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Synovial fluid lactic acid in septic and nonseptic arthritis.

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1499
SYNOVIAL FLUID LACTIC ACID IN SEPTIC AND
NONSEPTIC ARTHRITIS
R. EUGENE ARTHUR, MARK STERN, MAURO GALEAZZI, ANDREW R. BALDASSARE,
TERRY D. WEISS. JOHN R . ROGERS, and JACK ZUCKNER
We determined lactic acid levels by the lactic
dehydrogenase method in synovial fluid of 41 patients
with various rheumatic diseases, to test the concept that
significantly elevated values were diagnostic of septic
arthritis. Nine patients had septic arthritis, 15 rheumatoid arthritis (RA), and the remainder miscellaneous
conditions. In another 9 patients with different rheumatic diseases, including 1 with septic arthritis, synovial
fluid lactic acid was determined by both the lactic
dehydrogenase and gas-liquid chromatography methods. There was a wide scatter of values among patients
with septic and nonseptic inflammatory arthritis, and
much overlap occurred. We could not differentiate
septic arthritis from RA on the basis of synovial fluid
lactic acid levels. Results were similar with both procedures for determining lactic acid levels.
A simple and rapid laboratory test to aid in the
diagnosis of infectious arthritis would prove most
valuable. The patient with acute monarticular arthritis
or the patient with an acute flare superimposed on a
chronically inflamed joint from another condition,
~
From the Division of Rheumatology, St. Louis University
School of Medicine, St. Louis, Missouri.
R. Eugene Arthur, MD: former Fellow, Division of Rheumatology (current address: McBride Clinic, Orthopedic and Arthritis Center, Oklahoma City, Oklahoma); Mark Stem, MD: former
Fellow. Division of Rheumatology; Mauro Galeazzi, MD: former
Fellow, Division of Rheumatology; Andrew R. Baldassare, MD:
Associate Professor of Medicine, Division of Rheumatology; Terry
D. Weiss, MD: Associate Professor of Medicine. Division of Rheumatology; John R. Rogers, MD: Medical Arts Laboratory, Oklahoma City. Oklahoma; Jack Zuckner, .MD: Clinical Professor of
Medicine, Director, Division of Rheumatology.
Address reprint requests to Jack Zuckner, MD, Division of
Rheumatology, St. Louis University School of Medicine, 1325
South Grand Boulevard, St. Louis, MO 63104.
Submitted for publication May 1, 1981; accepted in revised
form July 2 5 , 1983.
Arthritis and Rheumatism, Vol. 26, No. 12 (December 1983)
such as rheumatoid arthritis (RA), requires special
consideration for the possibility of an infected joint.
The diagnosis may be difficult to determine, however,
particularly when the synovial fluid (SF) is not typically purulent or the Gram stain and cultures of the SF
are negative. Since early treatment of a septic joint is
vital to prevent destruction of cartilage and other joint
structures, early diagnosis becomes essential.
Certain diagnostic parameters for infection in
an articulation include fever, characteristic elevation
of the white blood cell (WBC) count in SF, and
decreased levels of SF glucose. These findings are
often helpful, but they frequently overlap with those of
other arthritides (such as RA) where similar changes
may be present. In certain infectious conditions, such
as gonococcal arthritis and sepsis due to anaerobes
and fungi, and in cases of partially or inadequately
treated sepsis, the Gram stain and culture of SF may
be negative and thus misleading. A delay of 24-48
hours awaiting culture results adds to the therapeutic
dilemma even though antibiotics are usually administered when sepsis is strongly suspected.
In 1978 Brook et a1 (1) proposed that SF lactic
acid concentration could be used to differentiate between flares of acute monarticular arthritis due to
sepsis (nongonococcal) and other inflammatory and
noninflammatory conditions. They determined SF lactic acid concentration by gas-liquid chromatography
(GLC) and found significantly higher concentrations in
nongonococcal septic joints than in all other conditions. They were also able to follow 1 patient with
serial SF lactic acid determinations during therapy for
a pseudomonas infection in a joint, and they found that
recovery correlated with falling SF lactic acid concentrations.
1500
ARTHUR ET AL
Table 1. Lactic acid in synovial fluid: septic, nonseptic inflammatory, and noninflammatory arthritis
Diagnosis (no.)
Group 1, Septic (9)
S nrtrerrs (6)
P aerirginoso (1)
Negative culture (2)
Group 11, Inflammatory (26)
Rheumatoid arthritis (15)
GouVpseudogout (4)
Reiter's syndrome (3)
Scleroderma (1)
Systemic lupus erythematosus ( I )
Polymyositis (1)
Ankylosing spondylitis (1)
Group 111, Noninflammatory (6)
Average lactic
acid level (mg/
dl) 2 standard
deviation
53.6 t 13.8
61.2 ? 18.9
33.9
41.0
43.4 t 7.2
54.3 2 11.2
28.0
20.4
54.0
19.4
57.0
9.0
24.4 ? 3.7
Range
(mddl)
5-135
5-135
9.9-72
4-160
4.1-160
1542.4
4-36.2
17-38
In this study, the lactic dehydrogenase (LDH)
method of lactic acid determination was used to further evaluate the diagnostic significance of changes in
lactic acid concentration in SF. This procedure was
used since it is more readily available in most hospitals
than is the GLC technique utilized by Brook et a1 (I).
Comparative levels were also obtained from these 2
methods of determining lactic acid concentration in SF
in a limited number of patients.
polarized light microscopy; 3 of the latter had gout and 1
pseudogout. There were also 4 miscellaneous isolated cases
in this group. Group 111 comprised 6 patients with osteoarthritis (OA).
Synovial fluid was aspirated under sterile technique
by direct needle entry into the involved joint. No grossly
bloody fluids were obtained. Fluids were paired with concomitant blood samples for comparison. Studies performed
on S F included total WBC count with differential, glucose,
lactic acid, C'3, C'4, total protein, Gram stain and culture for
pyogenic organisms, and crystal analysis. Simultaneous
blood samples were obtained for WBC count with differential, glucose, C'3, C'4, total protein, and lactic acid. All
studies were performed before antibiotic therapy was started. Some joints had mutiple subsequent SF studies. Fiftyseven fluid samples were aspirated from the 41 patients.
Specimens for lactic acid determinations were placed
in test tubes containing 10 mg potassium oxalate and 10 mg
sodium fluoride. The tubes were placed on ice and processed
within a few hours on a Dupont Automatic Clinical Analyzer. Photometric absorbance was read at 340 nm by an Abbott
ABA- 100 spectrophotometer. This is the standard laboratory
LDH procedure for determining lactic acid concentration. In
addition, isolated S F specimens were collected in perchloric
acid (1 ml of 10% perchloric acid). Others were kept for 7296 hours on ice to test results as related to temporal factors
in handling of the SF. Addition of hyaluronidase (0.1 ml) to
another S F was followed by lactic acid determination to
evaluate complicating factors possibly due to the physical
viscosity of the samples.
r
PATIENTS AND METHODS
Patients in the Arthritis Clinical and Research Center
at St. Louis University Hospital with acute monarticular or
polyarticular arthritis were studied. There were 41 patients,
25 female and 16 male. They were divided into 3 groups:
patients in Group I had septic arthritis, Group I1 had
inflammatory, nonseptic arthritis, and Group I11 had noninflammatory arthritis. Table 1 shows the diagnosis and number of patients in each group. Seven of 9 patients in Group I
had positive SF cultures, 6 for Staphylococcus airreits and 1
for Pseudomonas arruginosa. Two patients who did not
have a positive culture were included in the septic group.
One was a 65-year-old patient with acute synovitis in both
knees who had a temperature elevation to 103"F, severe
obstipation with fecal impaction, and hypertension. S F
obtained from each knee revealed WBC counts of
54,000/mm3 and 67,000/mm3 and glucose values of 2 and 4
mg%, respectively. The second was a 60-year-old patient
with acute monarticular arthritis who had a fever of 102"F,
SF WBC count of 138,000/mm3, and SF glucose of 2 mg%.
Both patients responded to antibiotic therapy. The presentation and clinical course of these 2 patients suggested septic
arthritis, and therefore they were included in Group I.
Fifteen of the 26 patients in Group I1 had RA, and all 15 met
the American Rheumatism Association criteria for definite
or classic RA (2). Three individuals had Reiter's disease and
4 had crystal-induced synovitis confirmed by compensated
150 -
-0-E
125 -
2
100
OI
+
Y
-
0
.
5
P
3
75..
a
>
0
IA
>
50
25
.
-.
.
-
I
STAPH
AUREU
..
.
cr
ILE
I
.
I PM 1
AS
OA
7
SEPTlCARlHRITIS
INFLAMMITORY NONSEPllC I R l H R I l I S
IN-INFLAMMATO
ARTHRITIS
Figure 1. Synovial fluid lactic acid values. RA = rheumatoid arthritis; Crystal = gout and pseudogout; PSS = progressive systemic
sclerosis; SLE = systemic lupus erythematosus; PM = polymyositis; AS = ankylosing spondylitis; OA = osteoarthntis.
SYNOVIAL FLUID LACTIC ACID
1501
1.
1
I
1
150
0
0 GROUP1
SEPTIC
X GROUP I1 INFLAMMATORY, NON SEPTIC
0 GROUP Ill NONINFLAMMATORV
0
0
oia II
WBClmm’
,
20.000
40,000
60.000
80.000
100,000 200.000 300.000 400.000
I
500,000
Figure 2. Synovial fluid lactic acid levels compared with white
blood cell (WBC) counts.
The SF lactic acid concentration of an additional 9
patients was determined by the GLC method of Brook et al
(1) as well as the LDH method to compare values obtained
by these 2 procedures. In 1 patient, infectious arthritis was
due to Hemophilus paraitfluenzae. Four patients had RA
and 4 had isolated miscellaneous conditions.
One SF had an inoculum of Staphylococcus epidermidis added in vitro and cultured for 48 hours. This SF was
from a patient with juvenile arthritis. Determinations of
lactic acid were performed by each method both before and
after inoculation.
Recovery studies were performed by each method by
adding known amounts of lactic acid to another SF sample.
RESULTS
There was a wide scatter of SF lactic acid
values among patients with infectious and nonseptic
inflammatory arthritis when the LDH method was
used. Much overlap occurred in these groups, as
illustrated on the scattergram of Figure 1. Lactic acid
values in the 9 patients in Group I ranged 5-135 mg/dl
Table 2.
Synovial fluid laboratory results*
Patients (no.)
Septic arthritis (9)
Mean
Range
Inflammatory, nonseptic (26)
Mean
Range
Noninflammatory (6)
Mean
Range
* WBC
with an average of 53.6 mg/dl; 4 determinations were
higher than the average (135, 79, 76, and 72 mg/dl).
The pseudomonas-infected SF had a lactic acid value
of 33.9 mg/dl. The 26 patients in Group I1 had values
ranging 4-160 mg/dl with an average of 43.4 mg/dl; 12
fluids were higher than 43.4 mg/dl with an average of
74.3 mg/dl for these 12. Six patients in Group 111
averaged 24.4 mg/dl (2 values were higher, 33 and 38
mg/dl). Table 1 shows the lactic acid values for the 3
groups, giving both average and range of values.
Lactic acid values are also listed for specific diagnoses. RA patients had a mean SF lactic acid of 54.3
mg/dl compared with a mean of 61.2 mg/dl in patients
with infection due to S aureus. In infectious arthritis
only the initial lactic acid value before treatment is
shown, although multiple determinations were obtained
on the SF.
Statistical analysis using Student’s t-test
showed no significant difference among any of the 3
groups: P > 0.1 in all cases. Also, the subgroup of RA
patients and the subgroup of S aureus sepsis patients
were compared with each other and with the major
groups in their entirety. No significant differences
were found ( P > 0.5).
Although SF WBC counts tended to be higher
in the septic group, there was no significant relationship between SF lactic acid concentrations and SF
WBC counts. This is demonstrated in Figure 2.
All S F findings for these patients are given in
Table 2. SF complement (C’3 and C’4), total protein,
glucose, WBC count, and lactic acid are tabulated. No
significant correlation of the lactic acid values with
these other factors was found. Similar studies performed on the serum likewise did not correlate with
the SF lactic acid levels.
One of the patients with RA and superimposed
infection due to S aureus was followed with serial SF
=
Lactic acid
(rnddl)
WBC
(/rnrn’)
Polys
(%I
4.7
53.6
5-135
116.470
7.40&483,000
89
84-56
12t
1-46
I .7-8.2
56.7
2 1-94
34.5
2-95
43.4
4-160
14,700
2,200-50,000
77
1 1-96
66
5-127
4.4
2.8-8 .O
36.8
22-85
11.3
1.5-32
219
55-550
10
2-22
3.2
1.5-4.0
30.6
20-58
11.5
1 .6-24
24.4
17-38
75
59-86
white blood cells; polys = polyrnorphonuclear leukocytes.
I‘ Excludes 4 patients, 1 with diabetes and 3 on intravenous glucose solutions before synovial fluid was obtained.
ARTHUR ET AL
Table 4. Comparison of lactic dehydrogenase (LDH) and gasliquid chromatography (GLC) methods for lactic acid determinations in synovial fluid
I lw.ow
CLINDAMVCIN
- 80,000
- 60,000
5
n
Patient
Diagnosis
LA
EH
Rheumatoid arthritis
Septic (H parainjuenzae)
Rheumatoid arthritis
Osteoarthritis
Internal derangement
Rheumatoid arthritis
Juvenile arthritis
Systemic lupus erythematosus
Rheumatoid arthritis
x
A
LACTIC ACID
- 40,000
I
fS
5
10
20
15
25
30
Figure 3. Serial synovial lactic acid and white blood cell (WBC)
determinations in a patient with infectious arthritis due to Staphylococcus aureus.
aspirations throughout the course of therapy. Because
of penicillin hypersensitivity, the patient was treated
with clindamycin administered intramuscularly in a
dose of 600 mg every 8 hours over a period of 5 weeks;
he refused intravenous therapy. There was a gradual
decrease in both SF lactic acid and SF WBC counts,
but the lactic acid never reached very low levels. This
is demonstrated in Figure 3.
Table 3 demonstrates the effect on SF lactic
acid values of different procedures for collecting and
treating SF samples. Samples collected in perchlorate
gave only slightly higher lactic acid values than those
collected in fluoride-oxalate tubes. Allowing samples
to sit at room temperature or in the cold for 4 days
before lactic acid was determined resulted in only a
minor variation in the results. Thus, the temperature at
which the sample was stored made little difference in
the SF lactic acid value after the reaction was stopped
with fluoride-oxalate or perchlorate. Addition of hyaluronidase to 1 SF sample had no effect on the SF lactic
Table 3.
FB
LS
MW
JL
ME
MR
Studies on lactic acid levels in synovial fluid
have been reported previously. Several have been
Modification
no.
Day
Temperature,
collecting tubes,
and time factors
1
1
2
4
1
2
4
I
2
5
Room
Room
Room
Cold
Cold
Cold
Cold
Cold
Cold
1
1
Room
Room
3
H yaluronidase
With
Without
4
40
56
34
20
8
72.4
18
12
66
DISCUSSION
Temperature
2
41.4
49.5
21
17.1
9.9
66.6
23.4
19.8
63.9
acid value. The results produced by these modifications were in all instances relatively minor, resulting in
no important influence on the findings.
Comparisons between the LDH and GLC methods for SF lactic acid determination are shown in
Table 4. There were only minor differences in results
obtained by the 2 methods on a given SF. All SF
samples were handled in a like manner.
SF from 1 patient (JL) whose SF was inoculated
in vitro with S epiderrnidis had a higher lactic acid
level than the control (Table 5 ) . No important differences in results were noted by either method for other
SF samples handled in this manner.
Recovery studies are shown in Table 6 and
Figures 4 and 5 . Both methods had nearly linear slopes
with correlation coefficients of almost 1 and slopes
intersecting the origin.
Lactic acid in synovial fluid with modified collection and preparation techniques
Patient
GLC.
mg/100
ml
~~
YW
- 20.000
LDH,
mg/100
ml
Perchlorate
(mddl)
27
24
27
105
-
17
17
22
33
33
Fluorideoxalate
(mddl)
20
20
20
82
83
90
-
-
1503
SYNOVIAL FLUID LACTIC ACID
Table 5. In vitro study after synovial fluid inoculation with
Sruph.vlococcus epidermidis
LDH*
(mg1100 ml)
GLCt
(mg/100 ml)
24.4
52.5
20.5
49.6
Control
Cultured 48 hours
* Lactic dehydrogenase method.
t Gas-liquid chromatography method.
physiologic investigations of respiratory gases and
lactic acid concentration in SF in various disease
states. Cummings and Norby (3) demonstrated a significantly lower pH in the SF of RA patients compared
with normal subjects. Other investigators (4-7)
showed a decrease in pH of SF from patients with RA
usually associated with a diminished pOZ and increased pC02 and lactic acid. Similar findings have
been described in SF of patients with juvenile arthritis
(8). These alterations may be explained by increased
glucose utilization and conversion to pyruvic acid and
lactic acid under anaerobic conditions in the inflamed
synovium of RA.
The possibility that lactic acid levels in body
fluids might serve to distinguish infectious and noninfectious conditions received support from the finding
of lactic acid elevations in spinal fluid of patients with
meningitis (9-1 1). These increased levels of lactic acid
were utilized for early detection and monitoring of the
infectious process in the central nervous system. Metabolic studies by Buckingham et al (12) revealed that
extracts from gram-negative organisms, such as Escherichia coli and Salmonella typhosa, produced marked
in vitro fibroblast production of lactic acid as well as
increased hyaluronic acid formation and glucose utilization. Gram-positive cocci, yeast, and mycoplasma
had no such stimulatory capabilities. SF studies by
Brook et a1 (1) revealed significant differences in lactic
acid levels in septic arthritis compared with nonseptic
inflammatory and noninflammatory arthritides. It was
their impression that very high lactic acid levels in SF
of patients with nongonococcal septic arthritis could
differentiate these patients from those with other inflammatory and noninflammatory conditions. Subsequent studies by the same group (13) demonstrated the
presence of 2 peaks of relatively long retention time on
the gas-liquid chromatogram of SF from patients with
septic arthritis, including gonococcal arthritis. There
was some overlap with other inflammatory conditions,
however. These two peaks represented volatile substances which corresponded to the retention times of
n-valeric and n-hexanoic acid. Other techniques have
also been used for determining lactic acid in SF,
namely an enzymatic kit method (14-16) and a simplified GLC method (17). Results with these procedures
were similar to those of Brook et a1 ( l J 3 ) . Washington
(18) found, with an enzymatic assay, elevated levels of
lactate in SF of patients with septic arthritis and in
some cases of nonseptic inflammatory and noninflammatory conditions; low lactate levels were often found
in patients in the latter 2 groups, but not in the septic
cases. These results concur with ours since it was not
possible to differentiate infectious arthritis on the basis
of the elevated SF lactate levels.
Our data do not corroborate the findings of
Brook et a1 (1,13) and other investigators (14-17,1921) who reported that lactic acid elevations in SF are
diagnostic of infectious arthritis. In our studies utilizing the LDH method, there was a wide scatter of SF
lactic acid values and considerable overlap, especially
between septic arthritis and RA. Results in these 2
groups were not significantly different. The main differences between our study and that of Brook et a1 (1)
were in the method of stopping the reaction after
obtaining the SF samples and in the technical proce-
Table 6. Recovery study of lactic acid determined by both the lactic dehydrogenase (LDH) and gasliquid chromatography (GLC) methods
Added lactic acid
Measured concentration
concentration
(mg/100 ml)
LDH
(mg/100 ml)
GLC
(mg/100 ml)
None
6.25
12.5
25
20
32.4c
36.0
42.0
57.6
88.2
143. I
231.3
37.6*
44.0
50.0
73.2
79.0
125.8
238.9
100
200
Concentration adjusted for synovial
fluid diluent
* Baseline synovial fluid lactic acid before addition of lactic acid
LDH
(mg/100 ml)
3.6
12.6
25.2
55.8
110.7
198.9
G LC
(mg1100 ml)
6.4
12.4
35.6
41.4
88.2
201.3
1504
ARTHUR ET A L
LDH
GLC
Method
Method
200-
200-
180
-
P 120
-
f
a
0
Y
+
-
Regresson Lme y = 1 0 1 x
1.5
Correlation coefficient 0 9 9 8
40
80
120
160
200
Lactic Acid Added (mg1100 ml)
=
lactic dehydrogenase; GLC
dure for determining lactic acid concentrations. Their
study used 50% sulfuric acid to stop the reaction. Our
SF samples were collected in fluoride-oxalate tubes
and kept on ice until the test was performed. In
additional cases in our study. collections were also
made into tubes containing perchloric acid. Results
were comparable by both of the methods we used for
stopping pyruvate production, although SF lactic acid
P
L
+
Regression line y = 1 .Ox
2.8
Correlation coefiiciint 0.98
40
80
120
180
80
40
120
160
200
Lactlc Acid Added (mg1100 ml)
Figure 4. Lactic acid recovery studies. LDH
200
Regression line y=O.98x
0.14
Correlation coefficient 0 . 9 9 4
200
Lactic Acid by GLC Method (mg1100 ml)
Figure 5. Correlation of lactic acid recovery studies. LDH = lactic
dehydrogenase; GLC = gas-liquid chromatography.
=
gas-liquid chromatography
values were a little higher when stopped in perchloric
acid. Results were shown to be fairly stable over a
period of 72 hours on 3 SF tested for this purpose, but
most of our determinations were actually run within a
few hours of obtaining the SF samples. Thus, the
method of stopping pyruvate production and subsequent handling of SF had little effect on interpretation
of the results. It might be conjectured that the lack of
correlation between our study and others (1,13-17,1921) was a consequence of the different procedures
used for determining lactic acid concentration, that is,
GLC in most of the other studies and the standard
LDH procedure in our investigation. However, direct
comparison of these 2 methods on SF samples from 9
of our patients gave very similar results. Also, recovery studies were linear by both methods. Riordan and
coworkers (19) likewise found similar lactic acid values when comparing the LDH and GLC methods.
Since the LDH method is a reliable and regularly used
procedure for the determination of lactic acid concentration in many body fluids, it seemed a more appropriate technique to pursue for determining the levels in
synovial fluid. SF lactic acid elevations were thus not
a reliable indicator for differentiating septic arthritis
from nonseptic arthritides.
We are not able to account for the difference
between our results and others. The present state of
knowledge of mechanisms of lactic acid production
correlates with our findings. Inflamed synovial tissue,
whether due to infection or to an inflammatory non-
I505
SYNOVIAL FLUID LACTIC ACID
septic type of arthritis, theoretically should lead to
anaerobic conditions locally a n d result in an elevation
of lactic acid in both situations. T h e in vitro demonstration of glucose utilization and lactic acid production by fibroblasts in response t o bacterial extracts
occurred with gram-negative bacteria a n d , therefore,
would not apply here, since gram-positive bacteria
produced the bulk of joint infections in the present
study and others (1,13-21). Leukocyte breakdown
products and released enzymes causing increased lactic acid levels should not b e a factor since leukocyte
counts in the synovial fluid of our patients did not
correlate with lactic acid levels. None of the above
factors apparently produced lactic acid alterations
which could differentiate between septic a n d nonseptic
inflammatory arthritis.
9.
10.
11.
12.
13.
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Behn AR, Mathews JA, Phillips I: Lactate UV-system: a
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1981
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acid, septic, arthritis, synovial, nonseptic, fluid, lactic
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