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Brief Reports
Microbiological Analysis of Pancreatic Abscess
Pancreatic abscess is a serious complication of pancreatic infection, which progresses to necrosis and pustulation [1- 5]. About
one-third of pancreatic abscesses are polymicrobial, caused mainly
by enteric facultative microorganisms and occasionally by Staphylococcus aureus [1-3]. However, since most studies have not
been based on modern anaerobic bacteriologic methodologies, the
frequency with which anaerobes cause such abscesses is unknown.
This retrospective report describes our 15 years of experience
in the bacteriologic study of pancreatic abscess with use of specific
methods for the recovery of aerobic and anaerobic bacteria. The
microbiological data were correlated with clinical and laboratory
findings.
Between June 1973 and June 1988, 46 specimens obtained by
surgical drainage of pancreatic abscesses that occurred following
acute pancreatitis were studied for the presence of aerobic and
anaerobic bacteria. The patients had been ill for a mean of 6.4
days (range, 3- 16 days) at the time of surgery, and 23 had had
previous episodes of acute pancreatitis. Excluded from analysis
were 19 cases of infected pseudocysts; 5 cases in which no clinical
data were available; 4 in which there was no bacterial growth; and
5 in which specimens were submitted in improper transport media.
Pancreatic abscess was diagnosed intraoperatively as an abscess
arising in or contiguous with the pancreas. Clinical and microbiological data were compiled. Patients' ages ranged between 32 and
85 years (mean, 56 years), and 31 patients were males.
Antimicrobial therapy was given to all patients before sample
collection. Specimens were obtained at surgery by either a swab or
needle aspiration and were transported and processed as previously
described [6]. Blood for culture was drawn from 42 (91 %) of the
patients [6]. Statistical analysis was performed by means of the
X 2 test or Fisher's exact test.
A total of 158 isolates (77 aerobic or facultative bacteria and
81 anaerobic bacteria) were recovered. The number of isolates per
abscess varied between one and five (average number, 3.4) (table
1). Aerobic or facultative organisms alone were present in 17
specimens (37%), anaerobes alone were present in 10 (22%), and
mixed aerobic-anaerobic organisms were present in 19 (41 % ) .
Eight specimens (17%) each yielded one organism: Escherichia
coli (4 cases), Klebsiella pneumoniae (2), Bacteroides fragilis
( 1), and Peptostreptococcus magnus (1). The predominant aerobes were E. coli, K. pneumoniae, streptococcus group D, and
S. aureus. The predominant anaerobes were Peptostreptococcus
species, B. fragilis group organisms, Clostridium species, Prevotella species, Veillonella species, and Fusobacterium species.
Table 1. Aerobic and anaerobic isolates recovered from 46 pancreatic abscesses between June 1973 and June 1988 at the u.s. Naval
Hospital, Bethesda, Maryland.
Organism
No. of isolates
Aerobic
Gram-positive
a-Hemolytic streptococcus
Group D streptococcus
4
3
II
Staphylococcus aureus
Staphylococcus epidermidis
6
2
Gram-negative
Proteus species
3
5
3
18
3
Pseudomonas aeruginosa
Pseudomonas species
Escherichia coli
Serratia marcescens
Enterobacter aerogenes
Eikenella corrodens
Citrobacter freundii
Klebsiella pneumoniae
4
2
I
12
77
Total, aerobic
Anaerobic
Gram-positive
Peptostreptococcus magnus
Peptostreptococcus micros
Peptostreptococcus prevotii
Peptostreptococcus asaccharolyticus
Peptostreptococcus anaerobius
Peptostreptococcus species
Streptococcus intermedius
Veillonella species
Bifidobacterium species
Eubacterium lentum
Propionibacterium acnes
Clostridium septicum
Clostridium peryringens
Clostridium species
5
I
3
6
4
7
3
6
2
I
4
2
4
I
Gram-negative
Fusobacterium nucleatum
Fusobacterium species
Bacteroides fragilis*
Bacteroides distasonis*
Bacteroides ovatus*
Bacteroides vulgatus*
Bacteroides thetaiotaomicron*
Bacteroides species
Prevotella melaninogenica
Prevotella intermedia
Prevotella disiens
2
3
6
3
2
4
2
4
2
3
I
Total, anaerobic
* These species all belong to the B. fragilis
The opinions and assertions contained herein are the private ones of the
writers and are not to be construed as official or reflecting the views of the
U.S. Department of Navy or the U.S. Naval Service at large.
Acknowledgments: The authors acknowledge the efforts of the staffs of
the microbiology laboratory and clinical wards at the U.S. Naval Hospital in
Bethesda, Maryland.
Reprints or correspondence: Dr. Itzhak Brook, P.O. Box 70412, Chevy
Chase, Maryland 20813-0412.
Clinical Infectious Diseases 1996;22:384-5
This article is in the public domain.
1996;22 (February)
81
group.
Bacteremia caused by organisms identical to those found in the
abscess occurred in 11 instances (26% of cultured cases). The
isolates in these cases were E. coli (4); streptococcus group D
(2); and K. pneumoniae, B. fragilis, Bacteroides vulgatus, Peptostreptococcus magnus, and Peptostreptococcus prevotii (1 each).
Conditions predisposing to pancreatic infections were found in 42
cases (95%). These included biliary disease in 20 cases (48%),
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1996;22 (February)
Brief Reports
385
alcoholism in 15 (36%), recent surgery in 7 (17%), trauma in 4
( 10% ), and endoscopic retrograde procedures in 3 (7%).
Complications occurred in 32 patients (70%); a single complication occurred in 27 instances and 2 complications occurred in
5. These included residual abscess (6), pancreatic fistula (5),
bowel necrosis (4), enterocutaneous fistula (2), and progressive
pancreatitis (1). Infectious complications following drainage occurred in 18 cases. These included intraabdominal abscess at a site
other than the pancreatic bed (7), pneumonia (5), urinary tract
infection ( 4 ), and wound infections (3). Reoperation for infection
was necessary in 10 patients.
Nine (19%) of the patients died: persistent pancreatic infection
was present in six, and three had terminal bleeding. No correlation
was found between the microbiological findings and age, sex, predisposing conditions, duration of clinical signs and symptoms, laboratory findings, the type of complications, and outcome. All patients
were treated with use of surgical drainage, supportive therapy, and
antimicrobial agents. The latter were aminoglycosides (39 cases),
clindamycin (19), amoxicillin (17), cefoxitin (12), metronidazole
(7) , methicillin (6) , ceftazidime ( 6), ticarcillinlclavulanate (4) , penicillin (2), vancomycin (2), and cefazolin (1).
This study demonstrates the polymicrobial aerobic and anaerobic bacteriology of pancreatic abscess. In contrast to previous
reports [1- 5], our study demonstrates a higher frequency of
isolation of anaerobes in general and of Peptostreptococcus
species and B. fragilis group organisms in particular. This finding may be due to the utilization of specific methods for specimen collection and transportation and for cultivation of anaerobes in our hospital and to the inclusion only of specimens
submitted for the recovery of both aerobic and anaerobic bacte-
ria. The recovery of anaerobic bacteria of mostly gastrointestinal origin from pancreatic abscesses is explained by the
predominance of such bacteria in the normal gastrointestinal
flora [7].
This study underscores the importance of obtaining specimens
for the recovery of both aerobic and anaerobic bacteria from pancreatic abscesses. Intensive surgical and medical means are the
hallmark of therapy for pancreatic abscess. Antimicrobial therapy
for mixed aerobic and anaerobic bacterial infection is required.
Whenever possible, the final choice of antimicrobial agents should
be made on the basis of the isolation of specific organisms, aerobic
as well as anaerobic.
Endocarditis as a Complication of a Transjugular
Intrahepatic Portosystemic Stent-Shunt
Herein we describe the case of a male patient with alcoholic
cirrhosis who had previously had episodes of variceal bleeding and
who died of acute native-valve endocarditis due to Staphylococcus
epidermidis following TIPS. Infective endocarditis is reported, to
our knowledge, for the first time as a complication of TIPS.
A 71-year-old male patient with chronic hepatic disease and
portal hypertension was admitted to our facility for TIPS on 2
August 1994. He had drunk 21iters of wine per day for 36 years. He
was first hospitalized 2 years previously because of hematemesis;
esophageal varices were found and sclerotherapy was initiated.
Subsequently, he was hospitalized 12 more times for hematemesis
and underwent sclerotherapy. In June 1994 the patient began undergoing sclerotherapy in weekly sessions. At that time the blood
pressure was 90 I 60 mm Hg; he was toothless and had parotid
enlargement, gynecoid body hair distribution, palmar erythema,
and gynecomastia. Aortic and mitral systolic murmurs were heard.
Laboratory findings were normal except for a hematocrit of 0.31,
a WBC count of 3.4 X 10 9 /L, a platelet count of 76 X 10 9 /L,
and a high "Y-glutamyl transpeptidase level. He was classified as
a Child-Pugh A.
His condition was the same when he was admitted on 2 August
for TIPS. Findings on a chest radiograph were normal. Two days
later TIPS was performed, and for 24 hours prophylaxis with ceftriaxone was administered. The procedure lasted 90 minutes; the
portocaval gradient was reduced from 25 em H 20 to 12 cm H 20.
The patient was stable until 8 August, when he became oliguric
and had sacral edema; rales were heard in the thorax. The blood
The transjugular intrahepatic portosystemic stent-shunt
(TIPS) is a nonsurgical method for creating a portosystemic
shunt. The internal jugular vein is entered, a catheter and a
curved needle are advanced through the inferior vena cava into
a right hepatic vein, and then an intrahepatic branch of the portal
vein is punctured to establish the shunt. The stent is a tubular
wire mesh mounted on a balloon catheter and dilated to bridge
the tissue tract between the vessels [1]. Complications are related to transhepatic needle puncture, transvenous access to the
portal vein, portal cannulation, the stent, the puncture site, portosystemic shunting, and contrast material. Excluding hepatic
encephalopathy and delayed stenosis or occlusion of the shunt,
an overall complication rate of < 10% can be expected [2].
Infective complications are seldom reported.
Reprints or correspondence: Dr. Javier Daniel Finkielman, Sexta Catedra
de Medicina, Hospital de Clinicas "Jose de San Martin," D.B.A., Cordoba
2351, piso 10, (1120) Buenos Aires, Argentina.
Clinical Infectious Diseases 1996;22:385-6
© 1996 by The University of Chicago. All rights reserved.
1058-4838/96/2202-0037$02.00
Itzhak Brook and Edith H. Frazier
Departments of Pediatrics and Infectious Diseases,
Us. Naval Hospital, Bethesda, Maryland
References
1. Shi ECP, Yeo BW, Ham JM. Pancreatic abscesses. Br J Surg 1984;71:
689-91.
2. Altimeter WA, Alexander JW. Pancreatic abscess: a study of 32 cases. Arch
Surg 1963; 87:80-9.
3. Holden JL, Bern TV, Roost LSR. Pancreatic abscess following acute pancreatitis. Arch Surg 1976; III :858-61.
4. Malangoni MA, Shallcross JC, Richardson JD, et al. Factors contributing to
fatal outcome after treatment of pancreatic abscess. Ann Surg 1986; 203:
605-13.
5. Gerzof SG, Banks PA, Robbins AH, et al. Early diagnosis of pancreatic
infection by computed tomography-guided aspiration. Gastroenterology
1987; 93: 1315-20.
6. Brook I. Recovery of anaerobic bacteria from clinical specimens in 12 years
at two military hospitals. J Clin Microbiol 1988; 26: 1181-8.
7. Gorbach SL. Intestinal microflora. Gastroenterology 1971; 60: 1110-29.