CONGENITAL DEFECT OF THE FIBULA 
BY 
F. J. COTTON, M.D. 
AND 
A. L. CHUTE, M.D. 
Reprinted from the Boston Medical and Surgical Journal of 
August 25 and September 1, iBgB 
DAMRELL & UPHAM, PUBLISHERS 
B OS T O N 
283 Washington Street 
1898 S. J. PA RKH ILL &. CO.. BOSTON, U.S.A. 
PRINTERS CONGENITAL DEFECT OF THE FIBULA. 
The cases we have to report are of those classed in 
the literature either as congenital defect of the fibula 
or as intrauterine fracture of the tibia, according as the 
one or the other feature has chanced to impress the 
individual observer. 
F, J. COTTON, M.D., AND A. L. CHUTE, M.D. 
The first case, G. H., a boy of seven years, was an 
inmate of the Marcella Street Home. There was no 
history of trauma at birth or before, no deformities 
noted as having occurred in the family. The deform- 
ity was first noticed when the child began to walk. 
The limp then noticed has rather increased with his 
growth, though the disability has never been extreme. 
The boy is now robust, and, except for the left leg, 
normally formed. This leg shows marked shortening, 
the tibia shows a bend forward, and the foot, which 
has but four toes, is in marked valgus. The total 
shortening is two and one-half inches, one-half inch of 
which is due to shortening of the femur. The girth 
of the left thigh is two inches less than on the right. 
The patella is distinctly smaller than on the sound 
side. The circumference of the calf is one and one- 
quarter inches less on the left. No trace of the fibula 
is to be felt. At the middle part of the tibia there 
is a distinct bend forward. Over the most salient 
point of this bend is a faint scar-like line something 
over one-half inch in length. 
The foot shows no equinus, and the whole sole is 
used in walking. The foot is, however, markedly 2 
everted when weight is borne on it, the inner malle- 
olus coming much nearer the ground than in the sound 
foot. There are but four toes, the great toe being 
considerably larger in all dimensions than that of the 
other foot, the other toes of normal size and shape. 
Examination with the fluoroscope and x-ray photo- 
Case T. 
graphs showed no trace of the fibula. There was de- 
fect of one toe and of the corresponding metatarsus. 
The astragalus, calcis, and probably the cuboid, are 
represented by a fused mass of bone of irregular shape ; 
the scaphoid and the three cuneiforms were normal, at 
least in position. 3 
The boy had, as a result of the shortening, a marked 
scoliosis, with rotation, the dorsal convexity to the left; 
Cose I. 
this disappeared on lying down. He had a marked 
limp, but never had any pain, and was active. The 4 
boy left the institution shortly after being seen, and 
has never had other treatment than a high sole. 
Case 11. E. F., a girl of eight, was also at the 
Marcella Street Home. The deformity in this case 
was very similar to that in Case I, but the disability 
greater. This child also is, save for the deformity of 
Case 71. 
the leg, normally formed, and, though small, yet of 
strong frame. 
The shortening in this case is two and three-eighths 
inches for the lower leg, and one-half inch for the 
thigh. The whole limb is evidently atrophic, the dif- 
ference in girth of the two thighs being three-quarters 
of an inch ; of the calves, two inches difference. The 5 
CaseX. 6 
femur at its lower end is obviously less in width. The 
patella is notably less in size. 
There is obviously a defect of the fibula, only in its 
lower quarter is anything to be made out, and there is 
no trace of an external malleolus the outer edge of 
the upper joint surface of the astragalus is palpable, 
during flexion and extension, where the external mal- 
leolus should be. 
The tibia, shortened but not thickened, is definitely 
bent, though at a very obtuse angle. The apex of this 
angle is about the junction of lower and middle thirds 
of the tibia, and is directed forward and slightly in- 
ward. There is no sign of thickening about the angle. 
Over the most salient point of this bend is a longi- 
tudinal scar-like depression, about three-eighths of an 
inch in length, which is more adherent to the bone 
than is the surrounding skin. 
The foot is held in equinus by contraction of the 
calf muscles, and is used in strong plantar flexion, 
showing considerable pronation when bearing weight. 
The peronei seem to be little if at all contracted. The 
foot itself, narrower than its fellow, and three-quarters 
of an inch shorter, is of sufficiently normal shape save 
for the lack of one metatarsus and its toe. The re- 
maining toes are normal in shape; in size about the 
same as those of the other foot. 
All voluntary and passive movements of the hip, 
knee and ankle, and of the foot, are normally carried 
out, except as limited by the shortening of the calf- 
muscles. There is no paresis, and no essential muscles 
are absent. The reflexes are normal. There is a sco- 
liosis due to the shortening which wholly disappears 
in the prone position. 
The presence of a large hairy mole on the thigh of 
the lame side is of interest, though probably of no 
significance. 7 
The x-ray examination showed a normal right leg; 
on the left the following anomalies: A considerable 
decrease in width of the lower epiphysis of the femur, 
no marked change in its thickness vertically. The 
upper epiphysis of the tibia, likewise of normal thick- 
ness but much less in width, shows in the photograph 
as three-eighths of an inch less. The intercondylar 
groove of the femur is much less marked than on the 
sound side. Below the head the tibia approaches the 
normal thickness and the shafts of the two tibiae are of 
about the same thickness. The lower tibial epiphysis 
is narrower (one and one-sixteenth vs. one and seven- 
sixteenths) and considerably thinner vertically. The 
epiphyseal line grows somewhat indistinct toward the 
outer side. The angle in the tibia does not show in 
the front view. Viewing the leg from the side with 
the fluoroscope one sees a definite but very obtuse 
angle in the bone without any thickening of the shaft. 
The fibula measures but three-fifths as much in 
length as the sound one, the shaft is little more than 
half the normal diameter. The upper epiphysis does 
not show on the plate though the conformation of the 
end of the bone suggests its presence, unossified. The 
lower epiphysis is present, of two-thirds the normal 
size, but so shifted upward that its tip comes opposite 
the epiphyseal line of the tibia; the external malleo- 
lus, therefore, does not enter into the articulation at 
the ankle. 
In the tarsus is a mass evidently representing fused 
astragalus and calcis, and probably scaphoid as well. 
The cuboid and three cuneiforms are distinct. The 
first and second metatarsals have the normal articu- 
lation, the third articulates with the outer cuneiform 
and with the cuboid, the fourth with the cuboid alone. 
The metatarsals and phalanges are, save for the defect 
of one toe and metatarsal, entirely normal. Case. TLh 9 
Case W 10 
Before being seen by us the child had had no treat- 
ment. With a view largely to correction of the scoli- 
osis, a tenotomy of the tendo-Achillis was performed 
and a boot with a high sole applied. This reduced 
the scoliosis to a minimum but the valgus position of 
the foot was rather aggravated. Accordingly, a sole 
support with double uprights was so arranged by rais- 
ing the heel end in the boot as to leave the foot in 
moderate plantar flexion. This apparatus in connec- 
tion with the high-soled boot has somewhat improved 
the gait. 
Case 111. J. R., age two years. Seen through 
the kindness of Dr. E. G. Brackett. Is an out-patient 
at the Children’s Hospital. 
At birth it was noticed that the child had but 
three toes on the right foot and that the foot was 
held in a queer position which, from the description 
of the parents, must have been a calcaneo-valgus. 
Under no other treatment than the mother’s manipu- 
lation this “queer” position has almost entirely dis- 
appeared. 
At present the right leg is one and one-half inches 
shorter than the left, all of this shortening appar- 
ently in the lower leg. The thigh and calf are both 
smaller than on the normal side and the shaft and 
condyles of the femur feel distinctly slenderer than 
on the left. The patella is not much over one-third 
the normal size. 
The tibia shows a bowing forward a little below 
the middle, with, however, very little lateral deviation. 
Over and about the bend the tissues are somewhat 
thickened but there is apparently no thickening of 
the bone. Over the bend anteriorly is a faint scar- 
like line half an inch in length. 
No fibula could be felt and the prominence of the 
external malleolus was wholly wanting. 11 
The radiographs, however, show a rudimentary 
fibula about two inches in length, the lower end of 
which is nearly one-half inch above the lower epi- 
physeal line of the tibia. Nothing is to be seen of 
either epiphysis, but from the shape of the lower end 
of the fibula it seems probable that the lower epi- 
physis exists, though it probably, as in the last case, 
does not reach the ankle-joint. The upper end of the 
fibula, unlike that in Case 11, tapers off gradually and 
there is no reason to suppose the presence of an 
epiphysis. 
The foot in this case has but three toes, sufficiently 
normal in size and shape, and is one and one-half 
inches shorter and much narrower than the left. It is 
held in very slight equinus, while the valgus deformity 
is extreme. The foot can be brought up nearly to a 
right angle with the leg, but correction of the valgus 
is only partly possible. This is evidently due to con- 
traction of the peronei, which are drawn tense long 
before tbe normal position can be attained. 
Radiographs show an apparent fusion of the talus 
and calcis. The cuboid is much smaller than normal, 
the scaphoid and the three cuneiforms somewhat 
small. Two metatarsals with the corresponding 
phalanges are wanting. 
The boy, who has walked for eight or ten months, 
has an extreme limp and is not active, but has no 
pain. He is now wearing a valgus shoe with aT- 
strap. 
In neither of the two cases (I and III) in which a 
complete history was obtainable could we get any 
account of hereditary deformity, prenatal trauma or 
abnormal labor. 
Many cases of this sort have been reported and 
there has been much discussion as to their etiology, 
with a number of theories to account for the rela- 12 
tively constant association of these apparently non- 
related deformities. 
Most of the earlier observers (Gurlt, Brodhurst, 
Swan and others) and some of the later (as Brinton, 
Ithen, Braun and Busachi) have believed the bend in 
the tibia a result of intrauterine fracture, while the 
scar was supposed to indicate compound fracture. 
The accepted etiology was either external trauma or 
excessive muscular contraction on the part of the 
fetus. These observers had no clear theory to ad- 
vance as to the cause of the defect of toes, metatarsus 
and fibula. 
Little accounted for the fracture which he accepted 
as proximate cause, by supposing an overaction of 
muscles due to some vice of innervation which, of 
course, explains nothing. 
Broca supposed a defect of development with 
fracture from muscular action. 
Adams believed the condition not an absence of the 
fibula but a fusion of tibia and fibula a view not 
borne out by dissections. 
Pressure from twin pregnancy and compression by 
the cord have been made to serve as causes, though 
with no support of facts. 
Blasius noting the lack of growth of the limb in 
later life found this hard to reconcile with the theory of 
trauma as a cause, but he advanced no other theory. 
Chance supposed compression in abnormal position 
(against other leg) by the cord to be the cause; the 
scar a result of decubitus. 
Fricke noting that the fetus in the fifth and sixth 
week shows a bend of the tibia and assuming the fac- 
tor in its straightening to be the growth of the fibula 
was inclined to assume, in cases where the fibula 
was wanting, a mere persistence or exaggeration of 
this fetal condition. 13 
Brinton, writing in 1884, considered the trauma 
primary and tried to explain the associated defects as 
in some vague way secondary. 
Ithen, in 1885 and Braun in 1886, still held to 
trauma; Braun holding the fibular defect to be a pre- 
disposing cause of the fracture, in that it weakened 
the leg. The defect he did not explain. Recognizing 
the uncertainty whether the dimple over the angle 
was or was not a true scar, he suggested the possi- 
bility of decubitus as a cause. 
Temesvary, six years later, reiterated these views, 
and the theory now usually accepted, that of amniotic 
pressure and adhesions, though suggested by Dareste 
in 1882, seems to have been overlooked by most 
authors until 1892, when Sperling, in a masterly 
paper, reviewed the whole subject and challenged all 
evidence supposed to prove that these so-called intra- 
uterine fractures were fractures at all, and pointing 
out the possible explanation of their causation by ab- 
normalities of the amnion. His arguments in brief 
were: 
A fracture in utero by indirect or direct violence 
would be hard to produce, the fetus being suspended 
in amniotic fluid and protected by the uterine and ab- 
dominal walls. 
Violence sufficient to produce such a fracture would 
usually at least produce miscarriage. 
If uterine pressure were the cause of fracture we 
should have fractures occurring with some frequency 
intra partum, when the intrauterine pressure is great- 
est ; in fact, however, such fractures occur only at or 
near full term, and as a result, not of intrauterine press 
ure alone, but of the counterpressure of the bony 
pelvis as well. 
Callus is practically never found in the cases seem- 
ing to belong to the class under discussion. 14 
The presence of the so-called scar is not valuable 
evidence of compound fracture it is not even proved 
that it is a scar. 
The defects of fibula and toes, so frequently associ- 
ated with the tibial bend, point to an origin as early as 
the second month of fetal life, for at this time the parts 
are laid down, and defects in the true sense cannot 
arise later. These defects cannot be, so far as we can 
see, either cause or result of the so-called fracture. 
Hence the association points to a common cause for 
both. It seems likely that both are due to pressure 
and pull of the abnormal amnion and its adhesions —• 
the more likely inasmuch as this seems to be the cause 
of other similar deformities. 
Haudek, in an extensive article in 1896, accepting 
Sperling’s conclusions, adds to the evidence the report 
of the microscopic examination of one of these so-called 
scars which he had excised. It showed no interrup- 
tion of the skin layers, and only such fibrous and 
atrophic changes as could best be explained as the re- 
sult of pressure, in short, could not be called true scar. 
He also called attention to the fact that defects of the 
radius, which in early fetal life lies exposed in supina- 
tion, are, with the associated defect of thumb and fin- 
gers, the not infrequent counterpart of defect of the 
similarly exposed fibula. 
Kirmisson notes in this connection the scar-like 
mark over the bowed ulna which occurs in some of 
these cases of radial defect. 
Nelaton, Kirmisson, Hoffa, Walsham and Hughes, 
and very recently Nasse, in the new Deutsche Ghir- 
urgie, accept these views in general, and of late other 
theories have been largely given up. Delanglade, in 
an article which has just appeared, accepts the am- 
niotic theory in general, but is inclined to lay more 
stress on narrowness of the amnion than on the action 15 
of adhesions a reservation also tacitly made by 
several others of the above list. 
In considering this list of theories we find that 
several need not detain us. The theory of changes in 
bone texture lacks all evidence. That the pressure of 
twin pregnancies is not the cause appears from the 
fact that we have found no note of a case where the 
child was one of twins. The defect is not a fusion of 
tibia and fibula for, as Gould has pointed out, the in- 
terosseous membrane is present. Moreover, where the 
fibula is defective in part only, its rudiment occupies its 
normal position. 
Fricke’s theory of persistence of the fetal bend does 
not account for the usual direction of the bend for- 
ward and inward, instead of forward and outward, and 
presupposes, without explaining, the absence of the 
fibula. 
The theory of nerve changes as a cause lacks evi- 
dence and is not in accordance with recent work which 
tends to show that growth in utero is independent of 
the nervous system (Schaper). 
There remain only the theories of damage to, or ab- 
sence of, original cell-elements, of fracture, and of 
amniotic changes. The arguments of Sperling and 
Haudek are, we think, enough to dispose of the 
fracture theory. It is conceivable and cannot be dis- 
proved that the defect may be one of development 
per se, but the theory of defect of development of 
rays ” lacks proof that such rays exist, and cannot 
explain the undoubted cases of defect of the fibula or 
radius without defects of the foot or hand. Ou any 
other theory of defect due to absence or faulty ar- 
rangement of original cell-groups, it is hard to see how 
to explain the relative constancy of type and the 
limited extent of the deformity. Nor can such a 
theory explain the tibial bend or the so-called scar. 16 
The amniotic theory, however, seems to explain all 
the lesions pretty clearly. We cannot but accept it 
as at least the most plausible theory yet advanced. 
The origin of the typical deformity would be, then, as fol- 
lows : Between the fifth and the eighth week, pressure 
of a too tightly-fitting amnion interferes with the de- 
velopment of the exposed fibula and the outer toe or 
toes of the exposed foot. Lack of space determines 
the bend of the growing tibia ; the adhesion which pro- 
duces the so-called scar is a result of contact of the 
most salient point of the tibia with the enveloping wall. 
The persistent lack of growth of the whole limb is prob- 
ably a result of deficient vessels and nerves due to the 
early pressure, as well as of disuse. 
As to the frequency of this deformity it is not so rare 
as would be supposed from some very short lists re- 
cently published. Haudek collected, with his own 
case, 103 in all, and we have found others to bring the 
list up to 127, including the cases here reported: 
Haudek’s list: Ztschr, f. Ortli. Chir., 1896, iv, 326 .... 103 
Kirmisson (besides 2 cases included by Haudek); Traits des 
mal. ch. d’ orlgine congen., Paris, 1898 ; Revue de Chirurgle, 
1897, p. 524 6 
Walsham and Hughes : Deformity of the Human Foot . . 1 
Steele : Transactions American Orthopedic Association, 1896, ix, 
175 3 
Frees : Transactions British Orthopedic Society, Birmingham, 
1896, i, 10 1 
Humphrey: On the Skeleton (cited by Gould, Transactions 
Pathological Society, xxxii, 153) 1 
Proudfoot; New York Journal of Medicine, 1846 (cited by Brin- 
ton, Transactions American Surgical Association, 1884, ii, 
425) 1 
Langton : St. Bartholomew’s Hospital Report, 1879, xv, 272 . 1 
Kaufmann : (cited by Braun, Arch. f. klin. Chir., xxxiv, 1886) . 1 
.r\_dU.l lllctillll • (Ol LcU Uy X>l dillllj xi.l i« Ik 1111» V_/ULII . j loOD) • I 
Delanglade : Rev. des Malad. de I’Enfance, April, 1898 . . 1 
Tyrie : Journal Anatomy and Physiology, xxviii, 4, p. 411, 1894 . 1 
McKenzie : New York Medical Journal, 1897, Ixv, 241 . . . 1 
Morestin : Revue des Malad. de I’Enfance, April, 1898. . . 1 
Rose : Gbl. f. Chirurgie, 1897, No. 12, p. 357 1 
Whitman : Rev. d’ Orthopedie, 1898, ix, 86 1 
Tubby : Deformities, 1896, p. 359 1 
Cases here reported by us 3 
Total 128 17 
Nasse1 speaks of having seen this defect repeatedly 
in v. Bergmann’s clinic but gives no detailed account 
of cases, and we find reference to a report by Bur- 
miester,2 which we have not verified. 
As to the details of cases reported, and the varia- 
tions occurring, the following notes are presented : 
The fibula defect is noted as total in 72 cases. 
A fibula of not over half the normal length with 
both epiphyses present, one or both small, is thrice 
noted. In Volkmann’s dissections, the upper epiphy- 
sis of the fibula w&s prolonged upward by a fibrous 
band. This band may, in part, replace a fibula which 
has no upper epiphysis (Braun) or may replace the 
whole fibula (Gould, Wagstaffe). Where an epiphysis 
is present it may show lack of ossification ; this is prob- 
ably the condition in Case II of our series. 
Where the lower epiphysis is present it may lie 
higher up than normal and not serve as a part of the 
ankle-joint. This is shown by Bidder’s dissections and 
by the radiographs of our Case 11. Probably this 
condition may often obtain, for in the absence of dis- 
sections or radiographs, where no external malleolus 
is to be felt, it is very hard to say whether a rudi- 
mentary fibula may not be present. 
A bend or angle of the tibia, directed forward and 
usually slightly inward, usually accompanied by the 
so-called scar, is noted in 67 of the published cases. 
The acuteness of the angle varies widely. There may 
be thickening of the tibia, or its head and shaft may 
be slenderer than normal. The shortening of the 
shaft is present to a greater extent than the bend can 
account for and may be marked. As to the lower end 
of the bone, it may show no obvious change or may 
1 Deutsche Chirurgie Lief, 66, i, Halfte sq. 165. 
2 Cerberten aus des Geb. des Guburkh. ii. Gynack. zum Feier von 
Carl Huger, Berlin, 1896, sq. 215 (1 plate). 18 
show a knobby internal malleolus and an oblique sur- 
face for the ankle articulation. 
This latter condition is the classical one in the cases 
of Yolkmann’s “ Congenital Dislocation of the Ankle.” 
It is a question, however, whether these cases do not 
belong in a separate class. The original cases, de- 
scribed by Volkmann, Kraske and Bidder, though they 
had defective fibulas, showed no defect of toes, were all 
bilateral, and all occurred in members of one family, 
seven out of seventeen of whom had the deformity. 
This hereditary character does not accord with either 
the facts or the theory of cases of fibula defect in gen- 
eral. For these few cases, however, the dissections 
reported prove a definite obliquity of the ankle-joint, 
primary, and the cause of the extreme deviation of the 
foot. Bidder found in one case that the lower epiphy- 
sis of the tibia, 1.2 cm. thick at the inner side, fell away 
to 2 mm. at the outer. 
We have no evidence of the existence of such ob- 
liquity in the majority of cases, but it is very probable 
that it exists to some extent. The radiograph of our 
Case I shows some obliquity and that of Case 111 
suggests it. 
Defect of one or more toes associated with the fibu- 
lar defect is noted expressly in 67 cases. In one case, 
however (Kirmisson), there were seven toes. Apart, 
from one case (Otto) where the great toe is said to 
have failed, the defect seems always to have affected 
the outer toes. Several cases are reported where all 
save the hallux were lacking. There is often some 
disproportion in size of the toes. Webbing, especially 
of the second and third, is frequent. In some cases 
there is associated defect of toes on the other foot with- 
out fibular defect. The metatarsals corresponding to 
the missing toes are uniformly absent. Some of the 
tarsal bones may be lacking or more often there is 19 
fusion of several of them: the calcis, talus, scaphoid 
and cuboid, or some of these, being especially likely to 
fuse. There seems to be no regular type of deformity 
here. The foot is in equinus, usually in equino-valgus 
of varying degree. In five cases, however, varus or 
equino-varus was reported. In one of our cases the 
position in the beginning seems to have been a cal- 
Czse $ 
caneo-valgus. The contracture of the tendo-Achillis 
accompanying the equinus is not entirely owing to the 
disuse of dorsal flexion in a short leg, for it may, as in 
a case of Bidder’s, occur where the deformity is bi- 
lateral and equal. 
In 21 cases the patella is noted as of less than nor- 
mal size. It may be wanting or, at least, not distin- 20 
guishable clinically. A lack of development of the 
whole limh, femur as well as tibia, is usual, varying 
widely in degree. Whether this may be in part, as 
Nasse seems to think, due to the atrophy of disuse, or 
from congenital deficiency of vessels and nerves, is 
hard to say. The shortening is progressive and its in- 
crease as the child grows is a very important factor in 
determining the disability. 
Braun reports two cases, of sixteen and seventeen 
years, with a shortening of 7 and of 8 cm. respectively 
the femur being responsible in each case for 2 cm. 
Blasius found in one case at ten years, 2 inches 
shortening; in another, at nine years, inches. 
Kirmisson had a case with 12 cm. shortening at two 
years, with atrophy of the whole extremity. 
Schnelle reported a case with 3 inches shortening at 
three years, 5 inches at ten years, 9 inches at twenty- 
nine years. 
Kaufmann found the increase of shortening between 
two and one-half and six and one-half years of age to 
be 2 cm. in one case. 
Kemke in a case seen at birth found the tibia lijr cm. 
short; at one and one-half years the shortening was 
cm. 
The deformities associated with fibular defect have 
been most various, including hare-lips, skull defects, 
visceral anomalies, etc.; but, as would be expected 
from the accepted theory, defects of the foot, as a 
whole, of the femur, of the whole upper extremity, or 
especially of the ulna, or radius and’ fingers, are most 
common. 
Before leaving this part of the subject it may be well 
to call attention to certain deformities of the leg which 
seem to be of similar origin with the fibular defect 
those where some constriction is apparently the cause. 
Case IV. Age four. An unreported case; seen 21 
by kindness of Dr. J. E. Goldthwait; has a shortened 
and deformed leg and foot, as shown in the accompany- 
>C<a>seJF 
ing figures. The x-ray shows no defect either of tibia 
or fibula, but at the point of constriction the bones lie 22 
in contact and seem to be fused. At this point there 
is also a bend in both bones forming an angle open 
forward. The site of constriction is marked by a deep 
sulcus, without scar, encircling the leg. The x-ray 
shows no ossilication in the foot; manipulation shows 
the presence of some bones, apparently fused, in part 
at least. Anterior to the tarsus, the foot is pulpy, and 
there must be extensive bony defects. The total 
shortening from knee to heel is inches, from knee 
to ankle inches. The deformed foot measures but 
2f inches in length, the normal. 5 inches. 
A case of deformity, strikingly similar to this, is re- 
ported by Ridlon,8 in which the circular depression 
about the ankle was associated with other similar con- 
striction rings, with spontaneous amputation of fingers, 
etc. 
Still another case is reported by Steele,4 where a 
depression just above the ankle, as from a cord, 
coexisted with defect of fibula and toes and bend and 
so-called scar of tibia. 
These cases, taken together, make it seem possible 
that this class of cases may also be due, not to strangu- 
lation by the umbilical cord, but, like those we have 
been considering, to abnormalities of the amnion, al- 
though the mechanism is not clear. 
Chance 5 cites similar cases, and explains them as a 
result of amniotic adhesions. 
The conditions to be considered in treatment are: 
The total shortening; the abnormal axis of the lower 
part of the tibia ; the equinus the shortened calf 
muscles; the valgus. These are present in varying 
proportions in different cases. There can, therefore, be 
no routine treatment. The total shortening may be so 
8 Ridlon : Transactions American Orthopedic Association, vol. ix, 
179, 1896. 
i Steele : Ibid, p. 175. 
5 Chance : Bodily Deformities, London, 1862, p. 135. 23 
great, especially if the other deformities of the limb are 
also extreme, that amputation will be the only resort. 
This has been repeatedly performed. So far as the 
shortening is due to the bend in the tibia, it is amena- 
ble to treatment by osteotomy or osteoclasis. Brinton, 
in one case, reduced the shortening in this way from 
2-J to 1-| inches, and Rose reports the successful cor- 
rection by osteotomy of a right angled bend in the tibia. 
Tenotomy of the tendo-Achillis has usually been neces- 
sary as an accessory to this as to other operations on 
these cases; it has also been performed as the only 
means of relief, but without much result. In some 
cases a wedge osteotomy has been performed, in one 
case (Langton) followed by non-union. There have 
been other unsatisfactory results after osteotomy, but 
there seems no reason, if the operation is carefully 
done, why the tibia cannot be accurately straightened 
in this way, as has been done by Rose, Brinton, Kir- 
misson and others, nor why there should be a return 
of the deformity, as has occurred (Kiister). 
As to avoidance, so far as may be, of the increase 
of shortening with the growth of the child, Nasse lays 
stress on early use of the limb, with proper support, 
to avoid atrophy from disuse. 
The equinus may always be remedied by tenotomy 
of the tendo-Achillis, which has so often been per- 
formed. The important fact to bear in mind in this 
connection is that the equinus is in large measure an 
attempt at necessary compensation of the total shorten- 
ing, and, if the ankle can be supported in the equinus 
position, it is hard to see what is to be gained by the 
tenotomy, unless, indeed, the shortening is so little 
that a moderately high sole will fully compensate it. 
The most difficult problem to treat has usually been 
the valgus deformity. This is not, at least in the ma- 
jority of cases, a valgus of pronalion and flattening 24 
alone but rather a tipping outward of the whole foot, 
including the astragalus, which has no external malle- 
olus to hold it into place. Moore 6 has recently re- 
ported cases of valgus, due to the removal of the fib- 
ula for disease, which show this mode of production of 
the deformity. In some cases, at least, an obliquity 
of the lower surface of the tibia determines the valgus; 
in others there is apparently no such obliquity. The 
tipping outward of the foot must also be favored by 
the irregularity of the articular surface of the astraga- 
lus ; also by the fact that the bones of the tarsus often 
are partly fused, and hence must have little mobility. 
These facts, probably, are the explanation of many 
failures in the use of the high sole after tenotomy of 
the tendo-Achillis, and must be carefully considered 
in outlining any treatment. 
In a proportion of the cases (as in Case 111 of our 
series) there is contracture of the peronei, as well as of 
the calf muscles, which necessarily prevents correction 
of the valgus until tenotomy is performed. The sec- 
tion of the peroneal tendons has been performed (Brin- 
ton, Nelaton, Walsham, Kirmisson and others) with 
good success. 
In cases where there was obliquity of the ankle- 
joint, a wedge osteotomy above the ankle has been 
performed by Riedinger and by Walsham with good 
result. Volkmann, in one such case, took a wedge out 
of the articular surfaces, securing correction of the 
valgus and anchylosis of the ankle. The result was 
fair. 
Simple resection of the ankle-joint has been done in 
number of cases. One of the most successful is a 
recent case by Rose, where the lost ankle motion was 
compensated by extra mobility in Lesfranc’s joint. If 
this anchylosis be so effected that the foot remains in 
6 Moore : Annals of Surgery, 1896, xxiy, 634. 25 
plantar flexion (Braun), this will lessen the necessary 
height of the sole. Where the deformity is bilateral 
this has, of course, no point, but in other cases seems 
desirable. The Wladimiroff-Miculicz resection, sug- 
gested by Kemke, but not carried out, would have no 
advantage. In two cases (Rincheval, Nasse) Barden- 
hauer’s operation, the splitting of the tibia, and the 
insertion of the talus in the split has been carried out. 
Nasse secured anchylosis in equinus. In both cases 
the result seems to have been satisfactory. 
In cases where the rudiment of the fibula, as shown 
by the x-ray, is of some size, but situated higher up 
than normal, it seems possible that an operation aim- 
ing to slide this down and fix it to the tibia as an ex- 
ternal malleolus, might be worth considering. It has 
apparently never been done. 
Attempts to remedy the defect by orthopedic 
apparatus have, on the whole, been about as satisfac- 
tory as the operative cases. The worth of operative 
procedures must vary with the case; but, in most 
cases, and especially where the limb as a whole is 
markedly atrophic, not much is to be expected. In a 
recent discussion by Kirmisson, Nelaton and others, it 
came out clearly enough that the results attained 
immediately after operation are not conclusive as to 
the end result. Bidder gives plates of two cases: one 
where Volkmann did ankle resection; the other one 
of Kiister’s, where there had been an osteotomy; 
they are not encouraging. Probably in any case, 
even if operated on, an apparatus of some sort must 
be worn to prevent recurrence or the rise of some 
new deformity. The limb is primarily defective as 
well as deformed, and correction of the deformity, 
even if complete, does not solve the whole problem. 
Probably, unless osteotomy promises some considera- 
ble gain in length, or in the position of the foot, or 26 
unless peroneal contracture interferes with the reduc- 
tion of the valgus, no operation, not even a tenotomy, 
will usually be worth while. If a valgus shoe with a 
high sole, sloped to fit the equinus, and with side 
irons, can be satisfactorily fitted, there seems no 
reason for tenotomy of the Achillis. 
To sum up (in so far as one may generalize where 
cases so vary): Osteotomy to be performed not merely 
because deformity exists, but only for definite indica- 
tions ; tenotomy only to reduce the valgus or as an ad- 
junct to osteotomy; resection of the ankle or Barden- 
hauer’s operation, where apparatus will not control the 
tipping of the ankle; amputation only in cases utterly 
unfit for other treatment; treatment of all ordinary 
cases by apparatus to support the ankle, and prevent 
valgus high sole to supplement the equinus in 
equalizing the shortening these would seem to be 
the general lines of treatment. The treatment seems 
to be at best unsatisfactory, and, as always in such 
cases, operation is to be avoided unless we have some 
clear gain in view. 
Appended is a partial bibliography; other references, 
especially to older and less accessible publications, 
with detailed citations of a number of cases, will be 
found in Haudek’s article : 
BIBLIOGRAPHY. 
Braun. Arch. f. klin. Chirurgie, 1886, xxxiv, 666. 
Brinton. Transactions American Surgical Association, 1884, ii, 
425. 
Gould. Transactions Pathological Society, 1881, xxxii, 152. 
Swan. Medical Press and Circular, 1879, xxvii, 160. 
Sperling. Ztschr. f. Gehurkh. n. Gyn., 1892, xxiv, 225. 
Haudek. Ztschr. f. Orth. Chir., 1896, iv, 326. 
Temesvary. Wiener klin. Woch., 1892, xlii, 1284. 
Kraske. Cbl. f. Chir., 1882 (supplement), page 85. 
Bidder. Langenheck’s Archiy., 1888, 37. 
Riedinger. Cbl. f. Chirurgie, 1889 (supplement), page 109. 
Kemke. luaug. Dissert., Konigsberg, 1893. 27 
Targett. Transactions Pathological Society, 1892, xliii, 126. 
Yolkmann. Deutsche Ztschr. f. Chir., 1872-73, ii, 538. 
Rincheval. Arch. f. klin. Chir., 1891, xlviii, 802. 
Hoffa. Orthoped. Chirurgie. 
Kirmisson. Traite. des mal. chir. d’origine congen., Paris, 1898. 
Tyrie. Journal Anatomy and Physiology, xxvii, 4, 1894, page 
411. 
Walsham and Hughes. Deformity of Human Foot, page 336 
and 534. 
Kirmisson. Revue de Chir., 1897, 524. 
Nasse. Deutsche Chirurgie, Lief. 66, i Halfte. 
Steele. Transactions American Orthopedic Association, vol. ix. 
McKenzie. New York Medical Journal, 1897, Ixv, 241. 
Rose. Cbl. f. Chirurgie, 1897, No. 12, 357. 
Delanglade. Revue des mal. de I’enfance, April, 1898. 
Morestin. Ihid, April, 1898. 
Chance. Bodily Deformities, London, 1862. 
Tubby. Deformities. 
Dunn. Transactions Pathological Society, 1889, vol. xlv, 272.  THE BOSTON— 
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