Document 140990

the
physician
siqr,:t;smedicine Reprinted with permission from McGraw-Hili, Inc. VOL. 20/N02/FEBRUARY 1992fTHE PHYSICIAN AND SPORTSMEDICINE © McGraw-Hili, Inc. 1
Vol 20 • No.2. February 92 • THE PHYSICIAN AND SPORTSMEDICINE
Conservative
Treatment of
Inflamed
Knee Bursae
G. Charles Roland, MD
Murray J. Beagley, MB, ChB
Patrick W. Cawley, OPA, RT
n
~
Knee bursitis often mimics other
pathologies, making correct di­
agnosis necessary to initiate ap­
propriate treatment. Most commonly af­
fected are the prepatellar, pes anserine,
tibial collateral ligament, and two infrap­
atellar bursae. Other common bursitic
conditions include Baker's cysts and
posttraumatic adventitious hemorrhagic
bursitis. Most of these can be treated
conservatively with aspiration of fluid
from the bursa, rest, ice, immobilization,
and injection of a corticosteroid and
analgesic combination. Some chronic
bursitic conditions may require surgical
excision of the bursa.
brief
any disorders involving the flexor
and extensor mechanisms of the
knee and associated bursae are be­
ing seen because the growing
munber of athletes tend to place high levels of
stress on their knees. These bLUsitic conditions
can be characterized both by etiology (acute
overuse, chronic overuse, traumatic, or infective)
M
Dr Roland is in private practice with the Orthopaedic Multi­
specialty Medical Group of San Diego. He is a clinical in­
structor in the Department of Orthopaedics at the University
of California at San Diego, an orthopedic consultant at Point
Loma College, and medical director of Bayside Sports
Medicine Clinic, all in San Diego. Dr Beagley is a research
scholar at the Orthopaedic Multispecialty Medical Group of
San Diego. Mr. Cawley is director of research for Don Joy
Co. in Carlsbad, California.
The stress of repetitive kneeling leads to a
relatively high incidence of prepatellar bursitis
among wrestlers.
THE PHYSICIAN AND SPORTSMEDICINE • Vol 20 • NO. 2. February 92
bursitis
en patient, routine x-rays of the affected joint
can generally distinguish them from the types of
bursitis that more commonly affect athletes.
Note that not all knee bursae are affected by bur­
sitis' but knowing the location of all the bursae
may aid diagnosis in those often affected.
Prepatellar Bursitis
Acute Nonpyogenic. Commonly known as
Figure 1. The clinical appearance of prepatellar bursitis in a
17-year-old male wrestler.
Figure 2. Surgically exposed prepatellar bursa of a 20-year-old
college wrestler.
and by location. Most often bursitis can be treat­
ed conservatively in a physician's office. Howev­
er, familiarity with the anatomic positions of the
commonly affected bursae is essential to cor­
rectly diagnose and treat the condition (see
"Identifying Bursae," page 72).
Other conditions that must be differentiated
from bursitis, such as crystal-induced bursitis,
rheumatoid arthritis, other chronic inflammato­
ry arthritides, and tumors or foreign bodies'" are
seldom seen in young, otherwise healthy ath­
letes. If these conditions are of concern in a giv­
coal miners, carpet layer's, or housemaids knee,
acute nonpyogenic bursitis of the prepatellar
bursa develops in response to frictional stress di­
rectly over the bursa, such as that caused by
repetitive kneeling. It is common among wres­
tlers and trampolinists (figure 1).3.5.7
Patients who develop acute nonpyogenic
prepatellar bursitis generally present with ten­
derness and swelling directly over the patella.
They have decreased range of motion of the knee
because pain limits movement as the skin tight­
ens over the patella during maximum flexion.e.9
Pyogenic. Pyogenic bursitis of the prepatellar
bursa develops as a result of penetrating or in­
tegumental injuries, including recent aspiration
of the bursa. The patient's history can thus alert
the physician to the diagnosis.
Patients who have pyogenic prepatellar bur­
sitis present with red, tender swelling directly
over the patella, and occasionally with associat­
ed cellulitis. Patients may also have inguinal
lymphadenopathy. Old wounds, puncture sites,
or abrasions may be evident. Pyogenic bursitis
may be indistinguishable clinically from non­
pyogenic bursitis; thus, microbiological study of
the aspirate is necessary.
Treatment. Using aseptic technique and a
wide-bore needle, phYSicians should initiate
treatment for prepatellar bursitis by aspirating
the fluid-filled bursa. In nonpyogenic bursitis,
the aspirate is a clear, serouslike fluid. Following
aspiration, physicians can inject the bursa with a
combined corticosteroid and local analgesic,
and prescribe rest, ice, compression, and eleva­
tion, which can be augmented with a posterior
splint or knee immobilizer.
In pyogenic bursitis, the aspirate is cloudy
and viscous. Culture of this fluid is always indi­
cated. Commonly, the pathogen is staphylococ­
cus; streptococcus is involved less frequently.
Vol 20 • No. 2' February 92 • THE PHYSICIAN AND SPORTSMEDICINE
bursitis
Because penicillin-resistant bacteria may be in­
volved, physicians should treat these infections
with a penicillinase-resistant penicillin until an­
tibiotic sensitivities are available.
If a patient's pyogenic bmsitis does not re­
spond to antibiotics, or the bursa is extremely
large, open drainage with excision of the bmsa
maybenecessruy 3.,Q." (figme2).
Chronic Inflammatory PrepateUar Bursitis.
Chronic inflammatory prepatellar bursitis may
result from repeated episodes of nonpyogenic
prepatellar bursitis or from a single resolved
episode of pyogenic bursitis. Repetitive mild
traumas or previous infection cause thickening
of the bmsal wall.
According to Sharrard,'2the surrounding vas­
cular network bleeds into the blll'Sa, resulting in
distention. However, the aspirate is often serous,
without evidence of blood staining. A normal
bursal wall has a characteristic frond pattern
and synovial lining containing secretory cells
(figure 3). Histologically, we (G.C.R.,M .J.B.,
P. Wc.) have been unable to demonstrate secre­
tory cells in chronically inflamed bmsallinings
(figme 4). We speculate that distension is caused
by transudation of fluid from tissue surrounding
the bursa.
Many patients feel little or no pain, and thus
do not seek medical attention until the bursa
has become grossly distended. They present
with large, fluctuant, nontender masses directly
over their patellas. These masses may extend
several inches up the thigh or several inches
down the anterior proximal tibia.
Treatment. Initial trea tment for chronic
prepatellar bursitis involves aspiration of fluid
from the bmsa and injection of a corticosteroid
to reduce the inflammatory reaction. Compres­
sion may help limit further distention of the bur­
sa. Repetitive aspirations may be necessruy.
If this conservative approach fails, surgical
excision of the bursa is indicated. Quayle and
Robinson" have described a smgical procedme
in which only the posterior wall of the bursa
is removed, preventing the skin from sticking
and scarring to the underlying tissue. This
procedure is easier to perform than excision of
the entire bursa, and it is less traumatic for
patients, resulting in fewer complications. In
Figure 3. Histologic specimen of normal bursal wall
with characteristic frond patterns and synovial lining. Note
the secretory cells (arrow).
Figure 4. Histologic specimen of excised posttraumatic
hemorrhagic bursal wall. As in other types of chronic bursitis,
secretory cells are absent.
\
the senior author's (G.C.R.'s) experience, this
procedure gives excellent results, and leaving
the anterior wall of the bursa intact does not
appear to predispose patients to recurrence of
bursitis. Following the operation, the surgeon
should institute suction drainage and prescribe
a posterior extension splint to immobilize the
knee for at least 10 to 14 days.
To help prevent recurrent chronic prepatellar
bmsitis and the other prepatellar bmsitis condi­
tions, physicians should recommend that pa­
tients use protective knee pads.
THE PHYSICIAN AND SPORTSMEDICINE • Vol 20 • No.2' February 92
.,
bursitis
Infrapatellar Bursitis
Infrapatellar bursitis may involve either the
superficial infrapatellar bursa or the deep infra­
patellar bursa.
Superficial InfrapateUar Bursitis. Bursitis of
the superficial bursa, like that of the prepatellar
bursae, develops following repetitive mild trau­
ma, such as kneeling on the bursa. In contrast to
the theory that the most consistently occurring
bursae develop during fetal life, Sharrard 12 has
postulated that the superficial infrapatellar bur­
sa is not an inborn structure, but one that devel­
ops only in response to repetitive kneeling. Un­
like prepatellar bursitis, though, infrapatellar
bursitis usually arises from kneeling in an up­
right position and therefore is commonly known
as vicar's knee. Generally, it heals well with com­
pression and ice packs and does not require
complete immobilization or drainage.
Deep Infrapatellar Bursitis. Bursitis of the
deep infrapatellar bursa may follow direct trauma
over the patellar tendon, such as striking the
knees on a hard surface during a fall. This bursitis
may be difficult to distinguish clinically from
posttraumatic rupture of the patellar tendon or
hemorrhage into the retropatellar fat pad. Pa­
tients who have these conditions all have pain
and tenderness over the patellar tendon, and they
are unable to fully flex or extend their knees. MRI
is frequently necessary to confirm the diagnosis.
Frictional or overuse injuries may also cause
deep infrapatellar bursitis, which is then charac­
terized by pain deep in the patellar tendon just
proximal to its insertion on the tibial tuberosity.
Fluid accumulation in the bursa may cause the
sac to bulge on either side of the patellar tendon.
The symptoms of Osgood-Schlatter disease
and patellar tendinitis may closely mimic those
of frictional or overuse deep infrapatellar bursi­
tis. Osgood-SdJ.latter disease may in fact coexist
with the bursitis. Radiography, which can dem­
onstrate tibial apophysitis and residual ossicles
present in the tendon, may help establish the di­
agnosis. Distinguishing patellar tendinitis from
deep infrapatellar bursitis is difficult, although
patients with the latter condition generally feel
pain deep to the tendon.
Identifying Bursae
Bursae are closed sacs or cystic spaces lined
with a synovial membrane that closelyresem­
bles that found in synovial joints. The anatom­
ic locations of the knee bursae vary-as do the
descriptions of their locations. Some bursae
are inconSistently found; some frequently form
communications with adjacent bursae or co­
alesce to form larger sacs. 1-4
Bursae that occur most consistently devel­
op during fetal life and are found interposed
between tendon or ligament sheaths and bony
prominences. These bursae, which promote
joint mobility and protect adjacent muscular
and skeletal tissues by reducing friction, 1 7 in­
clude bursae located circurnferentially around
the knee joint.
Anterior Bursae. Three bursae are located
on the anterior aspect of the knee: the large
prepatellar bursa, which lies between the
patella and the skin, is the most commonly in­
volved in bursitic conditions. The second, the
small superficial infrapatellar bursa, lies be­
tween the skin and the proximal portion of the
patellar tendon. The third, the smaller deep in­
frapatellar bursa, is found between the distal
patellar tendon and the proximal tibia (figures
Aand B).
Lateral Bursae. Four bursae commonly oc­
cur on the lateral aspect of the knee: The first
lies on the posterolateral aspect of the knee be­
tween the lateral head of the gastrocnemius
and the joint capsule. This bursa normally
communicates with the knee joint. Two other
bursae are located along the fibular collateral
ligament. One lies between this ligament and
the biceps tendon; the other lies between the
ligament and the popliteal tendon. The fourth
laterally occurring bursa lies between the
popliteal tendon and the lateral condyle of the
femur.
Medial Bursae. Four bursae commonly oc­
cur on the medial aspect of the knee: The first
Vol 20 • NO.2. February 92 • THE PHYSICIAN AND SPORTSMEDICINE
Illustrations: © 1992. Mary Albury-Noyes
lies between the medial head-of the gastrocne­
mius and the capsule. This bursa sometimes
includes an extension between the tendons of
the gastrocnemius and the semimembranosus
muscles. The second, the pes anserine bursa,
. lies between the tibial collateral ligament and
the tendon insertions of the sartorius, gracilis,
and semitendinosus muscles. The third lies be­
tween the tibial collateral ligament and tendon
of the semimembranosus. The fourth, the tib­
ial collateral ligament bursa, lies just beneath
the tibial collateral ligament and directly over
the medial meniscus. Occasionally people
. have a fifth bursa lying between the tendon of
the semimembranosus and the semitendi­
nosus muscles.
Bursae not fOlmd conSistently include ad­
ventitious bursae, which may develop later in
life in response to major trauma or to friction
or microtrauma over a bony prominence such
as a large exostosis.
In fetal life, the suprapatellar bursa is sepa­
rate, but after birth, it develops into an exten­
sion of the synovial cavity. Thus, it is more cor­
reet to refer to this entity as the suprapatellar
pouch or suprapatellar rejlexion.
Femur ,
Suprapatellar
pouch
Prepatellar .
bursa
.
Posterior joint
space
Patellar
tendon
Semimembranosus
bursa
Superficial
infrapatellar
bursa
Medial -----+i~
meniscus
Deep
infrapatellar
bursa
GastrOGA..mius --+!!!f!:lI!1
muscle
-;;'-+--,--,-'~
Tibia
Figure A_ Sagittal section of the knee through the medial femoral
condyle showing the positions of the commonly occurring bursae.
Gastrocnemius
muscle
References
1. Brantigan OC, Voshell AF: The tibial collateralliga­
ment: its function, its bursae and its relation to the
medial meniscus_J Bone Joint Surg (Am) 1943;25­
A(l): 121-131
Semimembranosus
muscle
2. Goss CM (ed): Gray's Anatomy of the Human Body,
ed 29. Philadelphia, Lea & Febiger, 1973, p 353
3. Kulund DN: The Injured Athlete. Philadelphia, JB
lippincott Co, 1982, pp 373-374
4. O'Donoghue DH, Allman FL: TI·eatment oflnjuries
to Athletes, ed 4. Philadelphia, WE Saunders Co,
1984, pp 466,475
5. Buckingham RB: Bursitis and tendinitis. Compr
Ther 1981;7(2):52-57
6. Dodson CF Jr: Common peri-patellar inflammato­
ry conditions. J Arkansas Med Soc 1979;75(9):330­
332
7: Justis JE: Affections of muscles, tendons, and asso­
ciated structures, in Edmonson AS, Crenshaw AH
(eds): Campbell's Operative Orthopaedics, ed 6. St
Louis, CVMosbyCo, 1980, pp 1404-1410
Figure B. Anteromedial view of the knee showing the positions of
the commonly occurring bursae.
THE PHYSICIAN AND SPORTSMEDICINE • Vol 20 • No. 2' February 92
bursitis
If fluid accumulatian daes cause the bursa to'
bulge, the physician shauld aspirate the fluid
and inject a cambined steroid-Iidacaine medi­
catian into. the bursa. Fallawing injectian,
hawever, a certain amaunt af steroid may be
absarbed into' the tendan itself, leaving it vul­
nerable to' rupture. Therefare, patients shauld
avaid for 2 weeks any activity that may put un­
due stress an the patellar tendan.
Pes Anserine Bursitis
Althaugh physicians mast aften see pes
anserine bursitis in alder, abese patients, it is be­
caming mare camman amang yaunger peaple,
particularly in runners. The pes anserine bursa's
pasitian an the anteromedial aspect afthe knee,
just beneath the pes anserinus tendans and aver
the tibial attachment af the tibial collateralliga­
ment, subjects it to. heavy frictianallaads during
activities such as running. This is particularly
true for patients who. have flatfaat and genu val­
gum, canditians that result in excessive prona­
tian and valgus stress at the knee. Running an
crowned hills ar roads may alSo. exacerbate the
problemY· I.
To. establish a diagnasis af pes anserine bursi­
tis, physicians must distinguish the canditian
fram a partial tear af the tibial attachment af the
tibial callateralligament. Patients who. have ei­
ther canditian repart paint tenderness aver the
proximal metaphyseal regian. Hawever, a pa­
tient who. has pes anserine bursitis shQuld nat
feel increased pain when valgus stress is applied
to. his or her knee at 30° flexian.
Treatment. To. treat pes anserine bursitis,
physicians shauld inject a carticasteroid and a
lacal analgesic directly into. the bursa and pre­
scribe ice therapy. Larssan and Baum13 have sug­
gested that Iidacaine alane be injected first, fal­
lawed by a mixture af 10.cal anesthetic and
carticasteroid if symptams persist. Surgery is
rarely required. Hawever, patients shauld rest
their knees until all symptams resalve; this farm
afbursitis may easily became chranic.
Tibial C611ateral Ligament Bursitis
Patients who. have tibial callateralligament
bursitis present with tenderness aver the tibial
callateralligament at the jaint line, clasely mim­
icking symptams assaciated with a medial
meniscus tear. Accarding to. Kerlan and GI<;lUS­
man,!5physicians shauld cansider a diagnasis af
tibial callateralligament bursitis when a patient
has these symptams withaut a histary af trauma
to. the knee.
Treatment. To. treat tibial callateralligament
bursitis, inject Iidacaine cambined with a steroid
directly into. the bursa, then encaurage a gradual
return to. full activity. When uncertain af the di­
agnasis in a patient who. has the typical symp­
tams, the seniar authar fallaws this treatment
first but proceeds with arthrascopy if treatment
is unsuccessful.
Bakers Cyst
A Baker's cyst traditianally has been cansid­
ered a herniatian af the synavial membrane at
the pasteromedial aspect af the knee caused by
an increase in intra-articular pressure (figure 5) .
Hawever, it naw appears that distensian af
the bursa(e) assaciated with the gastracnemius
and semimembranasus muscles is the same
canditian as Baker's cyst.' This distentian may
result fram inflammatary jaint disease, degener­
ative jaint disease, a meniscus tear, ar a cangeni­
tal defect. A ane-way valve mechanism may be
at wark, allawing fluid into the cyst but prevent­
ing it from returning to. the knee jaint. The
pumping actian af muscles while running ag­
gravates this problem, literally pumping fluid in­
to. the cyst. Marked fluid distentian may result
and may lead to. nerve and vessel impingement.
Or the cyst may rupture, causing swelling and
inflammatian in the calf that resemble the clini­
cal symptams af deep vein thrambasis. Baker's
cyst and deep vein thrombasis may caexist. A
venagram is aften necessary to. distinguish the
pathalagies.
A physician may demanstrate a cammuni­
cating Baker's cyst simply by injecting radi­
apaque dye into. the patient's knee jaint (fig­
ure 6). A cammunicatian is best seen after the
patient has exercised the knee jaint.
When a patient presents with a large, saft
mass an the pasteriar aspect af his ar her knee,
alSo. laak for papliteal aneurysm ar saft-tissue
Vol 20 • No. 2· February 92 • THE PHYSICIAN AND SPORTSMEDICINE
bursitis
tumor. These conditions are easily differentiated
by ultrasound or MRl. However, a biopsy may be
necessary to confirm the diagnosis of a soft-tis­
sue tumor.
Treatment. Aspiration and injection of a cor­
ticosteroid is the first line of treatment for a Bak­
er's cyst, but the results are usually disap­
pointing. Physicians must take care to avoid
neurovascular structures when aspirating the
fluid and injecting the medication.
Treatment of a chronic Baker's cyst caused by
meniscal pathology requires correction of the
underlying lesion. Meniscal derangement can
cause increased synovial fluid production, re­
sulting in increased intra-articular pressure. The
latter, in turn, can cause herniation through the
posteromedial capsule. Arthroscopic correction
of a meniscal tear is often sufficient to normalize
intra-articular pressure.
If cysts persist despite correcting the underly­
ing pathology, physicians can excise them and
carefully close any communication with the
knee joint. Postoperatively, physicians should
immobilize patients' knees in a slightly flexed
position for 3 to 4 weeks. The patient should
then begin a gradually progressive rehabilitative
program to restore strength and range of motion.
For congenital Baker's cysts in children, ob­
servation may be the best treatment; many re­
solve spontaneously.
Femur
r~r:;-: I~~-::"
Gastrocnemius
muscle (medial
head)
.'
Baker's cyst
Figure 5. Cross-sectional view of the knee showing a
common location for a Baker's cyst.
Hemorrhagic Adventitious Bursitis
As stated previously, adventitious bursae are
commonly found between bony prominences
and overlying soft tissue where friction is great:
for example, bursae seen in hallux valgus. Ad­
ventitious bursae may also form in the anterior
knee region between the skin and the extensor
mechanism following direct blunt trawna and
secondary organization of large hematomas.
Generally, hematomas undergo organization, ly­
sis, and resorption by the body. However, hema­
tomas around the knee undergo these changes
less readily than in other anatomic locations,
possibly because they are less exposed to sur­
rounding absorbent tissue and to the circulating
flow of blood.
Following direct blunt trauma to the anterior
Figure 6. A bursagram can demonstrate
communication between a bursa and the knee
joint. Here no communication is apparent.
THE PHYSICIAN AND SPORTSMEDICINE • Vol 20 • No. 2' February 92
..
bursitis
Direct, blunt trauma to the knee, such as that incurred in a collision or fall, may cause
posttraumatic hemorrhagic adventitious bursitis.
knee, blood pools between the skin, the superfi­
cial fascia, and the fascia investing the extensor
mechanism, particularly the retinaculum. A
large volume of this organizing clot may dissect
the fascia, forming a cleft. Repeated flexion and
extension of the knee can propel the clot cir­
cumferentially within the cleft, where it develops
a thick fibrous capsule or pseudosheath around
itself, forming a bursa. IS-I S With subsequent mi­
nor trauma, the newly developed adventitious
bursa may become more distended, probably as
a result of further hemorrhage into the bUrsa or
transudation of fluid from the surrounding tis­
sue. 12 The pseudosheath lining, like the inner
bursal lining in chronic bursitis, does not con­
tain any secretory cells.
Generally, traumatic bursae do not commu­
nicate with the joint, although one communi­
cating traumatic bursa has been reported. 19 Ra­
dioactive dye injected into the bursa and then
seen within the joint indicates disruption of the
underlying extensor mechanism.
Treatment. Early treatment of acute posttrau­
matic hemorrhagic adventitious bursitis involves
sterile aspiration and ice therapy to prevent fur­
ther bleeding and movement of the pooled
blood. Thepatient's knee should be compressed
and placed in a knee immobilizer in extension
for 1 to 2 weeks until healing is complete.
For patients who have chronic posttraumatic
hemorrhagic adventitious bursitis, the first line
of treatment should be aspiration followed by
injection of corticosteroids. If the fibrous sheath
has formed and fluid remains, surgical excision
may be indicated. Following excision, the physi­
cian should place a suction drain for 24 to 48
hours and immobilize the patient's knee in a
posterior splint in extension for at least 2 weeks.
In-Office Treatment
Most of the bursitic conditions that com­
monly affect athletes can be treated in the office
with aspiration, corticosteroids, and immobi­
lization. Specific treatment depends on the etiol­
ogy and pathogenesis of the condition. However,
initial diagnosis is paramount: Prompt, effective
treatment yields gratifying results at a low cost
and with little morbidity to the patient. It also
prevents the need-for further invasive proce­
dures. P9\II
Address correspondence to G. Charles Roland, MD, Or­
thopaedic Multispecialty Group of San Diego, 3565 Del
Rey St, Suite 302, San Diego, CA 92109.
Vol 20 • No.2' February 92 • THE PHYSICIAN AND SPORTSMEDICINE
r
bursitis
References
1. EllmanMH: Diagnosis and management of bursitis.
ComprTher 1984;10(8):14-20
2. Lagier R, Albert J: Bilateral deep infrapatellar bursitis
associated with tibial tuberosity enthesopathy in a
case of juvenile ankylosing spondylitis. Rheumatol
Int 1985;5(4):187-190
3. Mysnyk MC, Wroble RR, Foster 01; et al: PrepateUar
bursitis in wrestlers. Am J Sports Med 1986;14(1):46­
54
4. Taylor PW: Inflammation of the deep infrapatellar
bursa of the knee. Arthritis Rheum 1989;32(10):
1312-1314
5. Buckingham RB: Bursitis and tendinitis. Compr
Ther 1981;7(2):52-57
6. Cabaud HE: Nonligamentous problems-of the ath­
lete's lmee. Prim Care 1984;11 (1):89-100
7. Thun M, Tanaka S, Smith AB, et al: Morbidity from
repetitive knee trauma in carpet and floor layers. Br
J Industr Med 1987;44(9):611-620
8. Canoso JJ: Intrabursal pressures in the olecranon
and prepatellar bursae. J Rheumatol 19S0;7(4):570­
572
9. Smillie IS: Injuries of the Knee Joint, edA. Edin­
burgh, Churchill livingstone, 1970, p 358
10. Ho G Jr, Tice AD, Kaplan SR: Septic bursitis in the
prepatellar and olecranon bursa: an analysis of 25
cases. Ann Intern Med 1978;89(1):21-27
11. Quayle]B, Robinson MP: An operation for chronic
prepatellar bursitis. J Bone Joint Surg (Br) 1976;58­
B(4) :504-506
12. Sharrard WJ: Aetiology and pathology of beat lmee.
Brit J Industr Med 1963;20:24-31
13. Larsson LG, Baum J: The syndromes of bursitis. Bull
Rheum Dis 1986;36(1):1-8
14. Marquis AM: Pes anserine bursitis. ONA Journal
1978;6(10) :418-419
15. Kerlan RK, Glousman RE: Tibial collateral ligament
bursitis. Am J Sports Med 1988;16(4):344-346
16. Eskeland G, Eskeland T, Hovig T, et aJ: The ultra­
strucnue of normal digital flexor tendon sheath and
of the tissue formed around silicone and polyethyl­
ene implants in man. J Bone Joint Surg (Br) 1977;
59(2):206-212
17. Gelfand G, Birarenstock H: Hemorrhagic bursitis
and bone crisis in chronic adult Gaucher's disease: a
case report. Arthritis Rheum 1982;25(11):1369-1373
18. Vecchione TR!'Persistent post-traumatic pseu­
dosheath formation secondary to a movable orga­
nized blood cloo-JTrauma 1977;17(6):481 -482
19. Smason JB : Post-traumatic fistula connecting
prepatellar bursa;with lmee joint: report of a case. J
Bone Joint Surg (Am) 1972;54(7):1553-1554