Septic Bursitis in the Prepatellar and Olecranon Bursae An Analysis of 25 Cases GEORGE HO, Jr., M.D.; ALAN D. TICE, M.D.; and STEPHEN R. KAPLAN, M.D., F.A.C.P.; Providence,
Rhode Island
Five cases of septic prepatellar and 2 0 cases of septic olecranon bursitis are reported. All were men, with a mean age of 4 7 years. Seventeen had a history of recent trauma to the affected limb or sustained pressure on knees or elbows, or both, required by certain occupations. Septic bursitis was not associated with septic arthritis and could be easily distinguished from it by the characteristic bursal swelling and joint examination. Septic bursitis was misdiagnosed as nonseptic bursitis in eight cases despite characteristic bursal fluid leukocytosis ( > 1 0 0 0 cells/mm 3 ) and recovery of bacteria on culture. Staphylococcus aureus was identified in 22 cases; 7 6 % were resistant to penicillin. Intravenous antibiotics and bursal fluid drainage were uniformly successful. Oral antibiotic therapy was also successful unless the infection was extensive or there was underlying bursal disease. Early recognition, prompt therapy, and preventive measures are necessary to reduce the morbidity of septic bursitis.
T H E N U M E R O U S BURSAE of the body are subcutaneous
spaces lined with synovial membranes that secrete fluid to provide smooth and almost frictionless motion between contiguous muscles, tendons, bones, ligaments, and skin. Because of their superficial locations, the prepatellar and olecranon bursae are constantly at risk of being traumatized and becoming inflamed. The frequent occurrence of bursitis at these sites is exemplified by the use of such common terms as "housemaid's knee," "student's elbow," and in coal miners, "beat knee" and "miner's elbow." Occupational bursitis at deeper sites includes "weaver's bottom" and "waiter's shoulder." Bursae may also become inflamed without trauma, as in gout and rheumatoid arthritis (1). Our experience suggests that infections of bursae occur more frequently than the medical literature suggests. T h e only published series consisted of two cases of prepatellar bursitis (one due to Staphylococcus aureus, the other culture-negative) and four cases of olecranon bursitis (three due to S. aureus and one due to Streptococcus pneumoniae) (2). Single-case reports have included bursitis due to a variety of uncommon pathogens including Mycobacteri• From the subsections of Rheumatology and Infectious Disease of the Brown University Program in Medicine at the Providence Veterans Administration Hospital and the Roger Williams General Hospital; Providence, Rhode Island.
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um marinum (3), Sporothrix schenckii (4), and achloric algae (5). This report reviews five cases of septic prepatellar bursitis and 20 cases of septic olecranon bursitis with elaboration of their predisposing factors, clinical presentations, physical and laboratory findings, and results of treatment. Materials and Methods
Between July 1975 and September 1977, the authors saw six cases of septic bursitis at the Providence Veterans Administration Hospital and 11 cases at the Roger Williams General Hospital in Providence, Rhode Island. Data on eight additional cases were found by reviewing the bacteriology records at other Brown University-affiliated hospitals. All records were reviewed and, whenever possible, the patients were contacted for followup results. A diagnosis of septic bursitis was made on the basis of a positive culture or a positive Gram-stained smear of the bursal fluid. All fluid analyses were done by the respective hospital's laboratories. Culture techniques included plating the specimen on chocolate agar and inoculating it into thioglycollate broth. Antibiotic sensitivity testing was done by the standard Bauer-Kirby technique (6). In two cases, concentrations of antibiotics in serum and bursal fluid were measured by the agardiffusion method using trypticase soy agar seeded with Bacillus subtilis spores (7). Results
Twenty-five episodes of septic bursitis occurred in 24 patients. There were five cases of prepatellar bursitis and 20 cases of olecranon bursitis. One patient had olecranon bursitis (Patient 7), then later developed prepatellar bursitis (Patient 2). All 24 patients were men aged 17 to 84 years, with a mean of 47 years. PREDISPOSITION TO SEPTIC BURSITIS
In most cases there was a history of some associated disease, recent injury, or an occupation that involved frequent pressure on a bursa. Four of the five patients with septic prepatellar bursitis were engaged in work that produced frequent pressure on the prepatellar area (Table 1). They included a gardener, a carpet layer, a carpenter, and a stocker in a supermarket who knelt to place food items on lower shelves. Two of the five men (Patients 2 and 5) had both a recent injury and a history of chronic, work-related pressure on their knees. Of the 20 patients with septic olecranon bursitis, most had been engaged in work that predisposed to frequent trauma to the elbows, for example, gardening, plumbing, © 1978 American College of Physicians
21
Table 1. Septic Bursitis: Predisposing Factors and Duration of Symptoms
Patient
Age
Occupation
Recent Trauma *
Other Related Disorders
days
yrs Prepatellar 1 2
Duration of Symptoms Before Diagnosis f
Osteoarthritis of knees Previous prepatellar bursitis and septic olecranon bursitis None Chronic dyshidrotic eczema None
Knee laceration 14 days PTDx Knee abrasion 4 days PTDx None None Intrabursal steroid injection 14 days PTDx
N.R. 1 14
40
Laborer and glass cutter
Alcoholism
11
49
Custodian
Alcoholism
12
38
Janitor and bartender
13 14
37 58
Gymnastics instructor Unemployed
Chronic tophaceous gout with olecranon tophi, alcoholism, and liver disease None Gout and previous olecranon bursitis
15 16
60 49
Unemployed Unemployed
17
60
Unemployed draftsman
18
38
Unemployed
None Diabetes mellitus, previous olecranon bursitis, and schizophrenia Giant-cell arteritis treated with steroids, previous olecranon bursitis, and alcoholism Bacterial endocarditis and alcoholism
Not reported None Elbow injury followed by spontaneous bursal drainage 10 days PTDx Draining paronychia of middle digit of hand 5 days PTDx Infected forearm laceration 13 days PTDx Shallow cut over bursa 7 days PTDx Elbow injury followed by spontaneous bursal drainage 24 days PTDx None Minor scrape over bursa 3 days PTDx None None
3 N.R. 10
Salesman
Gout and uremia Previous prepatellar bursitis Chronic tophaceous gout with olecranon tophi, alcoholism, and mild azotemia None
19
30
Plumber
Former narcotics abuse
20
55
Retired truck driver
Erosive rheumatoid arthritis with olecranon nodules and mild azotemia
21
68
Retired plumber
22 23
51 44
Machine operator Security guard
Old injury to elbow with olecranon spur formation Gout None
24 25
48 50
Laborer Security guard
46 53
Clothes presser Gardener
19 17 23
Supermarket stocker Carpet layer Carpenter
84 53 57
Unknown Gardener Janitor
9
56
10
3 4 5 Olecranon 6 7 8
None Alcoholism, eczematoid dermatitis of hands with fissures
None Infected abrasion and cellulitis of hand 17 days PTDx Elbow abrasion during altercation 7 days PTDx Intrabursal steroids 6 weeks PTDx, spontaneous bursal drainage 2 days PTDx Abrasion over bursa 7 days PTDx None Excoriated pustule over bursa 1 day PTDx Elbow abrasion 2 days PTDx None
14 4
2 1 7 24 0 3 N.R. N.R. 1 17 7 2
7 6 1 2 1
* PTDx = before diagnosis. t N.R. = not recorded.
custodial work, and gymnastics (Table 1). Skin breakage in the form of a laceration, abrasion, or draining sinus over the olecranon bursa was evident in nine cases (Patients 8, 11, 12, 14, 19, 20, 21, 23, and 24), but only seven could recall the inciting injury. Four additional cases (Patients 9, 10, 18, and 25) had distal sites of infection. Other predisposing factors included olecranon gouty tophi in two patients and olecranon rheumatoid nodules in one. In addition to these three patients with bursal disease of known origin, three others had histories of previous olecranon bursitis of unknown cause (Patients 14, 16, and 17). Another patient (Patient 21) had a bony spur 22
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over the olecranon process secondary to an old injury. Additional factors among the patients with septic bursitis, which may have predisposed to bacterial infection, included steroid therapy for giant-cell arteritis (one case), alcoholism (seven cases), renal insufficiency (three cases), diabetes mellitus (one case), and intravenous narcotic abuse (one case). CLINICAL PRESENTATION
The duration of patient symptoms before diagnosis ranged from 1 to 14 days for prepatellar bursitis and as long as 24 days for olecranon bursitis (Table 1). The most 1
prominent symptoms on presentation were bursal swelling and pain, which were present in 100% and 92% of cases respectively. Two modes of onset were appreciated clinically. Eleven patients had an abrupt onset of intense symptoms (Patients 4, 6, 9, 10, 13, 17, 20, 22, 23, 24, and 25). These patients were frequently awakened from sleep because of pain or noted a rapid increase in pain during a few hours. In another nine patients the disease had a subacute onset (Patients 1, 2, 5, 8, 11, 12, 18, 19, and 21). These patients typically experienced mild symptoms shortly after some form of local trauma. This was followed in a few days by an increase in bursal swelling, redness, tenderness, and occasionally fever and chills. The duration of symptoms before diagnosis averaged 6 days in all the patients. The acute onset group experienced symptoms for an average of 2 days, and the subacute group 12 days before diagnosis. At the time of initial evaluation, four of the five patients with septic prepatellar bursitis were febrile with temperatures ranging from 38.2 °C to 38.9 °C. Prepatellar bursal swelling, pain, and tenderness were uniformly present. One patient had cellulitis around the bursa, and another had inguinal adenopathy. Of the five patients, three had infections of the right prepatellar bursa and two had infections of the left. Seven of the 20 patients with septic olecranon bursitis were febrile (38.5 °C to 40.3 °C). All cases had swollen bursae. Cellulitis was present in 74% of cases and regional adenopathy was documented in 25%. The two patients who denied pain and tenderness were diagnosed only when cultures showed bacterial growth. Ten infections involved the right olecranon bursa, and 10 involved the left. B U R S A L F L U I D ANALYSIS
Fluid was obtained from all infected bursae. Descriptions of fluid included: "serosanguinous," "purulent," "brown," "yellow turbid," "serous," "clear yellow," and "thick bloody pus." The amount of fluid removed was recorded in 20 cases. It ranged from a few drops to a maximum of 40 ml. In the patient with nodular rheumatoid arthritis and in both patients with tophaceous gout, a continuous drainage of fluid was observed at the time of diagnosis. Bursal fluid was examined for total leukocyte count and percentage of polymorphonuclear leukocytes (Table 2). The fluids that grew bacteria on culture had leukocyte counts from 1500 to 418 000 cells per mm 3 , with a mean of 77 236 cells per mm 3 . The percentage of polymorphonuclear leukocytes varied between 52% and 98%. After antibiotics were instituted and cultures became negative, repeat aspirations usually showed fewer cells than the initial taps (range, 4400 to 95 000 cells per mm 3 and mean of 21 712 cells per mm 3 ), but the percentage of polymorphonuclear leukocytes remained high (72% to 95%). Bursal fluid glucose measurements were done on three occasions. Values were found to be extremely low (4 and 15 mg/dl) in two cases and 55 mg/dl in one case (simultaneous serum glucose of 117 mg/dl). Birefringent crystals were found by compensated polarizing-light micros-
Table 2. Bursal Fluid Cell Count and Culture
Patient
4
6 9 10 11 13 14 15 21 22 23 24 25
Days on Antibiotics
Bursal Fluid Leukocytes
Polymorphonucleair Leukocytes *
0
cells/mm3 418 000
% 96
7 9 0 0 0 16 3 0 0 0 0 0 3 0 1 0 2 0 0 6 8
17000 11200 1500 44 800 16 800 7900 19 800 18000 5750 41500 8000 3400 95 000 300 000 262 000 6700 5100 3000 24 000 12 400 6000
72 83 90 97 86 90 93 95 N.R. 97 76 96 83 90 98 62 63 52 74 89 89
Culture
Staphylococcus aureus No growth No growth S. aureus S. aureus S. aureus No growth No growth S. aureus S. aureus S. aureus S. aureus S. aureus No growth S. aureus S. aureus S. aureus S. aureus S. aureus S. aureus No growth No growth
* N.R. = not recorded.
copy in the two cases in which chronic tophaceous gout had previously been established. Simultaneous serum and bursal fluid antibiotic levels were available in two patients taking oral antibiotics. Patient 24 was on dicloxacillin, 500 mg every 6 h. Ninety minutes after an oral dose, his serum dicloxacillin level was 2.5 jiLg/ml, and bursal fluid level was 1.2 jug/ml. Patient 25 received 500 mg of oral oxacillin every 6 h. After an oral dose, simultaneous serum and bursal fluid antibiotic levels were 6.5 and 5.3 juig/ml after 1 h, 5.0 and 4.7 jug/ml after 3 h, and 5.8 and 4.7 jxg/ml after 6 h on three separate days. BACTERIOLOGIC F I N D I N G S
The diagnosis of septic bursitis was made on the basis of a positive culture in 24 of the 25 cases. In one case (Patient 19) the diagnosis was based on the signs and symptoms of an infected bursa and the findings of Grampositive cocci on a smear of aspirated fluid. The culture did not grow an organism, presumably because oral antibiotic therapy had been started 7 days before bursal aspiration. Gram-stained smears of the initial bursal fluids were done in 23 cases; of these, only 15 were read as positive for bacteria. Of the 24 culture-positive cases, 22 grew 5. aureus. Of the other two cases, one patient with bacterial endocarditis had a group A, beta-hemolytic Streptococcus in both his olecranon bursa and his blood, and the other had both S. epidermidis and a group A, beta-hemolytic Streptococcus in fluid aspirated from a prepatellar bursitis near an infected laceration. Sixteen of the 21 strains of 5. aureus tested for antibiotic sensitivity were resistant to penicillin. All of the staphylococci were sensiHoetal. • Septic Bursitis
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23
Figure 1 . Elbow roentgenograms. Left. Normal. Right. Patient 2 3 . Note the soft-tissue density (arrows) outlining the inflamed olecranon bursa. The bony structures appear normal.
tive to methicillin, erythromycin, clindamycin, cephalothin, tetracycline, and chloramphenicol. Blood cultures (at least three in each patient) were done in 13 patients, but were positive only in the case with bacterial endocarditis. N o anaerobic bacteria were recovered from thioglycollate broth in any of these cases. OTHER LABORATORY F I N D I N G S
Blood leukocyte counts were done at the time of diagnosis in 23 cases. The counts ranged from 4400 to 22 900 leukocytes per mm 3 . A leukocytosis of more than 10 000 leukocytes per mm 3 was present in 14 cases. Westergren erythrocyte sedimentation rate was done within 2 days of diagnosis in nine cases. The mean was 43 m m / h with a range of 10 to 106 mm/h. Both the leukocyte count and the erythrocyte sedimentation rate returned toward normal with eradication of the infection. Radiologic examinations showed the characteristic soft-tissue density of a distended bursa without evidence of joint effusion (Figure 1). THERAPY A N D OUTCOME
Eight of 25 cases of septic bursitis were initially misdiagnosed and treated as nonseptic bursitis. All cases of septic bursitis required treatment with an antibiotic before a cure could be effected. The bacteria isolated were sensitive to the systemic antibiotics used in every case. All five cases of septic prepatellar bursitis were hospitalized and treated with intravenous antibiotics as soon as the diagnosis of infection was made. In Patients 1 and 3, incision and drainage of the infected bursae were done on the first day after diagnosis. They also received parenteral antibiotics for 3 and 4 days followed by oral drugs for 7 and 6 days, respectively. In the other three patients (Patients 2, 4, and 5), the bursae were not incised but were repeatedly aspirated for reaccumulation of fluid. An average of three aspirations was done in each case. The duration of parenteral antibiotic administration averaged 12.7 days followed by oral drug for 11.7 days. One patient (Patient 2) in the latter group received an intrabursal injection of cefazolin that resulted in intense local swelling and tenderness, which subsided after several days. All 24
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cases were without recurrences or residual symptoms after at least 10 months of follow-up. Patients with septic olecranon bursitis could be divided into three treatment groups, based upon initial treatment by their physician (Table 3). Group A patients were begun on parenteral antibiotics (Patients 6, 9, 10, 14, 18, 22, and 23). Group B patients failed to respond to initial oral antibiotics (Patients 8, 11, 12, 16, and 20). Group C responded to initial oral antibiotics (Patients 7, 13, 15, 17, 19, 21, 24, and 25). All group A patients were hospitalized and were usually given a supplemental course of oral antibiotics for variable time intervals. Three of these patients (Patients 9, 10, and 18) had sites of infection distal to the bursa. All group B patients were considered oral antibiotic failures because of clinical deterioration or lack of response while receiving oral medication. They all responded to subsequent parenteral therapy. Three group B patients (Patients 8, 12, and 20) had overt bursal disease from gout or rheumatoid arthritis. Also, one patient (Patient 16) of this group subsequently had a bursectomy done for chronic bursitis. Culture of bursal tissue at surgery showed no bacterial growth. For groups A, B, and C, durations of total antibiotic therapy averaged 23, 24, and 25 days, respectively, and the numbers of bursal aspirations averaged 2.7, 2.0, and 2.9, respectively. Other supportive measures used in the management of septic bursitis included analgesics and warm moist soaks. Discussion
In 1788, Monro (8) published A Description of All the Bursae Mucosae of the Human Body, which recognized over 140 bursae. Later Fullerton (9) described communications between the knee and several of its adjacent bursae with emphasis on their importance in the spread of infection. However, the prepatellar bursa is normally a closed space. Only in rare instances, such as traumatic fracture of the patella, has fistulization occurred between the prepatellar bursa and the knee joint (10). Bursography of the normal olecranon bursa delineates a self-contained potential space that does not communicate with the elbow joint (11). Thus, infection of either the prepatellar or olecranon bursa does not imply involvement of its respective joint, a point with therapeutic and prognostic import. This is in contrast to the involvement of the popliteal (Baker's) cyst in septic arthritis of the knee. Descriptions of infected bursae did not appear in the literature until the industrially compensable "beat" conditions were recognized in British coal miners. In the early 1950s Atkins and Marks (12) investigated these beat disorders of the knee and identified several factors that predisposed to infection: recent staphylococcal infections, a previous history of beat disorders, greasy skin, and a heavy growth of pathogenic staphylococci on the skin over the knee. They also noted that acute bursitis usually followed "either injury to the bursa (olecranon or prepatellar) or an extension to it of infection from an adjacent cellulitis" (12). Watkins and associates (13) postulated that most cases of simple acute bursitis in coal miners were due to trauma with hemorrhage into the bursa, which "occasionally became infected." Sharrard
(14) confirmed the rupture of large bursal blood vessels histologically and attributed it to the variable and often extremely high pressures measured over different parts of the knee during coal mining. True septic bursitis was thought to be rare and to be the result of a hemobursa that was secondarily infected from a nearby folliculitis or cellulitis (14). As modern industries became more interested in occupation-related disorders, awareness of workers' health and welfare effected improvement of working conditions and implementation of preventive measures against industrially related injuries and illnesses. The traditional occupational bursitis conditions were encountered less frequently; but their contemporary counterparts have begun to appear with the emergence of new technology. The association of artificial turf and increased frequency of traumatic bursitis in football players has been described (15). "Dialysis elbow" or hemorrhagic olecranon bursitis in uremic patients is believed to result from prolonged sustained pressure against the olecranon process during hemodialysis (16), although the anticoagulant effect of heparin and the arteriovenous communication might be contributing factors. The incidence of septic bursitis is not known, but it does not appear to be a rare disorder. In 1976, it accounted for 0.6 per 1000 admissions to the Roger Williams General Hospital and 1.2 per 1000 admissions to the Providence Veterans Administration Hospital. Septic bursitis is a disease of young and middle-aged men engaged in manual work. The male predominance cannot
Figure 2. Patient 2 3 . The distended bursa with desquamated skin is characteristic of septic olecranon bursitis.
Table 3. Septic Olecranon Bursitis: Treatment Groups and Clinical Features
Initial Parenteral Group A Treatment Patient number 7 Initial oral antibiotics (days) Parenteral antibiotics (days) 16.7 Follow-up oral antibiotics (days) 6.3 Total antibiotic therapy (days) 23.0 Number of aspirations (average) 2.7 Clinical features f Acute mode of onset 83% (5/6) Subacute mode of onset 17% (1/6) Fever 57% (4/7) Cellulitis 100% (7/7) Skin lesion 83% (5/6)
Oral Failure Group B 5
8
6.6
25.1
9.8
...
7.6
...
24.0
25.1
2.0*
2.9
25% (1/4) 67% (4/6) 75% (3/4) 33% (2/6) 40% (2/5) 12% (1/8) 80% (4/5) 43% (3/7) 80% (4/5) 50% (4/8)
* The three patients who had continuous bursal drainage were excluded. t Percentage based on (number present/number reported).
be solely accounted for by the Veterans Administration Hospital, because the majority of cases were encountered in community hospitals. Predisposition to trauma, be it accidental direct blows, inadvertent repetitive minor blows, or unnoticed constant pressure, appears to be the common denominator when occupations and other related disorders are taken into account (Table 1). Alcoholics are at risk of developing septic bursitis because of their propensity tp injury while intoxicated. A history of previous bursitis (present in four cases) probably reflects previous exposure to similar predisposing factors. As well as the element of injury, other factors such as steroid therapy, uremia, and diabetes mellitus may have increased the susceptibility of the host to infection. Local or distal skin disruption or infection was present in 58% of cases (Table 1). Bacterial seeding seemed likely in four cases (Patients 9, 10, 18, and 25) where distal sites of infection were evident on the affected extremity before the onset of bursal involvement. The patients with abrupt onset of symptoms had fewer identifiable skin lesions (6 of 10) than those with subacute onset (8 of 9). The subacute mode of onset presumably represented bacterial invasion of a previously traumatized bursa either by direct extension from a skin wound or via hematogenous spread. Even where visible skin wounds were not apparent, the avenue of bacteria introduction was still probably through the skin. The infected bursa was typically red, warm, tender, and tensely distended with a surrounding cellulitis (Figure 2). However, these physical findings may occur with gout or trauma and are not specific for infection. Regional adenopathy and fever were more specific but present in a minority of cases. The finding of a localized, fluctuant swelling over the patella or the olecranon process was often helpful in distinguishing septic bursitis from arthritis, in which the entire joint is inflamed. The patient with a bursal infection usually presented with his limb held in Hoetal. • Septic Bursitis
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Oral Success Group C
25
partial flexion. Joint motion, including rotation, was usually painless in septic bursitis except with full flexion and extension, which stretched and compressed the bursa. This contrasts sharply with septic arthritis, which produces pain with joint motion. Despite the characteristic clinical features of septic bursitis, eight of the 25 cases were initially misdiagnosed and treated as nonseptic bursitis. Aspiration of the inflamed bursa is the definitive diagnostic procedure and should be done in all cases of bursitis. Two cases in the present series (Patients 14 and 16) had painless bursal swelling and would have eluded correct diagnosis had aspiration not been done. On the other hand, the acute mode of onset in many bursitis cases may resemble an acute gouty attack. Although five cases had histories of gouty arthritis, sodium urate crystals were found only in the two with chronic tophaceous gout. Because the simultaneous occurrence of gout and infection in the same synovial space has been reported (17), all bursal fluid should be examined for urate crystals as well as cultured. In this series, the results of septic bursal fluid analysis generally paralleled those of synovial fluid from infected joints (18). Bacteria were seen on Gram-stained smears in only 65% of culture-positive bursal fluids. The leukocyte count in our culture-positive fluids was always greater than 1000 leukocytes per mm 3 , and usually more than 10 000 per mm 3 (Table 2). This is in contrast to the bursal fluid leukocyte count of traumatic nonseptic olecranon bursitis, which is usually less than 1000 cells/mm 3 (19). The low bursal fluid glucose levels are also clearly distinct from traumatic bursitis (19). The isolation of S. aureus from 22 of 24 cases is an interesting contrast to the recent report by Meislin and colleagues (20) who cultured S. aureus from only 38% of cases of cutaneous abscesses. The resistance to penicillin of the majority of the staphylococci isolated reflects the present sensitivities of pathogenic staphylococci (21), and should be considered in choosing initial antibiotic therapy. The bursal fluid antibiotic concentrations measured indicate that oral semisynthetic penicillins are able to penetrate bursal spaces and can reach levels near those in the serum. The levels obtained are well above the minimal inhibitory concentrations for the majority of strains of S. aureus (22). Intrabursal antibiotics were used in three cases without a clear indication of value but with an adverse reaction in Patient 2. Serial erythrocyte sedimentation rates and peripheral leukocyte counts, if initially elevated, were useful laboratory measurements that could be followed to substantiate clinical improvement. More specific indices of treatment effectiveness were the conversion of the bursal fluid cultures from positive to negative and the reduction in bursal fluid leukocyte concentration. Many different regimens of therapy were prescribed for the treatment of septic bursitis in the present series. The eight cases of olecranon bursitis that were initially misdiagnosed were inappropriately treated with either intrabursal corticosteroids or oral anti-inflammatory drugs (phenylbutazone or indomethacin). Intrabursal corticos25
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teroids delayed institution of antibiotics an average of 13 days. In contrast, there was a delay of only 4 days in those who received other anti-inflammatory drugs. We attribute the difference to the more potent effect of corticosteroids in suppressing the inflammatory response. Fortunately, there was no dissemination of infection and the end results were favorable in all cases when antibiotics were finally used. The three treatment groups (A, B, C) of septic olecranon bursitis were comparable in the duration of antibiotic therapy and the use of repeated aspirations to remove fluid (Table 3). Table 3 also gives a breakdown of the clinical features of the different groups. Group A patients were presumably treated with parenteral antibiotics initially because they were more likely to have a skin lesion with cellulitis and an acute onset of symptoms. All of these patients were cured with initial parenteral therapy. How many actually required the supplemental oral antibiotics is unknown. Patients of groups B and C were treated initially with oral antibiotics probably because they were clinically not as ill as the group A patients. The failure of oral drug treatment in group B may relate to a higher frequency of fever, skin lesions with cellulitis, and underlying bursal disease, as compared with group C. The case with rheumatoid nodules and the two cases with gouty tophi of the olecranon bursae were in group B. The oral failure cases were also more likely to have a subacute mode of onset, which may have made the physician believe the infection was not serious. The response of group C patients to oral antibiotics alone indicates that some patients can be treated as outpatients with oral drugs, despite an acute onset. Any decision regarding the type, route, and duration of treatment for septic bursitis must include consideration of the following factors: (a) underlying bursal disease, (b) rapidity of onset, (c) extent and severity of infection, (d) roentgenogram of the contiguous joint for evidence of fracture, and (e) examination of bursal fluid for crystals, leukocytes, and bacteria. The relative value of surgical drainage compared with repeated aspirations of a bursa, the route of antibiotic administration, and the duration of antibiotic therapy can only be assessed with prospective studies. In summary, septic bursitis is not as uncommon a disease as is indicated by published reports. We have delineated the likely predisposing factors, clinical spectrum, and laboratory findings in 25 cases, and outlined a diagnostic approach that includes a high index of suspicion based on occupational factors and a history of recent injury. In view of the bacteriologic findings, we recommend the initial use of a penicillinase-resistant semisynthetic penicillin after aspiration of the bursa for Gram stain and culture. Hospitalization and aggressive treatment with intravenous antibiotics are indicated in patients with extensive and underlying bursal disease. Adequate drainage of purulent fluid should be carried out in all patients with close follow-up, especially in outpatients on oral antibiotics. Interestingly, the two patients with cured septic prepatellar bursitis (the carpet layer and the carpenter) are wearing knee pads at their present jobs. Preventive mea-
sures are clearly indicated in those who are predisposed to bursitis by virtue of the work they do. These workers should also be encouraged to treat apparently minor lacerations and abrasions of the extremities seriously. ACKNOWLEDGMENTS: The authors thank Marjorie Stenberg, R.N., M.S., and Michael Turner, M.D., for help in editing, and Ms. Joan Sprague and Mrs. Dorothy Rosenberg for typing assistance. • Requests for reprints should be addressed to George Ho, Jr., M.D.; Veterans Administration Hospital; Davis Park; Providence R I 02908. Received 9 December 1977; revision accepted 11 April 1978.
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septic bursitis. J Florida Med Assoc 50:139-141, 1963 3. W I N T E R FE, R U N YON EH: Prepatellar bursitis caused by Mycobacterium marinum: case report, classification, and review of the literature. / Bone Joint Surg 47A:375-379, 1965 4. LEVINSKY WJ: Sporotrichial arthritis: report of a case mimicking gout. Arch Intern Med 129:118-119, 1972 5. NOSANCHUK JS, G R E E N B E R G RD: Protothecosis of the olecranon bursa caused by achloric algae. Am J Clin Pathol 59:567-573, 1973 6. B A U E R AW, K I R B Y W M M , SHERRIS JC, T U R C K M: Antibiotic suscep-
tibility testing by a standardized single disk method. Am J Clin Pathol 45:493-496, 1966 7. SABATH LD, M A T S E N JM: Assay of antimicrobial agents, in Manual of Clinical Microbiology, 2nd ed., edited by L E N N E T T E EH, SPAULDING EH, T R U A N T JP. Washington D.C., American Society of Microbiology, 1974
8. M O N R O A SECUNDUS: A Description of all the Bursae Mucosae of the Human Body. Edinburgh, Elliot, 1788 9. F U L L E R T O N A: The surgical anatomy of the synovial membrane of the knee joint. Br J Surg 4:191-200, 1916-17 10. SMASON JB: Post-traumatic fistula connecting prepatellar bursa with knee joint. J Bone Joint Surg 54A:1553-1554, 1972 11. W E S T O N WJ: The olecranon bursa. Aust Radiol 14:323-324, 1970 12. ATKINS JB, M A R K S J: The role of staphylococcal infection in beat disorders of miners. Br J Ind Med 9:296-302, 1952 13. W A T K I N S JT, H U N T TA, F E R N A N D E Z R H P , E D M O N D S OP: A clinical
study of beat knee. Br J Ind Med 15:105-109, 1958 14. SHARRARD WJW: Aetiology and pathology of beat knee. Br J Ind Med 20:24-31, 1963 15. LARSON RL, OSTERNIG LR: Traumatic bursitis and artificial turf. / Sports Med 2:183-188, 1974 16. C R U Z C, SHAH SV: Dialysis elbow: olecranon bursitis from long-term hemodialysis. JAMA 238:243, 1977 17. M C C O N V I L L E JH, POTOTSKY RS, C A L I A FM, PACHAS WN: Septic and
crystalline joint disease: a simultaneous occurrence. JAMA 231:841-842, 1975 18. GOLDENBERG DL, C O H E N AS: Acute infectious arthritis: a review of patients with nongonococcal joint infections. Am J Med 60:369-377, 1976 19. CANOSO JJ: Idiopathic or traumatic olecranon bursitis. Arthritis Rheum 20:1213-1216, 1977 20. M E I S L I N HW, L E R N E R SA, G R A V E S M H , M C G E H E E M D , K O C K A FE,
M O R E L L O JA, ROSEN P: Cutaneous abscesses. Ann Intern Med 87:145149, 1977 21. Ross S, RODRIGUEZ W, CONTRONI G, K H A N W: Staphylococcal susceptibility to penicillin G. JAMA 229:1075-1077, 1974 22. SABATH LD, G A R N E R C, W I L C O X C, F I N L A N D M: Susceptibility of
Staphylococcus ics. Antimicrob
aureus and Staphylococcus epidermidis to 65 antibiotAgents Chemother 9:962-969, 1976
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Rhode Island
Five cases of septic prepatellar and 2 0 cases of septic olecranon bursitis are reported. All were men, with a mean age of 4 7 years. Seventeen had a history of recent trauma to the affected limb or sustained pressure on knees or elbows, or both, required by certain occupations. Septic bursitis was not associated with septic arthritis and could be easily distinguished from it by the characteristic bursal swelling and joint examination. Septic bursitis was misdiagnosed as nonseptic bursitis in eight cases despite characteristic bursal fluid leukocytosis ( > 1 0 0 0 cells/mm 3 ) and recovery of bacteria on culture. Staphylococcus aureus was identified in 22 cases; 7 6 % were resistant to penicillin. Intravenous antibiotics and bursal fluid drainage were uniformly successful. Oral antibiotic therapy was also successful unless the infection was extensive or there was underlying bursal disease. Early recognition, prompt therapy, and preventive measures are necessary to reduce the morbidity of septic bursitis.
T H E N U M E R O U S BURSAE of the body are subcutaneous
spaces lined with synovial membranes that secrete fluid to provide smooth and almost frictionless motion between contiguous muscles, tendons, bones, ligaments, and skin. Because of their superficial locations, the prepatellar and olecranon bursae are constantly at risk of being traumatized and becoming inflamed. The frequent occurrence of bursitis at these sites is exemplified by the use of such common terms as "housemaid's knee," "student's elbow," and in coal miners, "beat knee" and "miner's elbow." Occupational bursitis at deeper sites includes "weaver's bottom" and "waiter's shoulder." Bursae may also become inflamed without trauma, as in gout and rheumatoid arthritis (1). Our experience suggests that infections of bursae occur more frequently than the medical literature suggests. T h e only published series consisted of two cases of prepatellar bursitis (one due to Staphylococcus aureus, the other culture-negative) and four cases of olecranon bursitis (three due to S. aureus and one due to Streptococcus pneumoniae) (2). Single-case reports have included bursitis due to a variety of uncommon pathogens including Mycobacteri• From the subsections of Rheumatology and Infectious Disease of the Brown University Program in Medicine at the Providence Veterans Administration Hospital and the Roger Williams General Hospital; Providence, Rhode Island.
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um marinum (3), Sporothrix schenckii (4), and achloric algae (5). This report reviews five cases of septic prepatellar bursitis and 20 cases of septic olecranon bursitis with elaboration of their predisposing factors, clinical presentations, physical and laboratory findings, and results of treatment. Materials and Methods
Between July 1975 and September 1977, the authors saw six cases of septic bursitis at the Providence Veterans Administration Hospital and 11 cases at the Roger Williams General Hospital in Providence, Rhode Island. Data on eight additional cases were found by reviewing the bacteriology records at other Brown University-affiliated hospitals. All records were reviewed and, whenever possible, the patients were contacted for followup results. A diagnosis of septic bursitis was made on the basis of a positive culture or a positive Gram-stained smear of the bursal fluid. All fluid analyses were done by the respective hospital's laboratories. Culture techniques included plating the specimen on chocolate agar and inoculating it into thioglycollate broth. Antibiotic sensitivity testing was done by the standard Bauer-Kirby technique (6). In two cases, concentrations of antibiotics in serum and bursal fluid were measured by the agardiffusion method using trypticase soy agar seeded with Bacillus subtilis spores (7). Results
Twenty-five episodes of septic bursitis occurred in 24 patients. There were five cases of prepatellar bursitis and 20 cases of olecranon bursitis. One patient had olecranon bursitis (Patient 7), then later developed prepatellar bursitis (Patient 2). All 24 patients were men aged 17 to 84 years, with a mean of 47 years. PREDISPOSITION TO SEPTIC BURSITIS
In most cases there was a history of some associated disease, recent injury, or an occupation that involved frequent pressure on a bursa. Four of the five patients with septic prepatellar bursitis were engaged in work that produced frequent pressure on the prepatellar area (Table 1). They included a gardener, a carpet layer, a carpenter, and a stocker in a supermarket who knelt to place food items on lower shelves. Two of the five men (Patients 2 and 5) had both a recent injury and a history of chronic, work-related pressure on their knees. Of the 20 patients with septic olecranon bursitis, most had been engaged in work that predisposed to frequent trauma to the elbows, for example, gardening, plumbing, © 1978 American College of Physicians
21
Table 1. Septic Bursitis: Predisposing Factors and Duration of Symptoms
Patient
Age
Occupation
Recent Trauma *
Other Related Disorders
days
yrs Prepatellar 1 2
Duration of Symptoms Before Diagnosis f
Osteoarthritis of knees Previous prepatellar bursitis and septic olecranon bursitis None Chronic dyshidrotic eczema None
Knee laceration 14 days PTDx Knee abrasion 4 days PTDx None None Intrabursal steroid injection 14 days PTDx
N.R. 1 14
40
Laborer and glass cutter
Alcoholism
11
49
Custodian
Alcoholism
12
38
Janitor and bartender
13 14
37 58
Gymnastics instructor Unemployed
Chronic tophaceous gout with olecranon tophi, alcoholism, and liver disease None Gout and previous olecranon bursitis
15 16
60 49
Unemployed Unemployed
17
60
Unemployed draftsman
18
38
Unemployed
None Diabetes mellitus, previous olecranon bursitis, and schizophrenia Giant-cell arteritis treated with steroids, previous olecranon bursitis, and alcoholism Bacterial endocarditis and alcoholism
Not reported None Elbow injury followed by spontaneous bursal drainage 10 days PTDx Draining paronychia of middle digit of hand 5 days PTDx Infected forearm laceration 13 days PTDx Shallow cut over bursa 7 days PTDx Elbow injury followed by spontaneous bursal drainage 24 days PTDx None Minor scrape over bursa 3 days PTDx None None
3 N.R. 10
Salesman
Gout and uremia Previous prepatellar bursitis Chronic tophaceous gout with olecranon tophi, alcoholism, and mild azotemia None
19
30
Plumber
Former narcotics abuse
20
55
Retired truck driver
Erosive rheumatoid arthritis with olecranon nodules and mild azotemia
21
68
Retired plumber
22 23
51 44
Machine operator Security guard
Old injury to elbow with olecranon spur formation Gout None
24 25
48 50
Laborer Security guard
46 53
Clothes presser Gardener
19 17 23
Supermarket stocker Carpet layer Carpenter
84 53 57
Unknown Gardener Janitor
9
56
10
3 4 5 Olecranon 6 7 8
None Alcoholism, eczematoid dermatitis of hands with fissures
None Infected abrasion and cellulitis of hand 17 days PTDx Elbow abrasion during altercation 7 days PTDx Intrabursal steroids 6 weeks PTDx, spontaneous bursal drainage 2 days PTDx Abrasion over bursa 7 days PTDx None Excoriated pustule over bursa 1 day PTDx Elbow abrasion 2 days PTDx None
14 4
2 1 7 24 0 3 N.R. N.R. 1 17 7 2
7 6 1 2 1
* PTDx = before diagnosis. t N.R. = not recorded.
custodial work, and gymnastics (Table 1). Skin breakage in the form of a laceration, abrasion, or draining sinus over the olecranon bursa was evident in nine cases (Patients 8, 11, 12, 14, 19, 20, 21, 23, and 24), but only seven could recall the inciting injury. Four additional cases (Patients 9, 10, 18, and 25) had distal sites of infection. Other predisposing factors included olecranon gouty tophi in two patients and olecranon rheumatoid nodules in one. In addition to these three patients with bursal disease of known origin, three others had histories of previous olecranon bursitis of unknown cause (Patients 14, 16, and 17). Another patient (Patient 21) had a bony spur 22
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over the olecranon process secondary to an old injury. Additional factors among the patients with septic bursitis, which may have predisposed to bacterial infection, included steroid therapy for giant-cell arteritis (one case), alcoholism (seven cases), renal insufficiency (three cases), diabetes mellitus (one case), and intravenous narcotic abuse (one case). CLINICAL PRESENTATION
The duration of patient symptoms before diagnosis ranged from 1 to 14 days for prepatellar bursitis and as long as 24 days for olecranon bursitis (Table 1). The most 1
prominent symptoms on presentation were bursal swelling and pain, which were present in 100% and 92% of cases respectively. Two modes of onset were appreciated clinically. Eleven patients had an abrupt onset of intense symptoms (Patients 4, 6, 9, 10, 13, 17, 20, 22, 23, 24, and 25). These patients were frequently awakened from sleep because of pain or noted a rapid increase in pain during a few hours. In another nine patients the disease had a subacute onset (Patients 1, 2, 5, 8, 11, 12, 18, 19, and 21). These patients typically experienced mild symptoms shortly after some form of local trauma. This was followed in a few days by an increase in bursal swelling, redness, tenderness, and occasionally fever and chills. The duration of symptoms before diagnosis averaged 6 days in all the patients. The acute onset group experienced symptoms for an average of 2 days, and the subacute group 12 days before diagnosis. At the time of initial evaluation, four of the five patients with septic prepatellar bursitis were febrile with temperatures ranging from 38.2 °C to 38.9 °C. Prepatellar bursal swelling, pain, and tenderness were uniformly present. One patient had cellulitis around the bursa, and another had inguinal adenopathy. Of the five patients, three had infections of the right prepatellar bursa and two had infections of the left. Seven of the 20 patients with septic olecranon bursitis were febrile (38.5 °C to 40.3 °C). All cases had swollen bursae. Cellulitis was present in 74% of cases and regional adenopathy was documented in 25%. The two patients who denied pain and tenderness were diagnosed only when cultures showed bacterial growth. Ten infections involved the right olecranon bursa, and 10 involved the left. B U R S A L F L U I D ANALYSIS
Fluid was obtained from all infected bursae. Descriptions of fluid included: "serosanguinous," "purulent," "brown," "yellow turbid," "serous," "clear yellow," and "thick bloody pus." The amount of fluid removed was recorded in 20 cases. It ranged from a few drops to a maximum of 40 ml. In the patient with nodular rheumatoid arthritis and in both patients with tophaceous gout, a continuous drainage of fluid was observed at the time of diagnosis. Bursal fluid was examined for total leukocyte count and percentage of polymorphonuclear leukocytes (Table 2). The fluids that grew bacteria on culture had leukocyte counts from 1500 to 418 000 cells per mm 3 , with a mean of 77 236 cells per mm 3 . The percentage of polymorphonuclear leukocytes varied between 52% and 98%. After antibiotics were instituted and cultures became negative, repeat aspirations usually showed fewer cells than the initial taps (range, 4400 to 95 000 cells per mm 3 and mean of 21 712 cells per mm 3 ), but the percentage of polymorphonuclear leukocytes remained high (72% to 95%). Bursal fluid glucose measurements were done on three occasions. Values were found to be extremely low (4 and 15 mg/dl) in two cases and 55 mg/dl in one case (simultaneous serum glucose of 117 mg/dl). Birefringent crystals were found by compensated polarizing-light micros-
Table 2. Bursal Fluid Cell Count and Culture
Patient
4
6 9 10 11 13 14 15 21 22 23 24 25
Days on Antibiotics
Bursal Fluid Leukocytes
Polymorphonucleair Leukocytes *
0
cells/mm3 418 000
% 96
7 9 0 0 0 16 3 0 0 0 0 0 3 0 1 0 2 0 0 6 8
17000 11200 1500 44 800 16 800 7900 19 800 18000 5750 41500 8000 3400 95 000 300 000 262 000 6700 5100 3000 24 000 12 400 6000
72 83 90 97 86 90 93 95 N.R. 97 76 96 83 90 98 62 63 52 74 89 89
Culture
Staphylococcus aureus No growth No growth S. aureus S. aureus S. aureus No growth No growth S. aureus S. aureus S. aureus S. aureus S. aureus No growth S. aureus S. aureus S. aureus S. aureus S. aureus S. aureus No growth No growth
* N.R. = not recorded.
copy in the two cases in which chronic tophaceous gout had previously been established. Simultaneous serum and bursal fluid antibiotic levels were available in two patients taking oral antibiotics. Patient 24 was on dicloxacillin, 500 mg every 6 h. Ninety minutes after an oral dose, his serum dicloxacillin level was 2.5 jiLg/ml, and bursal fluid level was 1.2 jug/ml. Patient 25 received 500 mg of oral oxacillin every 6 h. After an oral dose, simultaneous serum and bursal fluid antibiotic levels were 6.5 and 5.3 juig/ml after 1 h, 5.0 and 4.7 jug/ml after 3 h, and 5.8 and 4.7 jxg/ml after 6 h on three separate days. BACTERIOLOGIC F I N D I N G S
The diagnosis of septic bursitis was made on the basis of a positive culture in 24 of the 25 cases. In one case (Patient 19) the diagnosis was based on the signs and symptoms of an infected bursa and the findings of Grampositive cocci on a smear of aspirated fluid. The culture did not grow an organism, presumably because oral antibiotic therapy had been started 7 days before bursal aspiration. Gram-stained smears of the initial bursal fluids were done in 23 cases; of these, only 15 were read as positive for bacteria. Of the 24 culture-positive cases, 22 grew 5. aureus. Of the other two cases, one patient with bacterial endocarditis had a group A, beta-hemolytic Streptococcus in both his olecranon bursa and his blood, and the other had both S. epidermidis and a group A, beta-hemolytic Streptococcus in fluid aspirated from a prepatellar bursitis near an infected laceration. Sixteen of the 21 strains of 5. aureus tested for antibiotic sensitivity were resistant to penicillin. All of the staphylococci were sensiHoetal. • Septic Bursitis
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23
Figure 1 . Elbow roentgenograms. Left. Normal. Right. Patient 2 3 . Note the soft-tissue density (arrows) outlining the inflamed olecranon bursa. The bony structures appear normal.
tive to methicillin, erythromycin, clindamycin, cephalothin, tetracycline, and chloramphenicol. Blood cultures (at least three in each patient) were done in 13 patients, but were positive only in the case with bacterial endocarditis. N o anaerobic bacteria were recovered from thioglycollate broth in any of these cases. OTHER LABORATORY F I N D I N G S
Blood leukocyte counts were done at the time of diagnosis in 23 cases. The counts ranged from 4400 to 22 900 leukocytes per mm 3 . A leukocytosis of more than 10 000 leukocytes per mm 3 was present in 14 cases. Westergren erythrocyte sedimentation rate was done within 2 days of diagnosis in nine cases. The mean was 43 m m / h with a range of 10 to 106 mm/h. Both the leukocyte count and the erythrocyte sedimentation rate returned toward normal with eradication of the infection. Radiologic examinations showed the characteristic soft-tissue density of a distended bursa without evidence of joint effusion (Figure 1). THERAPY A N D OUTCOME
Eight of 25 cases of septic bursitis were initially misdiagnosed and treated as nonseptic bursitis. All cases of septic bursitis required treatment with an antibiotic before a cure could be effected. The bacteria isolated were sensitive to the systemic antibiotics used in every case. All five cases of septic prepatellar bursitis were hospitalized and treated with intravenous antibiotics as soon as the diagnosis of infection was made. In Patients 1 and 3, incision and drainage of the infected bursae were done on the first day after diagnosis. They also received parenteral antibiotics for 3 and 4 days followed by oral drugs for 7 and 6 days, respectively. In the other three patients (Patients 2, 4, and 5), the bursae were not incised but were repeatedly aspirated for reaccumulation of fluid. An average of three aspirations was done in each case. The duration of parenteral antibiotic administration averaged 12.7 days followed by oral drug for 11.7 days. One patient (Patient 2) in the latter group received an intrabursal injection of cefazolin that resulted in intense local swelling and tenderness, which subsided after several days. All 24
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cases were without recurrences or residual symptoms after at least 10 months of follow-up. Patients with septic olecranon bursitis could be divided into three treatment groups, based upon initial treatment by their physician (Table 3). Group A patients were begun on parenteral antibiotics (Patients 6, 9, 10, 14, 18, 22, and 23). Group B patients failed to respond to initial oral antibiotics (Patients 8, 11, 12, 16, and 20). Group C responded to initial oral antibiotics (Patients 7, 13, 15, 17, 19, 21, 24, and 25). All group A patients were hospitalized and were usually given a supplemental course of oral antibiotics for variable time intervals. Three of these patients (Patients 9, 10, and 18) had sites of infection distal to the bursa. All group B patients were considered oral antibiotic failures because of clinical deterioration or lack of response while receiving oral medication. They all responded to subsequent parenteral therapy. Three group B patients (Patients 8, 12, and 20) had overt bursal disease from gout or rheumatoid arthritis. Also, one patient (Patient 16) of this group subsequently had a bursectomy done for chronic bursitis. Culture of bursal tissue at surgery showed no bacterial growth. For groups A, B, and C, durations of total antibiotic therapy averaged 23, 24, and 25 days, respectively, and the numbers of bursal aspirations averaged 2.7, 2.0, and 2.9, respectively. Other supportive measures used in the management of septic bursitis included analgesics and warm moist soaks. Discussion
In 1788, Monro (8) published A Description of All the Bursae Mucosae of the Human Body, which recognized over 140 bursae. Later Fullerton (9) described communications between the knee and several of its adjacent bursae with emphasis on their importance in the spread of infection. However, the prepatellar bursa is normally a closed space. Only in rare instances, such as traumatic fracture of the patella, has fistulization occurred between the prepatellar bursa and the knee joint (10). Bursography of the normal olecranon bursa delineates a self-contained potential space that does not communicate with the elbow joint (11). Thus, infection of either the prepatellar or olecranon bursa does not imply involvement of its respective joint, a point with therapeutic and prognostic import. This is in contrast to the involvement of the popliteal (Baker's) cyst in septic arthritis of the knee. Descriptions of infected bursae did not appear in the literature until the industrially compensable "beat" conditions were recognized in British coal miners. In the early 1950s Atkins and Marks (12) investigated these beat disorders of the knee and identified several factors that predisposed to infection: recent staphylococcal infections, a previous history of beat disorders, greasy skin, and a heavy growth of pathogenic staphylococci on the skin over the knee. They also noted that acute bursitis usually followed "either injury to the bursa (olecranon or prepatellar) or an extension to it of infection from an adjacent cellulitis" (12). Watkins and associates (13) postulated that most cases of simple acute bursitis in coal miners were due to trauma with hemorrhage into the bursa, which "occasionally became infected." Sharrard
(14) confirmed the rupture of large bursal blood vessels histologically and attributed it to the variable and often extremely high pressures measured over different parts of the knee during coal mining. True septic bursitis was thought to be rare and to be the result of a hemobursa that was secondarily infected from a nearby folliculitis or cellulitis (14). As modern industries became more interested in occupation-related disorders, awareness of workers' health and welfare effected improvement of working conditions and implementation of preventive measures against industrially related injuries and illnesses. The traditional occupational bursitis conditions were encountered less frequently; but their contemporary counterparts have begun to appear with the emergence of new technology. The association of artificial turf and increased frequency of traumatic bursitis in football players has been described (15). "Dialysis elbow" or hemorrhagic olecranon bursitis in uremic patients is believed to result from prolonged sustained pressure against the olecranon process during hemodialysis (16), although the anticoagulant effect of heparin and the arteriovenous communication might be contributing factors. The incidence of septic bursitis is not known, but it does not appear to be a rare disorder. In 1976, it accounted for 0.6 per 1000 admissions to the Roger Williams General Hospital and 1.2 per 1000 admissions to the Providence Veterans Administration Hospital. Septic bursitis is a disease of young and middle-aged men engaged in manual work. The male predominance cannot
Figure 2. Patient 2 3 . The distended bursa with desquamated skin is characteristic of septic olecranon bursitis.
Table 3. Septic Olecranon Bursitis: Treatment Groups and Clinical Features
Initial Parenteral Group A Treatment Patient number 7 Initial oral antibiotics (days) Parenteral antibiotics (days) 16.7 Follow-up oral antibiotics (days) 6.3 Total antibiotic therapy (days) 23.0 Number of aspirations (average) 2.7 Clinical features f Acute mode of onset 83% (5/6) Subacute mode of onset 17% (1/6) Fever 57% (4/7) Cellulitis 100% (7/7) Skin lesion 83% (5/6)
Oral Failure Group B 5
8
6.6
25.1
9.8
...
7.6
...
24.0
25.1
2.0*
2.9
25% (1/4) 67% (4/6) 75% (3/4) 33% (2/6) 40% (2/5) 12% (1/8) 80% (4/5) 43% (3/7) 80% (4/5) 50% (4/8)
* The three patients who had continuous bursal drainage were excluded. t Percentage based on (number present/number reported).
be solely accounted for by the Veterans Administration Hospital, because the majority of cases were encountered in community hospitals. Predisposition to trauma, be it accidental direct blows, inadvertent repetitive minor blows, or unnoticed constant pressure, appears to be the common denominator when occupations and other related disorders are taken into account (Table 1). Alcoholics are at risk of developing septic bursitis because of their propensity tp injury while intoxicated. A history of previous bursitis (present in four cases) probably reflects previous exposure to similar predisposing factors. As well as the element of injury, other factors such as steroid therapy, uremia, and diabetes mellitus may have increased the susceptibility of the host to infection. Local or distal skin disruption or infection was present in 58% of cases (Table 1). Bacterial seeding seemed likely in four cases (Patients 9, 10, 18, and 25) where distal sites of infection were evident on the affected extremity before the onset of bursal involvement. The patients with abrupt onset of symptoms had fewer identifiable skin lesions (6 of 10) than those with subacute onset (8 of 9). The subacute mode of onset presumably represented bacterial invasion of a previously traumatized bursa either by direct extension from a skin wound or via hematogenous spread. Even where visible skin wounds were not apparent, the avenue of bacteria introduction was still probably through the skin. The infected bursa was typically red, warm, tender, and tensely distended with a surrounding cellulitis (Figure 2). However, these physical findings may occur with gout or trauma and are not specific for infection. Regional adenopathy and fever were more specific but present in a minority of cases. The finding of a localized, fluctuant swelling over the patella or the olecranon process was often helpful in distinguishing septic bursitis from arthritis, in which the entire joint is inflamed. The patient with a bursal infection usually presented with his limb held in Hoetal. • Septic Bursitis
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Oral Success Group C
25
partial flexion. Joint motion, including rotation, was usually painless in septic bursitis except with full flexion and extension, which stretched and compressed the bursa. This contrasts sharply with septic arthritis, which produces pain with joint motion. Despite the characteristic clinical features of septic bursitis, eight of the 25 cases were initially misdiagnosed and treated as nonseptic bursitis. Aspiration of the inflamed bursa is the definitive diagnostic procedure and should be done in all cases of bursitis. Two cases in the present series (Patients 14 and 16) had painless bursal swelling and would have eluded correct diagnosis had aspiration not been done. On the other hand, the acute mode of onset in many bursitis cases may resemble an acute gouty attack. Although five cases had histories of gouty arthritis, sodium urate crystals were found only in the two with chronic tophaceous gout. Because the simultaneous occurrence of gout and infection in the same synovial space has been reported (17), all bursal fluid should be examined for urate crystals as well as cultured. In this series, the results of septic bursal fluid analysis generally paralleled those of synovial fluid from infected joints (18). Bacteria were seen on Gram-stained smears in only 65% of culture-positive bursal fluids. The leukocyte count in our culture-positive fluids was always greater than 1000 leukocytes per mm 3 , and usually more than 10 000 per mm 3 (Table 2). This is in contrast to the bursal fluid leukocyte count of traumatic nonseptic olecranon bursitis, which is usually less than 1000 cells/mm 3 (19). The low bursal fluid glucose levels are also clearly distinct from traumatic bursitis (19). The isolation of S. aureus from 22 of 24 cases is an interesting contrast to the recent report by Meislin and colleagues (20) who cultured S. aureus from only 38% of cases of cutaneous abscesses. The resistance to penicillin of the majority of the staphylococci isolated reflects the present sensitivities of pathogenic staphylococci (21), and should be considered in choosing initial antibiotic therapy. The bursal fluid antibiotic concentrations measured indicate that oral semisynthetic penicillins are able to penetrate bursal spaces and can reach levels near those in the serum. The levels obtained are well above the minimal inhibitory concentrations for the majority of strains of S. aureus (22). Intrabursal antibiotics were used in three cases without a clear indication of value but with an adverse reaction in Patient 2. Serial erythrocyte sedimentation rates and peripheral leukocyte counts, if initially elevated, were useful laboratory measurements that could be followed to substantiate clinical improvement. More specific indices of treatment effectiveness were the conversion of the bursal fluid cultures from positive to negative and the reduction in bursal fluid leukocyte concentration. Many different regimens of therapy were prescribed for the treatment of septic bursitis in the present series. The eight cases of olecranon bursitis that were initially misdiagnosed were inappropriately treated with either intrabursal corticosteroids or oral anti-inflammatory drugs (phenylbutazone or indomethacin). Intrabursal corticos25
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• Annals of Internal Medicine • Volume 89 • Number 1
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teroids delayed institution of antibiotics an average of 13 days. In contrast, there was a delay of only 4 days in those who received other anti-inflammatory drugs. We attribute the difference to the more potent effect of corticosteroids in suppressing the inflammatory response. Fortunately, there was no dissemination of infection and the end results were favorable in all cases when antibiotics were finally used. The three treatment groups (A, B, C) of septic olecranon bursitis were comparable in the duration of antibiotic therapy and the use of repeated aspirations to remove fluid (Table 3). Table 3 also gives a breakdown of the clinical features of the different groups. Group A patients were presumably treated with parenteral antibiotics initially because they were more likely to have a skin lesion with cellulitis and an acute onset of symptoms. All of these patients were cured with initial parenteral therapy. How many actually required the supplemental oral antibiotics is unknown. Patients of groups B and C were treated initially with oral antibiotics probably because they were clinically not as ill as the group A patients. The failure of oral drug treatment in group B may relate to a higher frequency of fever, skin lesions with cellulitis, and underlying bursal disease, as compared with group C. The case with rheumatoid nodules and the two cases with gouty tophi of the olecranon bursae were in group B. The oral failure cases were also more likely to have a subacute mode of onset, which may have made the physician believe the infection was not serious. The response of group C patients to oral antibiotics alone indicates that some patients can be treated as outpatients with oral drugs, despite an acute onset. Any decision regarding the type, route, and duration of treatment for septic bursitis must include consideration of the following factors: (a) underlying bursal disease, (b) rapidity of onset, (c) extent and severity of infection, (d) roentgenogram of the contiguous joint for evidence of fracture, and (e) examination of bursal fluid for crystals, leukocytes, and bacteria. The relative value of surgical drainage compared with repeated aspirations of a bursa, the route of antibiotic administration, and the duration of antibiotic therapy can only be assessed with prospective studies. In summary, septic bursitis is not as uncommon a disease as is indicated by published reports. We have delineated the likely predisposing factors, clinical spectrum, and laboratory findings in 25 cases, and outlined a diagnostic approach that includes a high index of suspicion based on occupational factors and a history of recent injury. In view of the bacteriologic findings, we recommend the initial use of a penicillinase-resistant semisynthetic penicillin after aspiration of the bursa for Gram stain and culture. Hospitalization and aggressive treatment with intravenous antibiotics are indicated in patients with extensive and underlying bursal disease. Adequate drainage of purulent fluid should be carried out in all patients with close follow-up, especially in outpatients on oral antibiotics. Interestingly, the two patients with cured septic prepatellar bursitis (the carpet layer and the carpenter) are wearing knee pads at their present jobs. Preventive mea-
sures are clearly indicated in those who are predisposed to bursitis by virtue of the work they do. These workers should also be encouraged to treat apparently minor lacerations and abrasions of the extremities seriously. ACKNOWLEDGMENTS: The authors thank Marjorie Stenberg, R.N., M.S., and Michael Turner, M.D., for help in editing, and Ms. Joan Sprague and Mrs. Dorothy Rosenberg for typing assistance. • Requests for reprints should be addressed to George Ho, Jr., M.D.; Veterans Administration Hospital; Davis Park; Providence R I 02908. Received 9 December 1977; revision accepted 11 April 1978.
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Ho eta/. • Septic Bursitis
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