteophytes, and the range of 

motion may be decreased. The radio­

logical findings are characteristic.

FOOT PRONATION

This may give rise to considerable pain 

and disability in the runner. Several 

conditions may predispose to the devel­

opment of the pronated foot.3

•  Joint laxity

•  Heet valgus

•  Genuvarus

•  Tight tendo-Achilles

•  Subtalar varus

•  Forefoot supination

It is worth re-iterating the importance 

of assessing the whole limb before con­

centrating on the foot problem. Exam­

ine the running shoes for uneven wear 

and observe the patient from behind, as 

the position of the heels can only be ac­

curately assessed from this view.

CONGENITAL ABNORMALITIES

A number of congenital anomalies 

within the foot may be important to the 

athlete. Perhaps the most common of 

these is the condition of metatarsus pri­

mus varus which has a strong hereditary 

influence and may rise to hallux valgus.

Assessory ossicles may also occur. 

The “os trigonum” is a frequently found 

radiological anomaly. Most common in 

causing clinical symptoms is the so 

called “os naviculare” on the dorsome- 

dial aspect of the foot. This is simply an 

accessory navicular bone.

Tarsal coalition is an unusual but im ­

portant cause of pain in the adolescent. 

This gives rise to “peroneal spastic flat 

foot”. In this condition the patient com­

plains of pain on the posterolateral as­

pect of the ankle with exercise. This 

pain is related to the peroneal tendons 

which on clinical examination appear to 

be tender and the muscles in spasm. 

The medial arch of the foot is frequently 

dropped, hence the “flat foot” descrip­

tion. It is important to take adequate 

Xrays, including Harris oblique views 

of both heels in order to establish the 

possible presence of a tarsal coalition. 

CT Scanning may also be helpful.

ISELIN’S DISEASE

This condition, which affects the ado­

lescent, is another example of a chronic 

traction injury. In this instance, this 

involves the insertion of the peroneus 

brevus tendon into the base of the 5th 

metatarsal. Local tenderness may be 

elected in this area and radiological fea­

tures usually consist of a presence of a 

small flake of bone displaced from the 

apophysis, near the insertion of the ten­

don.

STRESS FRACTURES

Nearly 50% of stress fractures which oc­

cur in athletes involve the foot.4

The important clinical features con­

sist of gradually increasing and chronic 

pain which eventually make it imposs­

ible to continue with athletic activity.

Local tenderness is invariably 

present, and the radiological features in­

clude a periosteal reaction, and some­

times a fracture line. It is important to 

differentiate these conditions from 

malignancies, and therefore a precise 

history is essential. In the case of the 

“Jones fracture”, which occurs about 

2cms from the base of the 5th metatarsal 

the injury consists of a traction type of 

stress fracture, rather than one due to 

repeated compressive loading. This in­

jury should be differentiated from the 

avulsion fracture of the base of the 5th 

metatarsal, as the treatment is quite dif­

ferent and the prognosis without bone 

grafting much worse in the case of the 

Jones fracture.

FRACTURES AND 
DISLOCATIONS OF THE FOOT

These may follow many patterns, the 

clinical history and examination usually 

being revealing. The important feature 

is the development of considerable 

swelling within the first 24-48 hours.

Common areas of involvement in­

clude the subaltar joint, the talonavicu­

lar and calcaneocuboid joints (the 

so-called Chopart dislocation) and the 

tarsometatarsal joint (Lisfranc disloca­

tion). Deformity may be obvious on 

clinical examination. The metatarsal 

bones may be fractured as a result of

2 2 ___________________________________________________________
SPORTS M E D IC IN E  VOL. 5 NO. 2

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1 »•" d e ta ils  of c o m p o s itio n , in d ic a tio n s  c o n tra  in d ic a tio n s , s id e  e ffe c ts . d o s a g e  a n d  p re c a u tio n s  a r e  
-  *-lable o n  r e q u e s t fro m  R O C H E  P R O D U C T S  (P t y )  l t d  . P O  B o *  4 5 8 9  J o h a n n e s b u r g  2 0 0 0 . A d l.n e s  2 2 1 0

20 mg Tertojtjcam
V 3 1

TIlCQfTlL 20 "S'!
foOCHE

®  Tilcotil 20 mg
Each pacJt. ccŝajin$ 

pius

1 ™  -H M  'M l as solvent 

b a t o n  2 s  C  
K E E P  O U T  O F  
R E A C h  O F  C H I L D R E N

| S3] Reg. Nos. Vials: V/3. 1/238: H/34/128 
TILCOTIL = Trademark

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Tenoxicam  20m g

Nonsteroidal Anti-inflammatory Drug

RAPID ANTI­
INFLAMMATORY 
& ANALGESIC 
ACTION FOR THE 
TREATMENT OF 
SPORTS INJURIES

T h e  first I.V. and I.M. 
20m g once daily 
Parenteral Administration

For abridged product information 
please see page 24.

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S P O R T S  M E D IC IN E

‘TILCOTIL’ ROCHE
Components:
T e no xica m

Indications:
S y m p to m a tic  tre a tm e n t o f the 
fo llo w in g  p a in fu l in fla m m a to ry  and 
d e g en erative  d is o rd e rs  o f the 
m u s c u lo s k e le ta l system : 
rh e u m a to id  a rth ritis ; o s te o a rth ritis ; 
a n k y lo s in g  s p o n d y litis ; e xtra - 
a rtic u la r d is o rd e rs , e .g . te n d in itis , 
b u rs itis , p e ria rth ritis , g o u ty  
a rth ritis  (fo r ta b le ts ).

D osage:
2 0 m g once d a ily  at the sam e tim e  
each day. The p are n te ra l fo rm  is 
used fo r one o r tw o  d ays. For 
tre a tm e n t in itia tio n  in acute g o u ty  
a rth ritis  4 0  m g (2 ta b le ts ) once d aily 
fo r tw o  days fo llo w e d  by 20 m g 
once d a ily  fo r a fu rth e r five  days is 
re c o m m e n d e d .

C o n tra-in d icatio n s:
K no w n  h y p e rs e n s itiv ity  to  the d ru g . 
P atients in w h o m  s a lic y la te s  o r 
o th e r n o n s te ro id a l a n ti­
in fla m m a to ry  d ru g s  (N S A ID s) 
in d u ce  s y m p to m s  o f a sth m a , 
r h in itis  o r u rtic a ria . P atients w ho 
are s u ffe rin g  o r have s u ffe re d  fro m  
severe diseases o f the u p p e r 
g a s tro in te s tin a l tra c t, in c lu d in g  
g a s tritis , g a s tric  and duo de na l 
u lc e r. B efore a na esthe sia  o r 
s u rg e ry , ‘ T IL C O T IL ’ s h o u ld  n o t be 
g ive n  to p a tie n ts  at ris k  o f kidn ey 
fa ilu re , o r t o  p a tie n ts  w ith  increased 
ris k  o f b le e din g.
C o n c u rre n t tre a tm e n t w ith  
s a lic y la te s  o r o th e r N SAID s s h o u ld  
be a vo id e d .
P re g n a n c y  and la c ta tio n . 

P recautions:
S im u lta n e o u s  tre a tm e n t w ith  
a n tic o a g u la n ts  a n d /o r oral 
a n tid ia b e tic s  s h o u ld  be avo ide d  
u n le ss  the p a tie n t can be c lo s e ly  
m o n ito re d .
Renal fu n c tio n  (B U N , c re a tin in e , 
d e v e lo p m e n t o f o ed em a , w e ig h t 
g ain , e tc .) s h o u ld  be m o n ito re d , 
w he n  g iv in g  a NSAID to the e ld e rly  
o r to  p a tie n ts  w ith  c o n d itio n s  th a t 
c o u ld  increa se  th e ir ris k  of 
d e v e lo p in g  renal fa ilu re .

Packs:
T a ble ts 20 m g : 10 ’s, 3 0 ’ s.
V ial pack c o n ta in in g  1 vial active 
su b s ta n c e  and 1 a m p o u le  w a te r fo r 
in je c tio n .

crushing injuries.

In all cases, early diagnosis is import­

ant in order to allow treatment (includ­

ing early reduction of any dislocation) 

to begin.

OSTEOCHONDROSES

These have been described involving 

many of the tarsal and metatarsal bones. 

The most commonly observed exam­

ples include Kohler’s Disease of the 

navicular and Frieberg’s infraction of 

the head of the 2nd metatarsal. Re­

peated trauma has been thought to be an 

important aetiological factor, but this is 

not certain. Localised tenderness will be 

present and may sometimes suggest a 

stress fracture. However, the radiologi­

cal features are characteristic. The areas 

affected become flattened and sclerotic.

NEUROMAS

Morton’s Neuroma, usually in the third 

interdigital cleft on the plantar aspect of 

the foot, is the most common condition 

of this kind to affect the athlete. How­

ever, a less frequent condition known as 

Joplin’s Neuroma may involve the cuta­

neous nerve on the dorsal aspect of the 

hallux. This is frequently due to re­

peated trauma from tight running 

shoes. Local exquisite tenderness is 

characteristic of these conditions. In the 

case of the Morton’s neuroma trans­

verse compression of the metatarsal 

heads may elicit pain on clinical examin­

ation. In addition there may be paras- 

thesiae distal in the area of supply, and a 

local positive Tinel sign.

HALLUX VALGUS

Hallux valgus is a problem which more 

often affects the female runner. The 

aetiological factors include the wearing 

of tight fashionable shoes and the inher­

ited condition of metatarsus primus 

varus. Clinical examination frequently 

reveals a tender bunion overlying the 

head of the 1st metatarsal with the well 

known lateral angulation of the hallux. 

The sesamoids may become involved 

and be locally tender on the plantar 

aspect.

HALLUX RIGIDUS

This commonly affects long distance 

runners and is a condition of degenera­

tive arthritis of the 1st metatarso­

phalangeal joint. The history is import­

ant in that the patient will complain 

bitterly of pain and stiffness in the joint. 

Local tenderness may be present. The 

range of movement is grossly decreased 

and is painful. The Xray findings are 

those of a degenerative arthritis of the 

joint.

OTHER CAUSES OF FOREFOOT 
PAIN

The sesamoid bones may become in­

flammed or fractured in the absence of 

other surrounding pathology. They are, 

on occasion, subject to stress fracture. 

However, the simple Verruca vulgaris 

may give rise to pain and local tender­

ness in the plantar skin and should be 

considered.

It is worth remembering that ingrow­

ing toenails and athletes foot are not un­

common in runners and may be difficult 

to treat.

SUMMARY

The above account of the physical 

examination of the foot and ankle is by 

no means comprehensive with respect 

to all the conditions which may be 

found. However the problems which 

commonly affect the athlete have been 

detailed. It is most important to re­

iterate that full assessment of the patient 

is necessary in all cases, and that mala­

lignment problems may give rise to 

ankle and foot pain.

REFERENCES

1. Maron B R . “Orthopaedic aspects o f Sports 

M edicine” in Sports Medicine, Appenzeller 

O , and Atkinson R. Ed. Urban and Schwar- 

zenberg, Ballimore-Munich, 1983.

2. Schepsis A A  and Leach R E . “Surgical m an­

agement o f Achilles tendinitis”. The 

American Journal of Spons Medicine Vol 

15(4), 308-315,1987.

3. Noble CA. “Excessive distances are major 

causes o f injury”. SA Sports Medicine, No 3, 
4-5,1978.

4. Maiheson G O , Clement D B , McKenzie 

D C . “Stress fractures in athletes. A study of 

320 cases”. The American Journal of Sports 

Medicine. Vol 15(1). 46-58,1987.

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SPORTS M E D IC IN E  VOL. 5 NO. 2

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