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  • Research article
  • Open Access

Clinical characteristics of pyogenic spondylitis and psoas abscess at a tertiary care hospital: a retrospective cohort study

Journal of Orthopaedic Surgery and Research201813:302

https://doi.org/10.1186/s13018-018-1005-9

  • Received: 16 June 2018
  • Accepted: 15 November 2018
  • Published:

Abstract

Background

Psoas abscess and pyogenic spondylitis are intractable diseases that require long-term treatment, but the clinical characteristics and causative organisms have not been fully investigated. Herein, we describe the clinical characteristics of these diseases and evaluate the factors associated with in-hospital mortality and the presence of gram-negative rods as causative microorganisms.

Methods

All patients diagnosed with pyogenic spondylitis or psoas abscesses at a tertiary hospital were included. We retrieved the clinical data (age, sex, outcome, length of hospital stay, disease, bacteria, medication, comorbidities, and treatment status), vital signs (blood pressure, heart rate, and body temperature), and laboratory test results (blood cell count, liver function, renal function, electrolytes, blood sugar, and C-reactive protein) of all patients. The outcomes were in-hospital deaths and positive cultures of gram-negative rods.

Results

We analyzed 126 patients consisting of 69 (55%) men with a population mean age of 72 years. Seventy-two patients had pyogenic spondylitis and 54 had psoas abscesses. Eleven patients (8.3%) died during admission. The causative bacteria were gram-positive cocci in 63 patients (50%) and gram-negative bacteria in 19 patients (15%). The multivariate logistic model showed that blood urea nitrogen (BUN) (odds ratio [OR] 1.04, 95% confidence interval [CI] 1.02–1.06) and cardiovascular diseases (OR 7.02, 95% CI 1.55–31.8) were associated with in-hospital mortality. Platelets less than 150,000/μL (OR 3.14, 95% CI 1.02–9.65) and higher aspartic aminotransferase (OR 1.02, 95% CI 1.00–1.03) were associated with gram-negative rods.

Conclusions

Patients with suspected psoas abscesses or pyogenic spondylitis having a high BUN level and a history of cardiovascular diseases have a higher risk of mortality.

Keywords

  • Pyogenic spondylitis
  • Psoas abscess
  • Mortality

Background

Pyogenic spondylitis and psoas abscesses are caused by Staphylococcus aureus, often in areas with a low prevalence of tuberculosis [13]. Patients often have underlying diseases such as malignancies, diabetes mellitus, chronic renal failure, and cirrhosis, as well as long-term corticosteroid use [48]. These diseases are diagnosed using a combination of imaging techniques such as computed tomography (CT) or magnetic resonance imaging (MRI) and specimen cultures; however, diagnosis may often be difficult if the patient has few symptoms.

While some studies have reported the underlying diseases associated with pyogenic spondylitis and psoas abscesses [48], few have discussed the risk factors for a poor prognosis. It is also important to decide whether to administer antibiotics targeting gram-negative rods because bacteria other than Staphylococcus should be considered in some circumstances. Because clinical characteristics and risk factors associated with mortality or bacterial strains have not been well investigated, we described the clinical characteristics of patients with pyogenic spondylitis and psoas abscesses and investigated the factors associated with in-hospital deaths and the presence of gram-negative rods at the time of diagnosis. In addition, we compared the differences in clinical characteristics and outcomes between pyogenic spondylitis and psoas abscess, if any.

Methods

Study design and patients

We conducted a historical cohort study of all patients diagnosed with pyogenic spondylitis or psoas abscesses from 2000 to 2014 at Shimane Prefectural Central Hospital, a tertiary care hospital in Japan. Inclusion criteria were (1) patients who were diagnosed with pyogenic spondylitis or psoas abscesses by the physician in charge, (2) confirmation of the clinical diagnosis by radiological images, and (3) no apparent other causes that may mimic pyogenic spondylitis or psoas abscesses. There were no exclusion criteria. The diagnosis of pyogenic spondylitis and psoas abscess was confirmed using either CT or MRI. Bacteria associated with lesions or blood cultures were identified. Surgical interventions, such as percutaneous drainage, surgical drainage, and laminectomy, were determined by the physician in charge. The antimicrobial treatment was determined by the physician in charge based on the culture results and sensitivity analyses. Until the culture results were available or if the causative species could not be determined, empirical treatments based on established guidelines were administered.

We retrieved clinical data, vital signs, and laboratory test results of the patients from the Integrated Intelligent Management System database of Shimane Prefectural Central Hospital between August 1998 and August 2014. The Institutional Review Board of Shimane Prefectural Central Hospital approved this study. Since all data were obtained as part of our routine daily practice, informed consent was waived by the institutional review board.

Measurements

Clinical data included age, sex, the primary complaint, days from admission to diagnosis of pyogenic spondylitis or psoas abscess, and comorbidities (diabetes, hypertension, hyperlipidemia, cardiac disease, cerebrovascular disease, neurological disease, liver disease, renal disease, malignancy, and surgical history).

We also collected data regarding patient vital signs (systolic blood pressure [SBP], diastolic blood pressure [DBP], heart rate, and body temperature) and laboratory test results (white blood cell count [WBC], hemoglobin, platelet cell count [Plt], C-reactive protein [CRP], aspartic aminotransferase [AST], alanine aminotransferase [ALT], blood sugar, serum albumin [Alb], total bilirubin, lactate dehydrogenase [LDH], blood urea nitrogen [BUN], creatinine [Cr], sodium, and potassium) at the time of diagnosis.

We also collected data regarding treatment modalities (intravenous antimicrobial use and surgical treatments), as well as in-hospital deaths and the length of time in the hospital.

Statistical analyses

Continuous variables are presented as the mean and standard deviation (SD) or median and interquartile range (IQR), and categorical variables as numbers and percentages. We compared continuous variables with the Student’s t test or the Wilcoxon rank-sum test on the basis of the distributions. We compared categorical variables with the χ2 test when appropriate; otherwise, we used Fisher’s exact test. To explore the factors associated with in-hospital mortality and the presence of gram-negative rods, we constructed multivariate logistic regression models. We analyzed all patients to identify factors associated with in-hospital mortality but selected only culture-positive patients to investigate the factors associated with gram-negative rods.

Included continuous variables were unmodified; however, the units for WBCs and Plts were 100 and 10,000, respectively. For convenience, platelets were only analyzed if less than 150,000/μL. Potential variables were the measured clinical variables described above, and final models were determined after backward selection. Associations are expressed as odds ratio [OR] and 95% confidence intervals [CI]. All statistical analyses were performed using Stata12. All reported p values were two-tailed, and p values < 0.05 were considered statistically significant.

Results

Patient characteristics

A total of 126 patients (72 with pyogenic spondylitis [57%] and 54 with psoas abscesses [43%]) (Table 1) were studied. Their mean age was 72 ± 11 years (range 37–95 years). The number of male patients was 69 (55%). Lumbago or back pain was more frequent in pyogenic spondylitis (49 [68%] vs. 23 [43%], p = 0.004), whereas shock was more frequent in psoas abscesses (9 [17%] vs. 2 [2.8%], p = 0.009) (Table 1).
Table 1

Patients characteristics

 

All

Pyogenic spondylitis

Psoas abscess

p value

n = 126

n = 72

n = 54

Variables

n (%) or mean ± SD or median [IQR]

 

Male

69 (55)

38 (53)

31 (57)

0.61

Age, year

72 ± 11

74 ± 10

70 ± 11

0.07

Length of stay, days

60 [39–97]

60 [41–106]

58 [36–94]

0.06

In-hospital death

11 (8.7)

3 (4.1)

8 (15)

0.05

Invasive interventions

54 (43)

25 (35)

29 (54)

0.045

 Percutaneous drainage

50 (40)

21 (29)

29 (54)

0.006

 Operation

6 (4.8)

5 (6.9)

1 (1.9)

0.24

  Laminectomy

4 (3.2)

4 (5.6)

0 (0.0)

0.13

  Surgical drainage

2 (1.6)

1 (1.4)

1 (1.9)

1.00

Days after admission to diagnosis, day

0 [0–11]

0 [0–5]

2 [0–20]

0.0167

Days after admission to diagnosis, day ≥ 14 days

28 (22)

10 (14)

18 (33)

0.016

Antibiotics use, days

28 [17–42]

28 [18–42]

30 [15–42]

0.79

 Over 6 weeks

38 (30)

23 (32)

15 (28)

0.70

Symptoms

 Lumbago or back pain

72 (57)

49 (68)

23 (43)

0.004

 Fever

51 (40)

32 (44)

19 (35)

0.30

 Shock

11 (8.7)

2 (2.8)

9 (17)

0.009

Classification

 Type A*

33 (46)

 Type B*

18 (25)

 Type C*

21 (29)

 Multiple abscesses

30 (56)

Co-morbidities

102 (81)

56 (78)

46 (85)

0.36

Hospitalized for comorbidity

57 (45)

27 (38)

30 (56)

0.044

Hospitalized for other infections

17 (13)

6 (8.3)

11 (20)

0.07

Bacterial detection

84 (67)

45 (63)

39 (72)

0.34

 Gram-positive cocci

63 (50)

35 (49)

28 (52)

0.72

 Gram-negative rods

19 (15)

8 (11)

11 (20)

0.15

 Mycobacterium

2 (1.6)

2 (2.8)

0 (0.0)

0.51

Vital signs

 SBP, mmHg

132 ± 31

137 ± 28

127 ± 35

0.10

 DBP, mmHg

75 ± 18

78 ± 15

70 ± 20

0.0151

 Body temperature,  °C

37.3 ± 1.1

37.4 ± 1.1

37.2 ± 1.1

0.27

 Heart rate, /min

89 ± 19

88 ± 19

89 ± 19

0.30

Laboratory data

 WBC, × 102/μL

113 ± 51

106 ± 41

122 ± 61

0.07

 Hb, g/dL

11.3 ± 2.2

11.7 ± 1.8

10.7 ± 2.5

0.0116

 Plt, × 104/μL

22.8 ± 11.8

24.8 ± 11.5

20.0 ± 11.9

0.0234

 CRP, mg/dL

11.1 ± 9.8

9.4 ± 8.4

13.3 ± 11.0

0.0233

 T-bil, mg/dL

0.8 ± 0.5

0.8 ± 0.4

0.8 ± 0.5

0.75

 Alb, g/dL

3.3 ± 0.6

3.4 ± 0.6

3.1 ± 0.7

0.0045

 AST, IU/L

33 ± 30

31 ± 28

37 ± 31

0.26

 ALT, IU/L

26 ± 23

26 ± 25

24 ± 19

0.73

 LDH, IU/L

261 ± 123

239 ± 88

290 ± 153

0.0233

 Blood sugar, mg/dL

152 ± 71

141 ± 66

165 ± 76

0.06

 BUN, mg/dL

25.6 ± 22.8

20.9 ± 10.6

32.0 ± 32.0

0.0069

 Cr, mg/dL

1.3 ± 1.7

1.0 ± 0.8

1.7 ± 2.5

0.0178

 Na, mmol/L

137.0 ± 5.0

137.2 ± 5.1

136.7 ± 4.8

0.57

 K, mmol/L

4.0 ± 0.6

4.0 ± 0.5

3.9 ± 0.7

0.42

*Classification by Pola et al. [17]

All 126 patients received antibiotic treatment. One patient received only oral antibiotics. A total of 54 (43%) patients received invasive interventions, and they were more frequent in psoas abscesses (29 [54%] vs. 25 [35%], p = 0.045). The invasive interventions included 50 percutaneous drainage (40%), 4 laminectomy (3.2%), and 2 surgical drainage (1.6%). Two patients received multiple treatments, one patient received percutaneous drainage and laminectomy, another patient received percutaneous drainage and surgical drainage.

There were 11 in-hospital deaths (8.7%). Although there was one death (0.8%) within 14 days and 10 deaths (7.9%) 14 days after admission, these were not statistically significant (p = 0.82). When we compared the number of deaths before, and 60 days after admission, there were 6 deaths (4.8%) and 5 deaths (4.0%), respectively.

The number of patients who had comorbidities was 102 (81%), including 36 (29%) with hypertension, 32 (25%) with a surgical history, 21 (17%) with malignancies, 19 (15%) with diabetes, 15 (12%) with neurological diseases, 18 (14%) with cardiac disease, and 15 (12%) with cerebrovascular disease (Table 2).
Table 2

Co-morbidities of patients and status at hospitalization

 

All

Pyogenic spondylitis

Psoas abscess

p value

n = 126

n = 72

n = 54

Variables

n (%)

 

Co-morbidities

102 (81)

56 (78)

46 (85)

0.36

 Diabetes

19 (15)

10 (14)

9 (17)

0.80

 Hypertension

36 (29)

23 (31)

13 (24)

0.43

 Hyperlipidemia

7 (5.6)

5 (6.9)

2 (3.7)

0.70

 Cardiac diseases

18 (14)

8 (11)

10 (18)

0.31

 Cerebrovascular disease

15 (12)

6 (8.3)

9 (17)

0.17

 Neurological disease

15 (12)

8 (11)

7 (13)

0.79

 Dementia

4 (3.2)

4 (5.6)

0 (0.0)

0.13

 Alcoholism

4 (3.2)

1 (1.4)

3 (5.6)

0.31

 Neurosis

2 (1.6)

1 (1.4)

1 (1.9)

1.00

 Schizophrenia

2 (1.6)

0 (0.0)

2 (3.7)

0.18

 Mental retardation

2 (1.6)

1 (1.4)

1 (1.9)

1.00

 Depression

2 (1.6)

1 (1.4)

1 (1.9)

1.00

 Epilepsy

1 (0.8)

0 (0.0)

1 (1.9)

0.43

 Parkinson’s disease

1 (0.8)

1 (1.4)

0 (0.0)

1.00

 Pulmonary disease

7 (5.6)

3 (4.2)

4 (7.4)

0.46

 Liver disease

7 (5.6)

4 (5.6)

3 (5.6)

1.00

 Renal disease

8 (6.3)

3 (4.2)

5 (9.3)

0.29

 Malignancy

21 (17)

9 (13)

12 (22)

0.16

 Operation

32 (25)

17 (24)

15 (28)

0.68

 Others

30 (24)

17 (24)

13 (24)

1.00

 Osteoporosis

5 (4.0)

4 (5.6)

1 (1.9)

0.39

 Pancreatitis

2 (1.6)

1 (1.4)

1 (1.9)

1.00

 Thyroid disease

3 (2.4)

1 (1.4)

2 (3.7)

0.58

 Inguinal hernia

1 (0.8)

0 (0.0)

1 (1.9)

0.43

 Malignant syndrome

1 (0.8)

1 (1.4)

0 (0.0)

1.00

 Hypoadrenalism

1 (0.8)

1 (1.4)

0 (0.0)

1.00

 Gastrointestinal ulcer

4 (3.2)

2 (2.8)

2 (3.7)

1.00

 Glaucoma

3 (2.4)

2 (2.8)

1 (1.9)

1.00

 Discitis

1 (0.8)

1 (1.4)

0 (0.0)

1.00

 Cholecystitis

1 (0.8)

1 (1.4)

0 (0.0)

1.00

 Pemphigoid

1 (0.8)

1 (1.4)

0 (0.0)

1.00

 Spinal stenosis

1 (0.8)

0 (0.0)

1 (1.9)

0.43

 Rheumatoid arthritis

1 (0.8)

0 (0.0)

1 (1.9)

0.43

 Reflux esophagitis

2 (1.6)

1 (1.4)

1 (1.9)

1.00

 Ureteral stent placement

1 (0.8)

0 (0.0)

1 (1.9)

0.43

 Common bile duct stone

1 (0.8)

1 (1.4)

0 (0.0)

1.00

Status at hospitalization

 Hospitalized for comorbidity

57 (45)

27 (38)

30 (56)

0.044

 Medical department*

40 (32)

19 (26)

21 (39)

0.18

 Surgical department**

17 (13)

8 (11)

9 (17)

0.43

 Hospitalized for other infections

17 (13)

6 (8)

11 (20)

0.07

 Urinary tract infection

7 (5.6)

1 (1.4)

6 (11)

0.042

 Sepsis

4 (3.2)

2 (2.8)

2 (3.7)

1.00

 Pneumonia

2 (1.6)

0 (0.0)

2 (3.7)

0.19

 Cholangitis

1 (0.8)

1 (1.4)

0 (0.0)

1.00

 Liver abscess

1 (0.8)

0 (0.0)

1 (1.9)

0.43

 Pulmonary tuberculosis

1 (0.8)

1 (1.4)

0 (0.0)

1.00

 Infectious arthritis

1 (0.8)

1 (1.4)

0 (0.0)

1.00

*Comorbidities treated at medical department: blood stream infection 1, cardio-pulmonary arrest 1, cerebral infarction 1, cholangitis 1, congestive heart failure 2, diabetes 1, drug eruption 1, fever of unknown origin 2, gastric ulcer 1, leukemia 1, liver abscess 1, lumbago 2, malignant lymphoma 1, myeloma 2, neuralgia 1, Paget disease 1, pneumonia 3, pulmonary tuberculosis 1, renal failure 3, schizophrenia 1, sepsis 3, skin damage 1, transient ischemic attack 1, urinary tract infection 7

**Comorbidities treated at the surgical department: abdominal trauma 1, burn injury 1, colon cancer 2, fall trauma 1, gastric cancer 2, hip pain 1, ileus 3, infectious arthritis 1, internal iliac artery aneurysm 1, knee pain 1, normal pressure hydrocephalus 1, subarachnoid hemorrhage 2

Laboratory testing and physical examinations indicated that CRP (13.3 ± 11.0 vs. 9.4 ± 8.4 mg/dL, p = 0.02), LDH (290 ± 153 vs. 239 ± 88 IU/L, p = 0.02), BUN (32.0 ± 32.0 vs. 20.9 ± 10.6 mg/dL, p = 0.007), and Cr (1.7 ± 2.5 vs. 1.0 ± 0.8 mg/dL, p = 0.02) were higher in psoas abscess cases (Table 1).

Hospital courses

The median time from admission to diagnosis was 0 days (IQR 0–11, minimum 0 and maximum 185). In many cases, hospitalization occurred after the diagnosis of pyogenic spondylitis and psoas abscess (Table 1). The number of patients diagnosed with these diseases ≥ 14 days after hospitalization was 28 (22%) (median 31 days; IQR 21–50, minimum 14 and maximum 185). These patients developed pyogenic spondylitis or psoas abscesses during the course of hospitalization. There were 57 patients who were admitted for other comorbidities: medical department (40 patients) and surgical department (17 patients). Hospitalization for other infections were 17 patients. Comorbidities between pyogenic spondylitis and psoas abscess patients were generally similar (Table 2). Pyogenic spondylitis was diagnosed more rapidly than psoas abscesses (14% in ≥ 14 days vs. 33%, p = 0.016). The duration of antibiotics use was a median of 28 days (IQR 17–42, minimum 0 and maximum 206). Thirty-eight patients (30%) received intravenous antibiotics for 6 weeks. There was no statistical difference in the long-term use of antibiotics among patients (p = 0.70).

The median length of hospitalization was 60 days (IQR 39–97, minimum 4 and maximum 429). Eleven (8.7%) patients died during the hospitalization period.

Factors associated with in-hospital deaths included a lower SBP (110 ± 35 vs. 134 ± 30 mmHg, p = 0.02), a lower DBP (62 ± 19 vs. 76 ± 17 mmHg, p = 0.03), lower Alb (2.9 ± 0.8 vs. 3.3 ± 0.6 mg/dL, p = 0.02), higher AST (40 ± 19 vs. 33 ± 31 IU/L, p = 0.02), higher ALT (29 ± 11 vs. 25 ± 23 IU/L, p = 0.04), higher LDH (327 ± 114 vs. 254 ± 122 IU/L, p = 0.01), higher BUN (53.5 ± 45.3 vs. 22.9 ± 17.5 mg/dL, p = 0.02), and higher Cr (1.7 ± 0.9 vs. 1.3 ± 1.8 mg/dL, p = 0.005) (Table 3). The multivariate logistic model showed that BUN (OR 1.04, 95% CI 1.02–1.06) and cardiovascular disease (OR 7.02, 95% CI 1.55–31.8) were associated with in-hospital mortalities (Table 4).
Table 3

Factors associated with in-hospital mortality

 

Death

Alive

p value

(n = 11)

(n = 115)

Variables

n (%) or mean ± SD or median [IQR]

 

Male

7 (64)

62 (54)

0.75

Age, year

73 ± 10

72 ± 11

0.80

Length of stay, days

57 [34–86]

60 [39–98]

0.68

Diseases

 Psoas abscess

8 (73)

46 (40)

0.038

 Invasive interventions

6 (55)

48 (42)

0.31

 Percutaneous drainage

6 (55)

44 (38)

0.23

 Operation

1 (9.1)

5 (4.3)

0.43

 Laminectomy

0 (0.0)

4 (3.5)

1.00

 Surgical drainage

1 (9.1)

1 (0.9)

0.17

 Co-morbidities

9 (82)

93 (81)

1.00

 Diabetes

1 (9.1)

18 (16)

1.00

 Hypertension

4 (36)

32 (28)

0.51

 Hyperlipidemia

1 (9.1)

6 (5.2)

0.48

 Cardiac diseases

4 (36)

14 (12)

0.05

 Cerebrovascular disease

1 (9.1)

14 (12)

1.00

 Neurological disease

2 (18)

13 (11)

0.62

 Pulmonary diseases

0 (0.0)

7 (6.1)

1.00

 Liver disease

0 (0.0)

7 (6.1)

1.00

 Renal disease

1 (9.1)

7 (6.1)

0.53

 Maligancy

2 (18)

19 (17)

1.00

 Operation

1 (9.1)

31 (27)

0.29

 Others

2 (18)

28 (24)

1.00

Bacteria

 Gram-positive cocci

7 (64)

56 (49)

0.53

 Gram-negative rods

0 (0.0)

19 (17)

0.21

 Unknown

3 (27)

38 (33)

1.00

Vital signs

 SBP, mmHg

110 ± 35

134 ± 30

0.0196

 DBP, mmHg

62 ± 19

76 ± 17

0.0310

 Body temperature,  °C

36.9 ± 1.1

37.4 ± 1.1

0.12

 Heart rate, /min

93 ± 13

89 ± 19

0.33

Labo data

 WBC, × 102/μL

115 ± 56

113 ± 51

0.88

 Hb, g/dL

10.2 ± 2.8

11.4 ± 2.1

0.07

 Plt, × 104/μL

20.4 ± 18.8

23.0 ± 11.0

0.17

 CRP, mg/dL

17.8 ± 12.2

10.4 ± 9.3

0.06

 T-bil, mg/dL

1.1 ± 0.7

0.8 ± 0.5

0.11

 Alb, g/dL

2.9 ± 0.8

3.3 ± 0.6

0.0220

 AST, IU/L

40 ± 19

33 ± 31

0.0245

 ALT, IU/L

29 ± 11

25 ± 23

0.0376

 LDH, IU/L

327 ± 114

254 ± 122

0.0134

 Blood sugar, mg/dL

156 ± 42

151 ± 73

0.26

 BUN, mg/dL

53.5 ± 45.3

22.9 ± 17.5

0.0197

 Cr, mg/dL

1.7 ± 0.9

1.3 ± 1.8

0.0053

 Na, mmol/L

134.6 ± 10.0

137.3 ± 4.2

0.86

 K, mmol/L

4.0 ± 0.5

4.0 ± 0.6

0.68

Table 4

Multivariate logistic model for death

 

Odds ratio

95% confidence interval

BUN, mg/dL

1.04

1.02–1.06

Cardiovascular diseases

7.02

1.55–31.8

Microbiological examinations

Causal microorganisms were identified in 85 patients (67%), including gram-positive bacteria in 63 patients (50%), gram-negative rods in 19 patients (15%), and others or undetermined (Table 5).
Table 5

Causative bacteria

Bacteria

All (n = 126)

n (%)

Identified

85 (67)

 Gram-positive cocci

63 (50)

 Staphylococci

51 (40)

 MSSA

28 (22)

 MRSA

12 (9.5)

 CNS

11 (8.7)

 Enterococci

3 (2.4)

 Streptococci

8 (6.3)

 Gram-negative rods

19 (15)

Escherichia coli

7 (5.6)

 Klebsiella

3 (2.4)

 Prevotella

3 (2.4)

Proteus mirabilis

2 (1.6)

Citrobacter koseri

1 (0.8)

 Bacteroides

4 (3.2)

 Mycobacterium

2 (1.6)

Tuberculosis

1 (0.8)

 Nontuberculosis

1 (0.8)

 Other bacteria

2 (1.6)

 Unknown

41 (33)

MSSA methicillin-sensitive Staphylococcus aureus, MRSA methicillin-resistant Staphylococcus aureus; CNS coagulase-negative Staphylococcus; Enterocucci Enterococcus faecium 1, Enterococcus faecalis 2; Streptcocci alpha-hemolytic Streptococcus 1, Streptococcus agalactiae (type B group) 3, Streptococcus intermedius 1, Streptococcus sanguinis 1, Streptococcus pneumoniae 2; Klebsiella Klebsiella pneumoniae 2, Klebsiella oxytoca 1; Prevotella Prevotella oris 1, Prevotella melaninogenica 1, unidentified 1; Bacteroides Bacteroides fragilis 3, Bacteroides thetaiotaomicron 1; other bacteria: Corynebacterium sp. 1

Factors associated with gram-negative rods included lower Plts (15.8 ± 9.6 vs. 22.9 ± 12.3 × 10,000/μL, p = 0.0134; Plt < 1.5 × 104/μL, 11 [58%] vs. 20 [30%], p = 0.034) and higher ASTs (57 ± 57 vs. 32 ± 23 IU/L, p = 0.0236) (Table 6). The multivariate logistic model showed that platelets less than 150,000/μL (OR 3.14, 95% CI 1.02–9.65) and higher aspartic aminotransferase (OR 1.02, 95% CI 1.00–1.03) were associated with gram-negative rods (Table 7).
Table 6

Factors associated with gram-negative rods

 

GNR

Others

p value

(n = 19)

(n = 66)

Variables

n (%) or mean ± SD or median [IQR]

 

Male

13 (68)

33 (50)

0.20

Age, year

71 ± 9

72 ± 12

0.41

Psoas abscess

11 (58)

29 (44)

0.31

In hospital death

0 (0.0)

8 (12)

0.19

Invasive intervention

11 (58)

35 (53)

0.80

 Percutaneous drainage

10 (53)

33 (50)

1.00

 Operation

2 (11)

3 (4.5)

0.31

 Laminectomy

2 (11)

2 (3.0)

0.22

 Surgical drainage

0 (0.0)

1 (1.5)

1.00

Co-morbidities

15 (79)

52 (79)

1.00

 Diabetes

3 (16)

9 (14)

0.73

 Hypertension

5 (26)

12 (18)

0.52

 Hyperlipidemia

2 (11)

3 (4.5)

0.31

 Cardiac diseases

4 (21)

9 (14)

0.48

 Cerebrovascular disease

5 (26)

8 (12)

0.15

 Neurological disease

3 (16)

9 (14)

0.73

 Pulmonary disease

0 (0.0)

4 (6.1)

0.57

 Liver disease

1 (5.3)

4 (6.1)

1.00

 Renal disease

0 (0.0)

4 (6.1)

0.57

 Malignancy

1 (5.3)

12 (18)

0.28

 Operation

6 (32)

17 (26)

0.77

 Others

6 (32)

12 (18)

0.22

Vital signs

 SBP, mmHg

124 ± 27

131 ± 32

0.40

 DBP, mmHg

75 ± 18

72 ± 16

0.58

 Body tempereture,  °C

37.7 ± 1.3

37.4 ± 1.1

0.59

 Heart rate, /min

91 ± 17

91 ± 20

0.83

Laboratory

 WBC, ×102/μL

138 ± 69

120 ± 49

0.42

 Hb, g/dL

11.8 ± 2.0

11.1 ± 2.1

0.16

 Plt, ×104/μL

15.8 ± 9.6

22.9 ± 12.3

0.0134

 Plt < 1.5 × 104/μL

11 (58)

20 (30)

0.034

 CRP, mg/dL

17.1 ± 9.5

12.6 ± 9.8

0.07

 T-bil, mg/dL

1.0 ± 0.6

0.8 ± 0.4

0.18

 Alb, g/dL

3.2 ± 0.6

3.2 ± 0.6

0.70

 AST, IU/L

57 ± 57

32 ± 23

0.0236

 ALT, IU/L

31 ± 23

27 ± 25

0.22

 LDH, IU/L

292 ± 126

264 ± 108

0.37

 Blood sugar, mg/dL

147 ± 83

157 ± 73

0.23

 BUN, mg/dL

26.9 ± 14.9

25.2 ± 20.6

0.19

 Cr, mg/dL

1.3 ± 1.2

1.3 ± 1.7

0.24

 Na, mmol/L

136.9 ± 3.7

137.0 ± 4.7

0.86

 K, mmol/L

4.0 ± 0.6

3.8 ± 0.5

0.66

GNR gram-negative rods

Table 7

Multivariate logistic model for gram-negative rods

 

Odds ratio

95% confidence interval

Plt < 1.5 × 104/μL

3.14

1.02–9.65

AST, IU/L

1.02

1.00–1.03

Discussion

We showed the epidemiology of pyogenic spondylitis and psoas abscesses, as well as the factors associated with in-hospital mortality and the presence of gram-negative rods in patients’ cultures at a single center. The factors associated with mortality were an elevated BUN and a history of cardiovascular disease. The factors associated with a positive culture of gram-negative rods included higher AST and lower Plt laboratory results.

Previous studies have reported that the predisposing factors for bacterial spondylitis or psoas abscesses were diabetes mellitus, malnutrition, substance abuse, human immunodeficiency virus infection, malignancy, long-term steroid use, chronic renal failure, liver cirrhosis, and sepsis [48]. Some reports have showed that CRP or WBCs were associated with recovery [9, 10], although our study showed that CRP was also associated with gram-negative rods.

Staphylococcus was found in 50–88% of patients in prior studies [3, 11, 12], and our study showed a similar percentage (60%). Among gram-negative bacteria identified in our study, Escherichia coli was found in 5.6%, which was slightly higher than the 2.8% reported in previous studies [11, 13]. Mycobacterium tuberculosis is a frequent cause of psoas abscesses in regions where tuberculosis is common (e.g., southern China) [1, 2]; however, the proportion of patients with tuberculosis among pyogenic spondylitis cases decreased to about 24% in these areas [3]. Tuberculosis is common in Japan, yet there was only one case of tuberculosis in our study, which may reflect an early diagnosis before progression to severe tuberculosis or before the incidence of tuberculosis decreased in Japan [14].

In previous studies, delay of treatment, old age, sepsis, and E. coli infection were reported as mortality risk factors [11, 15]. There were no differences in mortality between patients with and without gram-negative rods and between elderly and younger patients in our study. We assumed that all patients were promptly treated after the diagnosis. If the treatment was delayed, this factor might be associated with mortality. A previous report revealed an association between endocarditis and pyogenic spondylitis [16]; however, there were no cases of endocarditis in our study. Psoas abscesses are generally reported to have higher morbidity and mortality. One study reported that the mortality rate of primary and secondary abscesses was 2.4% and 19%, respectively, and may approach 100% in untreated cases [1]. Our study had a similar mortality rate (15%), including primary and secondary psoas abscesses, although we could not differentiate them.

When the causative microorganism could not be identified, clinicians must administer an empirical treatment. The empirical treatment policy of the institution was following: (1) vancomycin ± cefazolin in general and (2) meropenem or similar antibiotics when gram-negative bacteria was likely in the setting of previous organism or infections of other sites. Those patients with an elevated BUN or cardiovascular comorbidity were at a higher risk of mortality. Therefore, such patients should receive broad-spectrum antibiotics as well as aggressive drainage and other intensive supportive therapies. The factors associated with gram-negative rods should also be a guide for empirical treatments. The prevalence of gram-negative rods was low, but those with lower platelet counts or elevated ASTs may be at a higher risk of gram-negative rod infections. These patients should receive antibiotics that target gram-negative rods as an initial therapy.

A new classification of pyogenic spondylodiscitis has been reported [17]. The new classification was based on clinical symptoms and radiological findings and associated with recurrence rate and mortality. Since our study had a retrospective design, we could not obtain the information necessary to reclassify our patients and our risk factors should be re-evaluated in future studies incorporating the new classification.

In this study, BUN and a history of cardiovascular disease were associated with in-hospital deaths. Low Plts (< 150,000/μL) and high ASTs were associated with gram-negative rods after performing multivariate analyses. For the group with a higher risk of in-hospital mortality, aggressive drainage should be considered in addition to intensive antimicrobial combination therapy. Although the frequency of gram-negative rods was low, the use of wide-spectrum antibiotics should be considered for the group with a high probability of having gram-negative rods based on these risk factors.

This study has some limitations. First, since our study had a retrospective design, we were unable to measure all factors. Second, we investigated a total of 126 patients, and this sample size is insufficient for robust multivariate analyses. We also could not break down into small homogenous group due to small sample size. However, our primary purpose was to describe the general picture of patients who were diagnosed in daily practice. Third, since we focused solely on patients with pyogenic spondylitis or psoas abscesses and did not analyze all patients who presented with fever and lower back pain, there is a possibility of missed cases. However, considering that our institution is a teaching hospital with easy access to imaging technology, we believe that the number of missed cases is low. Fourth, bacteria were not identified in all cases. Therefore, factors related to gram-negative bacteria should be interpreted with caution. Fifth, there were no established protocols for antibiotics and surgical treatments because this study was a retrospective observational study. The effect of treatment modalities on mortality should be considered. Sixth, we could not classify the psoas abscesses as primary and secondary. If we had been able to differentiate between primary and secondary psoas abscesses, we might have indicated another risk factor for mortality as reported in the previous study. Seventh, there were many variables we compared between pyogenic spondylitis and psoas abscess. The issue of multiple comparisons and the resultant significance should be considered to interpret the results.

Conclusion

In clinical practice, pyogenic spondylitis and psoas abscesses are likely to be severe in the presence of low blood pressure, malnutrition, liver failure, and kidney dysfunction. When deciding which antibiotic to use, the possibility of gram-negative bacteria should be considered in patients with low Plts and liver dysfunction.

Abbreviations

Alb: 

Albumin

ALT: 

Alanine aminotransferase

AST: 

Aspartic aminotransferase

BUN: 

Blood urea nitrogen

CI: 

Confidence interval

CNS: 

Coagulase-negative Staphylococcus

Cr: 

Creatinine

CRP: 

C-reactive protein

CT: 

Computed tomography

DBP: 

Diastolic blood pressure

GNR: 

Gram-negative rods

IQR: 

Interquartile range

LDH: 

Lactate dehydrogenase

MRI: 

Magnetic resonance imaging

MRSA: 

Methicillin-resistant Staphylococcus aureus

MSSA: 

Methicillin-sensitive Staphylococcus aureus

OR: 

Odds ratio

Plt: 

Platelet cell count

SBP: 

Systolic blood pressure

SD: 

Standard deviation

WBC: 

White blood cell count

Declarations

Acknowledgments

We express appreciation to Ms. Emi Onoda, medical secretary for performing data extraction.

Funding

This work was partly supported by a grant from the Ministry of Health, Labor and Welfare of Japan (H28-ICT-004) and JSPS KAKENHI Grant Numbers 26293159 and 18H03032.

Availability of data and materials

The datasets analyzed during the current study are available from the corresponding author by request.

Authors’ contributions

TN and TM designed the study and analyzed the datasets. TN, KoK, YY, JM, and KiK performed the data collection. TN and TM wrote and revised the manuscript. All authors read and approved the final manuscript.

Ethics approval and consent to participate

This study was approved by the Ethics Review Board of Shimane Prefectural Central Hospital (R14–060). Since all data were obtained as part of our routine daily practice, informed consent was waived by the institutional review board.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interest.

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Authors’ Affiliations

(1)
Department of Infectious Diseases, Shimane Prefectural Central Hospital, Izumo, Japan
(2)
Clinical Education and Research Center, Shimane Prefectural Central Hospital, Izumo, Japan
(3)
Department of Clinical Epidemiology, Hyogo College of Medicine, Nishinomiya Hyogo, 663-8501, Japan
(4)
Department of Orthopedics, Shimane Prefectural Central Hospital, Izumo, Japan
(5)
Department of Emergency Medicine, Shimane Prefectural Central Hospital, Izumo, Japan
(6)
Department of General Medicine, Shimane Prefectural Central Hospital, Izumo, Japan
(7)
Department of Pediatrics, Shimane Prefectural Central Hospital, Izumo, Japan

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© The Author(s). 2018

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