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Idiopathic or Traumatic Olecranon Bursitis.

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1213
IDIOPATHIC OR TRAUMATIC
OLECRANON BURSITIS
CLINICAL FEATURES AND BURSAL FLUID ANALYSIS
JUAN J. CANOSO
Thirty cases of idiopathic olecranon bursitis were
studied. Most had previous local trauma. The process was
unilateral and often associated with nontender pitting
edema in cases of short duration. Ten patients exhibited a
bony spur at the olecranon process, and amorphous calcific deposits were seen in 6. The bursal fluid was hemorrhagic with a xanthochromic supernatant, and the mucin
clot test was poor or fair. Leukocyte count averaged
878/mm3, predominantly mononuclears. Many cells contained inclusion bodies. Glucose, total protein, and complement (C3) concentration averaged 80,60, and 60%of
the respective serum values.
Little information is available on the characteristics of bursal fluid (BF) in specific disease states, and
the most detailed study in human BF included samples
from superficial and deep bursae affected by various
disease processes (1). The present report describes the
clinical and BF findings in 30 consecutive patients with
the idiopathic or traumatic form of olecranon bursitis.
From the Arthritis and Connective Tissue Disease Section,
Boston University Medical Center, and the Medical Service, Boston
Veterans Administration Hospital.
Juan J. Canoso, M.D.: Assistant Professor of Medicine, Boston University School of Medicine, and Chief, Rheumatology Section,
Boston VA Hospital.
Address reprint requests to Juan J. C---so, M.D., Room
Avenue, Boston,
1OD-93, Boston VA Hospital, 150 South Huntink
Massachusetts 02130.
Submitted for publication December 21, 1976; accepted
March 22, 1977.
~
Arthritis and Rheumatism, Vol. 20, No. 6 (July-August 1977)
MATERIALS AND METHODS
All patients were seen by the author at the Boston
Veterans Administration Hospital between September 1974
and October 1976. AP and lateral radiographic studies of both
elbows were obtained. Bursa1 fluid was analyzed according to
standard techniques for synovial fluid (2). Glucose, total protein, bilirubin, lactic dehydrogenase (LDH), and urate (Technicon SM and Dupont ACA in small samples), as well as
complement (C3) by radial immunodiffusion (Hyland) were
determined in paired samples of serum and BF.
The following etiologies were excluded: gout, by a
negative search for crystals in sediment of spun BF; rheumatoid arthritis and other systemic rheumatic diseases, by absence of clinical criteria; and sepsis; by negative aerobic and
anaerobic cultures of the BF.
RESULTS
Table 1 lists the clinical and BF analysis findings.
All patients were male-a reflection of the hospital population. The bursal swelling had been noted for a median of 17 days; the range was 4 hours to 180 days.
Repetitive trauma, such as the habit of leaning on the
elbow, or a discrete blow to the olecranon process preceded the swelling in most cases. The bursal swelling was
unilateral in all and was usually painless and nontender.
Pitting peribursal edema extending down the posterior
aspect of the forearm (Figure 1) was present in 7 of 14
patients seen within 2 weeks of onset, and was absent in
those who consulted later (P < 0.01).
Radiographically, bony spurs that were often bilateral but smaller in the unaffected side were seen in 10
Table 1. Characteristics of Patients and Bursa1 Fluid in 30 Cases of Idiopathic or Traumatic Olecranon Bursitis (0s)
Volume
(ml)
Color/
Super.
17
5
D
14
15
65/M
D
20
8
4
48/M
D
90
11
5
79/M
No
14
15
6
56/M
No
4
1.5
7
50/M
R
35
10
8
53/M
R
17
3
9
62/M
R
30
9
10
63/M
R
2
5
11
43/M
R
6
8
12
43/M
No
Un
0.75
13
57/M
No
3
1.75
14
48/M
R
28
3
15
50/M
R
60
10
16
50/M
R
4hr
6
17
83/M
No
28
5
18
79/M
No
14
5
19
56/M
R
75
2
20
53/M
R
3
0.75
21
44/M
D,R
27
20
22
45/M
D
35
15
23
84/M
D
II
7
24
56/M
No
6
1.5
25
57/M
D,R
10
15
26
58/M
R
3
8
27
57/M
R
28
20
28
54/M
No
28
12
29
65/M
No
180
0.5
30
56/M
D
2
4
Bloody/
xantho
Bloody/
xantho
Bloody/
xantho
Pink/
xantho
Pink/
xantho
Straw/
straw
Pink/
xantho
Pink/
xantho
Pink/
xantho
Straw/
straw
Pink/
xantho
Bloody/
ND
Straw/
straw
Pink/
xantho
Pink/
xantho
Pink/
xantho
Pink/
xantho
Pink/
xantho
Pink/
xantho
Straw/
straw
Pink/
xantho
Pink/
xantho
Pink/
xantho
Bloody/
pink
Pink/
xantho
Pink/
xantho
Pink/
xantho
Pink/
xantho
Pink/
ND
Pink/
xantho
Patient
Age/
Sex
Previous Duration of
Trauma* OB(days)
1
39/M
D
2
51/M
3
*D: discrete; R: repetitive.
Viscosity
Much
Clot
WBC Mononuclear
(md)
Cells (9%)
Inclusion
Cells (96)
RBC
(md)
Decr
Poor
550
98
ND
39,000
Decr
Poor
1,150
40
85
14,400
Decr
Poor
200
98
60
27,000
Decr
Poor
50
100
50
14,800
Decr
Fair
250
93
100
9,300
Decr
Fair
500
98
10
1,100
Decr
Poor
1,300
98
100
36,900
Decr
Fair
3,400
36
50
8,600
Decr
Fair
700
88
30
208,000
Decr
Fair
900
95
10
1,050
Decr
Poor
50
100
100
7,150
Decr
Fair
ND
100
10
ND
Decr
Poor
1,140
88
10
450
Decr
Poor
250
100
10
28,200
Decr
Poor
300
100
50
2 1,450
Decr
Poor
200
100
50
28,800
Decr
Poor
850
100
30
192,000
Decr
Poor
700
100
15
88,000
Decr
Poor
4,700
70.
10
3 1.950
Decr
ND
I50
86
20
3.050
Decr
Poor
200
98
70
42,000
Decr
Poor
100
86
10
58,500
Decr
Poor
200
88
5
68,400
ND
Poor
800
34
0
Hct 25%
Decr
Poor
800
96
25
2 1.250
Decr
Poor
100
98
20
53.300
Decr
Poor
900
54
40
43,800
Decr
Poor
I50
92
40
42.950
Decr
Fair
3,450
80
90
22.000
Decr
Poor
1,100
16
60
49.400
OLECRANON BURSITIS
patients. Amorphous calcific deposits were found in 6 .
After drainage of the fluid the bottom of the bursa on
palpation was granular or nodular, with flat, hard nodules up to 5 mm in diameter.
The BF was pink or bloody and the supernatant
was xanthochromic. The white cell count (WBC) averaged 878/mm9 (range 504,700). Mononuclear cells predominated with an average of 84% (range 16-100). In
most fluids a high percentage of cells contained nonbirefringent, round cytoplasmic inclusion bodies. The
cytology of the fluid included lymphocytes and macrophages predominantly, the latter containing vacuoles
and inclusion bodies which stained gray, blue, or occasionally purple with the Wright-Giemsa stain. In some
instances erythrophagocytosis was noted. Larger mononuclear cells with a central nucleus and without inclusions, as well as polymorphonuclear cells with various degrees of nuclear degeneration, were also noted. In
5 specimens studied, hematoxylin-eosin, PAS, iron
(Mallory); and Sudan IV stains failed to stain the inclusion bodies. The erythrocyte count had a median of
28,800/mm3 and a range of 450 to a hematocrit of 25%.
Table 2 shows the results of glucose, total protein, bilirubin, LDH, urate, and complement (C3) determinations in BF and paired serum samples. Glucose and
protein values represented approximately 80% and 60%
of the corresponding serum values. Total bilirubin and
LDH were significantly higher in BF ( P < 0.01 by the t
test for paired samples). Bursa1 fluid complement represented 60% of concurrent serum values. Serum/BF protein and complement ratios were plotted and noted to
rise concomitantly with a linear regression coefficient of
0.81. Characteristics of the BF such as WBC, percentage
of polymorphonuclear cells, percentage of cells with
inclusions, and glucose and complement levels did not
correlate with duration of bursitis or presence of peribursal edema.
DISCUSSION
The most notable features in the present study
related to the characteristics of the bursal fluid. The
poor quality of the mucin clot, the modest elevation of
the bursal fluid WBC in which mononuclear cells predominated, the evidence of hemorrhage and hemolysis,
and the numerous cells with inclusion bodies delineated
a fairly constant and unique fluid pattern. Similar findings have been observed in the subcutaneous calcanceous bursitis of the horse (3) as well as in an earlier
study on human BF (1). Higher WBC and lower glucose
1215
Fig 1. Distention of the olecranon bursa and massive pitting edema of
forearm of Patient 24.
levels in the latter study may have been the result of the
inclusion of cases of rheumatoid arthritis.
Trauma and recurrent intrabursal hemorrhage
may have been involved in the pathogenesis of the
olecranon bursitis, as the history of the patients suggested. It is known that repeated intraarticular injection
of blood is followed by a chronic synovitis (4).Also, in
miners who were aspirated or operated immediately after the onset of prepatellar bursitis, the bursa was found
to be distended by blood ( 5 ) . Finally, surgical specimens
from patients with chronic bursitis revealed loss of cellu-
CANOSO
1216
Table 2. Glucose. Total Protein, Bilimbin. Lactic Dehydrogenase (LDH). Llrate. and Complement (C3)
in Paired Samples o j Bursal Fluid and Serum
Bursal Fluid
No.of
Observations
Average
SD*
Range
24
25
6
6
6
9
79
4.3
3.1
596
6.5
81
22
1.1
1.7
198
2.1
25
(42-125)
(2.3-6)
(1.2-5.6)
(400-875)
(4-9.6)
(45-115)
Serum
Average
SD
Range
~~~~
Glucose (mg/dl)
Total protein (g/dl)
Bilirubin (mg/dl)
LDH (mU/dl)
Urate (mg/dl)
Complement (C3) (mg/dl)
99
7
0.5
139
6.3
130
25
0.5
0.15
13
2.1
51.7
(75-192)
(6.1-7.8)
(0.3-0.7)
(120-160)
(4.2-9.5)
(56-225)
* Standard deviation.
lar lining, necrosis, and fissuring of the bursal membrane that would certainly favor recurring bleeding
upon application of tangential forces (6). A possible
alternative or contributory role of hydroxyapatite crystals on the pathogenesis of the olecranon bursitis cannot
be excluded within the context of the present study.
However the purple inclusion bodies noted in the arthritis associated with hydroxyapatite crystals were uncommon (7), amorphous calcific deposits were present in
only 6 patients, and the extracellular, nonbirefringent
round bodies described in calcific (hydroxyapatite) periarthritis (8) were not seen.
There is a structural resemblance between bursal
and synovial membrane (9,lO) and both can be involved
in disease processes such as trauma, infection, gout, and
rheumatoid arthritis (10). However certain characteristics in the BFs studied-such as the poor quality of the
mucin test-were at variance with findings in hemorrhagic traumatic arthritis (1 1 ), suggesting a substantial
biologic difference between subcutaneous bursae such as
the olecranon bursa, and synovial joints and their bursal
expansions.
ACKNOWLEDGMENTS
The author is indebted to Mary A. Lambert, B.S.,
from the Department of Pathology, for expert technical assistance in preparing special stains, to the Medical Illustration
Department for photographic assistance, to Dr. G. Peterson
for patient referral, and to Drs. Alan S. Cohen and Kenneth
D. Brandt for encouragement and helpful suggestions.
REFERENCES
1. Rope, MW, Bauer W: Synovial Fluid Changes in Joint
Disease. Cambridge, Harvard University Press, 1953, pp
120-121
2. Cohen AS, Brandt KD, Krey PR: Synovial fluid, Laboratory Diagnostic Procedures in the Rheumatic Diseases.
Second edition. Edited by AS Cohen. Boston, Little,
Brown and Company, 1975, pp 1-62
3. Van Pelt RW, Riley WF Jr: Traumatic subcutaneous calcaneal bursitis (capped hock) in the horse. J Am Vet Med
ASSOC153:1176-1180, 1968
4. Roy S, Ghadially FN: Synovial membrane in experimentally-produced chronic hemarthrosis. Ann Rheum Dis
28:402-414, 1969
5. Sharrard WJW: Pressure effects on the knee in kneeling
miners. Ann R Coll Surg Engl 36:309-324, 1965
6. Rubens-Duval A: L’hygroma: rkvision histologique. Rev
Rhum Ma1 Osteoartic 39:183-187, 1972
7. Schumacher HR Jr, Tse R, Reginato AJ, et al: Hydroxyapatite-like crystals in synovial fluid cell vacuoles: a
suspected new cause for crystal-induced arthritis. Arthritis
Rheum 19:821, 1976 (abstr)
8. McCarty DJ Jr, Gatter RA: Recurrent acute inflammation associated with focal apatite crystal deposition. Arthritis Rheum 9:804-8 19, 1966
9. Becker W, Rauterberg K: Zur Mikromorphologie auskleidender Gewebe der Bursa. Arch Orthop Unfallchir
68: 197-203, 1970
10. Bywaters EGL: The bursae of the body. Ann Rheum Dis
24:215-218, 1965
11. Ropes MW, Bauer W: Synovial Fluid Changes in Joint
Disease. Cambridge, Harvard University Press, 1953, pp
78-82
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