INTRAPERITONEAL

INFECTIONS AND
ABSCESSES
JOSE CARLO B. VALENCIA, M.D., FPCP, FPSMID
June 23, 2023
• small amount of fluid is normally present in the peritoneal
space
• protein content (mostly albumin) of <30g/L
• <300 WBCs, predominantly mononuclear cells/uL
• With bacterial infection: Increase in WBC, influx of PMNS
Intraperitoneal Infections
• enzymes or organisms leak into the normally sterile peritoneal cavity
 inflammation
• Inciting events: disruption to anatomic barrier
• Rupture of appendix, diverticulum, ulcer
• Weakening of bowel wall due to ischemia, tumor or inflammation
(IBD)
• Adjacent inflammatory disease (pancreatitis, PID)
• Occurs in two stages
• Peritonitis
• Abscess
Primary (Spontaneous) Bacterial Peritonitis
• without an apparent source of contamination
• versus secondary
• the type of organism and presentation is different
• In adults: SBP commonly occurs in conjunction with liver cirrhosis
• metastatic cancer, postnecrotic hepatitis, chronic active hepatitis,
congestive heart failure systemic lupus erythematosus (SLE) and
lymphedema
• Always develop in patients with preexisting ascites, but,
uncommon in general (10% of cirrhotic patients)
Primary (Spontaneous) Bacterial Peritonitis
Cause: not definitely established
• involve hematogenous spread of organisms in a patient with diseased liver and
altered portal circulation resulting in a defect in the usual filtration function
• Organisms multiply in ascites, a good medium for growth
• Proteins of complement cascade are found in the peritoneal fluid, with lower levels
in cirrhotic patients than in patients with ascites of other etiologies
• Opsonic and phagocytic properties of PMNS are diminished in patients with
advanced liver disease
Primary (Spontaneous) Bacterial Peritonitis
• Cause: not definitely established
• Cirrhosis is associated altered gut microbiota, including increased prevalence of
potentially pathogenic bacteria such as Enterobacteriaceae
• Small intestinal bacterial overgrowth is present and is linked with pathologic bacterial
translocation and SBP
• Factors: deficiency in Paneth cell defensins, reduced intestinal motility, decreased
pancreatobiliary secretions and potral hypertensive enteropathy
Primary (Spontaneous) Bacterial Peritonitis
• Most common manifestation: fever (80%)
• Ascites- found virtually always predates infection
• Abdominal pain, an acute onset of symptoms and
peritoneal irritation during physical examination
• but absence of which does not exclude the diagnosis
Primary (Spontaneous) Bacterial Peritonitis
• Non localizing symptoms (malaise, fatigue or
encephalopathy) without clear etiology should also
prompt consideration of SBP
• Sample ascitic fluid of any cirrhotic patient with fever and
ascites
• >250 PMNS/uL is diagnostic- does not apply with
secondary peritonitis
Primary (Spontaneous) Bacterial Peritonitis
• Microbiology
• E coli is most commonly encountered
• Gram positive such as streptococci, enterococci and
even pneumococci are sometimes found
• Widespread use of quinolones to prevent SBP,
frequent hospitalization exposure to broad
spectrum antibiotics have led to change in the
etiology of infections in patients with cirrhosis, with
more gram positive and extended spectrum-B
lactamase (ESBL) producing organisms
Primary (Spontaneous) Bacterial Peritonitis
• Microbiology
• Risk for MDRO: nosocomial origin of infection, long-term
norfloxacin prophylaxis, recent infection with MDRO and recent B-
lactam antibiotics
• In SBP, anaerobes are less frequent than in secondary peritonitis
(mixed flora)
• If multiple organisms are recovered in the peritoneal fluid in a
patient with suspected SBP, reconsider the diagnosis and search
for a source of secondary peritonitis
Primary (Spontaneous) Bacterial Peritonitis
• Diagnosis
• Is not easy
• Depends on the exclusion of primary intraabdominal source of
infection
• Contrast-enhanced CT is useful in identifying an intrabdominal
source of infection
• May be difficult to recover organisms from cultures of the
peritoneal fluid- low burden of organism, collect at least 10 mL
Primary (Spontaneous) Bacterial Peritonitis
• Diagnosis
• Obtain blood cultures- bacteremia is frequent
• Maximize yield by collecting specimen for cultures
prior to administration of antibiotics
• Plain film of the abdomen: ascites
• Chest and abdominal radiography should be done
in patients with abdominal pain to exclude free air,
which signals a perforation
Primary (Spontaneous) Bacterial Peritonitis
• Treatment
• Directed at the isolate from blood or peritoneal fluid
• Gram staining of peritoneal fluid: often negative
• While waiting for culture result: cover for GNB and GP
cocci
• 3rd gen cephalosporin: cefotaxime, ceftriaxone
• Piperacillin Tazobactam 4.5g IV q8
• Empirical coverage for anaerobes is NOT necessary
Primary (Spontaneous) Bacterial Peritonitis
• Treatment
• Albumin for patients with Crea >/= 1 mg/dL, BUN >/ = 30 mg/dL or
total bilirubin >/= 4 mg/dL
• Narrow down antibiotic therapy once specific pathogen is
specified
• Patients usually respond to appropriate antibiotic therapy
• At least 5 days of antimicrobials if with rapid improvement and
blood cultures are negative
• Up to 2 weeks if with bacteremia and for those with slow
improvement
Primary (Spontaneous) Bacterial Peritonitis
• Primary Prevention
• Observational studies and meta-analysis: raised the concern that gastric acid suppression
(PPI) may increase risk of SBP, but no prospective studies yet establish whether avoidance of
such therapy may prevent SBP
• Non-selective beta blockers (propranolol) may prevent bacterial peritonitis
• Chronic antibiotic prophylaxis
• Ascitic fluid total protein <1/5g/dL
• Crea >/= 1.2 mg/dL
• BUN >/=25 mg/dL
• Serum Na </= 130 mg /dL
• Liver failure (Child Pugh score >/= 9 and bilirubin >/= 3 mg/dL)
• 7-day course of prophylaxis is recommended for patients with cirrhosis and GI bleeding
Primary (Spontaneous) Bacterial Peritonitis
• Secondary Prevention
• SBP has a high rate of recurrence
• 70% experience recurrence within 1 year
• Antibiotic prophylaxis is recommended for patients with history of SBP to reduce the
rate to 20% and improve short-term survival rates
• Prophylactic regimens for adults with normal renal function
• Ciprofloxacin 500 mg weekly
• Norfloxacin 400 mg/day
• Cotrimoxazole 800/160 mg tab/day
• However, long-term administration increase the risk of severe staphylococcal
infections
Secondary
Peritonitis
• Develops when bacteria contaminate the
peritoneum as a result of spillage from an
intraabdominal viscus
• Mixed flora: facultative GN bacilli and anaerobes
predominate , especially if source is colonic
• Early infection: host response is directed towards
containment
• Exudate contains fibrins and PMNs
• Early death due to GN sepsis and to potent
endotoxins
• GNB, especially E. coli are common blood isolates,
but Bacteroides fragilis bacteremia, also occurs
Secondary Peritonitis
• Severity of abdominal pain and clinical course depend on the inciting process
• Organism isolated also vary from the source of the initial process and the normal flora in
the site
• Secondary peritonitis can result form chemical irritation/and or bacterial contamination
• Ruptured gastric ulcer release low-pH gastric contents that will serve as chemical irritants
• Normal flora of the stomach same organisms in the oropharynx but in lower
numbers, bacterial burden NEGLIGIBLE vs ruptured appendix
Secondary Peritonitis
• Normal flora in the colon: 99.9% anaerobes
• Leaking of colonic contents: does not cause significant chemical peritonitis but infection
is intense due to the heavy bacterial load
• Local symptoms depend on the inciting event
• Epigastric pain: ruptured gastric ulcer
• Appendicitis: initially vague, periumbilical discomfort and nausea followed by
localization in the RLQ hours after
• Once infection spread in the peritoneum pain increases
• Patients lie motionless, knees drawn up to avoid stretching the nerve fibers of the
peritoneal cavity
• Coughing, sneezing (increases pressure in the cavity) is associated with sharp pain
Secondary Peritonitis
• Abnormal PE: voluntary and involuntary guarding of anterior abdominal musculature
• Tenderness, especially rebound are later findings
• Febrile, with leukocytosis and left shift to band forms
• Recovery of organism from peritoneal fluid is easier in secondary than in primary
peritonitis
• Emergent studies (abdominal CT) to find the source should be undertaken of the patient
is stable
• If unstable: Surgery
Secondary Peritonitis
• Treatment
• Early antibiotics aimed at aerobic GNB and anaerobes
• Community acquired, mild-moderate
• Broad-spectrum penicillin with beta lactamase inhibitor
• Combination of fluroquinolones or 3rd gen cephalosporin PLUS metronidazole
• Patients in ICUs and or with associated healthcare associated infections should
receive antibiotics targeting resistant GNB such as Pseudomonas aeruginosa
• Usually requires both surgical intervention to address the inciting process and
antibiotics to address the bacteremia and to decrease the incidence of abscess
formation, and wound infection and to prevent distant spread of infection
Intraabdominal
Abscesses
Jose Carlo Valencia, MD, FPCP, FPSMID
Intraperitoneal Abscess
• Abscess formation is common in untreated peritonitis if overt GN sepsis either does not
develop or develops but it is not fatal

• Pathogenesis and Immunity

• Disagreement disease state vs host response
• Abscess: infection of variable organism and PMNS contained in a fibrous capsule
• BUT it is also a process by which the host confines microbes to a limited space- preventing further
spread
• Cause significant symptoms and patients are quite ill
Intraperitoneal Abscess
• Pathogenesis and Immunity
• Bacteroides fragilis appears to be uniquely virulent
• Critical virulence factor: capsular polysaccharide complex
• Polysaccharide A evokes host response that localizes bacteria with abscess
• Polysaccharide A adheres to mesothelial cells which stimulates TNF alpha and iCAM1 by
peritoneal macrophages

• Clinical Presentation
• 74% are intraperitoneal or retroperitoneal vs visceral
• Most result from fecal spillage from a colonic source, peri appendiceal and diverticular
abscesses occur commonly
• Usually form within weeks of the development of peritonitis
Intraperitoneal Abscess

• Diagnosis
• Scans have considerably facilitated diagnosis of intraabdominal
abscess
• Abdominal CT: highest yield
• Ultrasound: RUQ, kidneys and pelvis
• Abscesses contiguous with or contained within a diverticula are
particularly difficult to diagnose with scanning procedures
• Barium enema occasionally may detect a diverticular abscess
not diagnosed with other procedures
Intraperitoneal Abscess
• Treatment
• Identification of focus of infection
• Administration of broad-spectrum antibiotics: only adjunct
• Performance of drainage
• Empiric antibiotics should be the same as that discussed for secondary peritonitis
• Most clinical failures are due to failure to drain the abscess and thereby achieve
source control
• Duration of antibiotic depends on the presumptive source has been control
• Adequate source control: 4-5 days
VISCERAL ABSCESS
Liver abscess
• Liver is the organ most subject to the development of abscess
• May be solitary or multiple
• May arise from hematogenous spread of bacteria or from local
spread from contiguous sites of infection within the peritoneal
cavity
• In the past, ruptured appendicitis is the most common source
• Currently, biliary tract is the most common
• FEVER is the most common presenting sign
• If biliary in origin: RUQ pain, guarding
VISCERAL ABSCESS
Liver abscess
• Non-specific symptoms: chills, anorexia, weight loss, nausea, vomiting may also develop
• Only 50% has RUQ tenderness or jaundice
• Fever of unknown origin may only be the manifestation, especially in the elderly
• Elevated serum alkaline phosphatase is the most reliable laboratory finding, seen in 70%
of patients
• 1/3 to 1/2 of patients have bacteremia
• Suggested by Chest Xray: elevated right hemidiaphragm, right basilar infiltrate or right
sided pleural effusion
VISCERAL ABSCESS
Liver abscess
• Biliary source: enteric GNB and enterococci are common
• Klebsiella pneumoniae liver abscess has been well described in Southeast Asia
• Ampicillin/amoxicillin therapy within the previous 30 days have been associated with
virulent hypermucoviscous K pnemoniae phenotype

• Liver abscess from pelvic and other intraperitoneal source: mixed flora
VISCERAL ABSCESS
Liver abscess
• Amoebic abscess are not uncommon
• Serology gives >95% positive result
• PCR testing has also been used
VISCERAL ABSCESS
Liver abscess
• Treatment
• DRAINAGE is the mainstay of therapy
• Can be percutaneous or surgical
• Growing interest of medical treatment alone for pyogenic abscess
• Same empiric regimen as secondary bacterial peritonitis
VISCERAL ABSCESS
Liver abscess
• Blood culture and diagnostic aspirate should be obtained prior to
initiation of therapy
• Mortality rate despite treatment: 15%
• Factors that predict failure of percutaneous drainage and favors
surgery:
• Multiple, sizable abscesses, viscous abscess that plugs the
catheter, associated diseases requiring surgery (biliary disease),
presence of yeast, lack of clinical response to percutaneous
drainage
VISCERAL ABSCESS
Splenic abscess
• Less common than liver abscess
• Degree of suspicion should be high since it is usually fatal if left untreated
• Bacterial endocarditis is the most common associated infection
• Can develop in patients who have received extensive immunosuppressive therapy and in
patients with hemoglobinopathies or other hematologic disorders
VISCERAL ABSCESS
Splenic abscess
• 50% of patients have abdominal pain, only ½ of these is localized in LUQ
• Splenomegaly is found in 50% of cases
• Fever and leukocytosis is generally present
• CT scan is the most sensitive tool
• UTZ is less sensitive
• Streptococcal species are the most common bacterial isolates followed by S. aureus –
reflecting associated endocarditis
VISCERAL ABSCESS
Splenic abscess
• Splenectomy with adjunctive antibiotics has been the traditionally considered as
standard treatment and remains the best approach for complex, multilocular or multiple
abscesses
• Percutaneous drainage has worked well for singe, small (<3cm) abscesses in some studies
• Patients undergoing splenectomy should be vaccinated against encapsulated organism
(Streptococcus pneumoniae, Hemophilus influenzae, Neisseria meningitis)
• The most important factor in successful treatment of splenic abscess is early diagnosis
VISCERAL ABSCESS
Perinephric and Renal Abscesses
• Not common
• 75% arise from a urinary tract infection
• Infection ascends from the bladder to the kidney with pyelonephritis preceding abscess
formation
• Areas of abscess developing within the parenchyma may rupture into the perinephric
space
• Most important factor associated with development of perinephric abscess is
concomitant nephrolithiasis obstructing urine flow
VISCERAL ABSCESS
Perinephric and Renal Abscesses
• Organisms frequently encountered: E. coli, Proteus spp, Klebsiella spp
• The urease of Proteus spp splits urea, creates a more alkaline and more
hospitable environment for bacterial proliferation, frequently found in
association with large struvite stones (Staghorn calculi)
• Presentation is quite non-specific
• Flank pain and abdominal pain are common
• 50% are febrile
• Pain may be referred to the groin or leg, with extension of infection
VISCERAL ABSCESS
Perinephric and Renal Abscesses
• Diagnosis is frequently delayed
• Mortality rate is appreciable, although lower than in the past
• Should most seriously considered when a patient presents with symptoms and signs of
pyelonephritis and remains febrile after 4 to 5 days of treatment
• Moreover,
• if urine culture yields polymicrobial flora, patient is known to have renal stones or when
fever and pyuria coexist with sterile urine culture
VISCERAL ABSCESS
Perinephric and Renal Abscesses
• UTZ and CT scan are most useful
• If a renal abscess is diagnosed, nephrolithiasis must be excluded, specially with high
urinary pH suggest the presence of urea-splitting organism
• Treatment: (percutaneous) drainage and antibiotic therapy
VISCERAL ABSCESS
Psoas Abscess
• Arise from hematogenous source, contiguous spread from intrabdominal or pelvic
process, from contiguous bony structures (vertebral bodies)
• Associated osteomyelitis is common in psoas abscess
• Mycobacterium tuberculosis is a frequent cause of psoas abscess
• S aureus and anaerobic GNB is usually associated in the US
• Presentation: fever, lower abdominal or back pain referred to the hip or knee
• CT scan is the most useful diagnostic technique
• Treatment: surgical drainage and antibiotic therapy