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10 February 2014
Karlos Noel R. Aleta, MD
Lecture-based trans
Peritonitis

LEARNING OBJECTIVES CRITERIA FOR DIAGNOSIS

 To know the different types, causes and manifestations of  Two or more of following criteria are met:
peritonitis o Temp: >38°C (100.4°F) or <36°C (96.8°F)
 To know the different types, causes and manifestations of o Heart rate >90 bpm
intra-abdominal abscesses o Respiratory rate >20 bpm or PaCO2 <32 mmHg or
 To know the management of peritonitis and intra- mechanical ventilation
abdominal abscesses o WBC count >12,000/L or <4000/L or >10%
immature/band forms
INTRODUCTION
 Intrabdominal Infections: one of the most common and CLINICAL SPECTRUM OF INFECTIONS AND SIRS
most important challenges on surgeon INFECTION Identifiable source of microbial insult
o Skills of surgeon- require repeated laparotomies SIRS refer to the table above
o STAR- Stage Abdominal Restoration SEPSIS Identifiable source of infection + SIRS
 Despite ancillary diagnostics, diagnosis is still dependent on
SEVERE SEPSIS Sepsis + organ dysfunction
clinical criteria
Sepsis + cardiovascular collapse
 A mutidisciplinary approach may be as important for SEPTIC SHOCK
(requiring vasopressor support)
survival as surgery
 A critically ill patient may require intensive care support
 Peritoneal cavity is three times that of the surface ROUTES OF ENTRY
area of the skin, thus, it is a huge area to be infected  Bacteria may enter the cavity via 4 portals
 Mortality from peritonitis is about 10% (even in good units)  penetrating wound
EXTERIOR
 infection at laparatomy, PD
PATHOPHYSIOLOGY  gangrene of viscus
INTRA-ABDOMINAL
 Inflammation of the peritoneal cavity evokes series of  perforation of fluid
VISCERA
events.  post op leak
 An inflammatory response to peritoneal injury: BLOODSTREAM  as part of septicemia
o Resulting in influx of protein-rich fluid FEMALE GENITAL  acute salpingitis
 Activation of complement cascade TRACT  puerperal infection
 Up-regulation of peritoneal mesothelial cell activity  ADULTS:
 Invasion of peritoneum with PMN’s, neutrophils and o 30% post-op complication
macrophages o 20% acute appendicitis
 Stimulation of cytokine and chemokine production o 10% perforated peptic ulcer

 Local Consequences CLASSIFICATION

o Transmigration of granulocytes from peritoneal  Primary
capillaries to mesothelial surface  Secondary
o Dilatation of peritoneal blood vessels  Tertiary
o Enhanced permeability  Peritonitis from peritoneal dialysis
o Peritoneal edema
o Formation of protein-rich exudate PRIMARY  Monomicrobial
SECONDARY  Polymicrobial
 First line of defense: clearance of noxious agents via the TERTIARY  Nosocomial (Gram (-), Staph, Fungi)
lymphatics of parietal peritoneum, diaphragm and
omentum
PRIMARY
 Fibrin formation acts to wall off infection  Infection of the peritoneal cavity not directly related to
o Associated with abscess formation other intra-abdominal abnormality
 Majority are bacterial infections commonly known as
HOST RESPONSE – 5 key factors Spontaneous Bacterial Peritonitis (SBP)
1. Inoculum size  Usually occurs in the presence of ascites from variety of
2. Virulence of contaminating organisms underlying conditions
3. Presence of adjuvants within peritoneal cavity  In pre-antibiotic era, it accounted for ~10% of pediatric
4. Adequacy of local, regional, systemic host defenses abdominal emergencies
5. Adequacy of initial treatment  Associated with post necrotic cirrhosis & nephrotic
syndrome
 In adults, 25% from alcoholic cirrhosis
SIRS
o Post-necrotic cirrhosis, lymphedema, metastatic disease,
 After a severe insult, accompanied by an inability to
SLE, CAH, CHF
regulate inflammatory response
 WHY?
CIRRHOTIC PATIENTS
 Proinflammatory cytokines
 Hematogenous → most likely
o TNF-α
o IL-1, IL-6, IL-12 o Organisms removed by liver from circulation may
o IFN-γ contaminate hepatic lymph pass through permeable
lymphatic walls into ascetic fluid

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 Peritonitis

o Portosystemic shunting → greatly decrease hepatic o CHON concentration

clearance on bacteremia & increase opportunity for o Gram staining/Culture sensitivity  anaerobic or aerobic
metastatic infection → susceptible sites ~ ascetic
collection DIAGNOSIS
o Importance of intrahepatic shunting in pathogenesis  Patients with (+) cultures with few leukocytes and no s/sx
of disease emphasized by infrequency in non-liver  bacterascites  early colonization before host response
ascetic conditions  Mortality of patients with low leukocyte response is same as
o Hepatic reticuloendothelial system important in patients with high leukocyte response
removal of bacteria from circulation  Conversely (-) ascitic fluid culture ~ culture negative
 ↓ activity in cirrhotics neutrocytic ascites  (+) blood culture in 1/3 of these
 ↓ in phagocytic activity in cirrhotics ~ severity of patients
disease  Diagnostic if GS yield is positive; more commonly negative
 Bacteremia ~ 75% with aerobic – may be negative in
TB PERITONITIS (TBP) anaerobic
 Most likely hematogenous spread from  Usually same organism isolated in peritoneal fluid is
remote focus/foci (mostly from lung) recovered in blood
ROUTE  Direct entry of tubercle bacili into the
OF peritoneal cavity from lymph node, intestine, SECONDARY
SPREAD genital tract with active disease is possible  Most common cause of peritonitis
 TBP may become clinically evident after  From perforation of a hollow viscus or other intra-
primary focus has healed abdominal pathology
 Gradual onset – fever, weight loss, malaise,  Requires surgical intervention in virtually all cases
night sweats, abdominal distension  Understanding of the anatomic spaces of the peritoneal
MANIFES-  Abdomen “doughy”, may not be rigid cavity is crucial
TATIONS  Surgery/Laparoscopy: Multiple nodules
scattered over peritoneal surface and
omentum
o Adhesions, variable amount of peritoneal
fluid

ROUTES OF ENTRANCE
 Enteric bacteria
o Access into peritoneal cavity by directly traversing intact
intestinal wall
o Animal studies
o Multiplicity of species of anaerobic organisms in
peritoneal fluid with infrequent bacteremia
 Pre-pubertal girls
o Ascending of genital origin
o Pneumococci in both vaginal secretions & peritoneal fluid
o Alkaline pH, vs acidic pH during post-pubertal, is less
inhibitory to bacterial growth
 Transfallopian
o (+) IUD
o Spread of gonococcal or chlamydial peri-hepatitis (Fitz-
Hugh-Curtis syndrome)
o Presumably via fallopian tube and paracolic gutters to
subphrenic space
o May also be hematogenous

CLINICAL PRESENTATION
 Pediatrics: acute febrile illness often confused with acute
appendicitis because of its s/sx
 Adults – Cirrhotic patients: atypical, fever with or
without abdominal symptoms
 Primary peritonitis: differential diagnosis for acute
decompensation of CLD especially with hepatic
encephalopathy

DIAGNOSIS
 Laparotomy: diagnosis of primary peritonitis with certainty
to exclude intra-abdominal pathology
 Examination of peritoneal fluid: surmise diagnosis of
peritonitis
o Cell CT / Diff CT

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 Peritonitis

PATHOLOGIC EFFECTS
 Widespread absorption of toxins from large inflamed
surface
 Associated paralytic ileus
o Loss of fluid
o Loss of electrolytes
o Loss of CHON
 Gross abdominal distension- elevation of diaphragm

SPECIAL INVESTIGATION
CBC  marked leukocytosis
SERUM AMYLASE  acute pancreatitis
CHEST X-RAY (upright)  pulmonary pathology
ABDOMINAL X-RAY  free gas
 free gas, pinpoint diagnosis,
CT SCAN
peritoneal fluid
ASPIRATION  pus like, bile, urine, feces

MANAGEMENT
 Recurring themes of treatment in peritonitis:
o Resuscitation- load with fluids and electrolytes
o Antibiotics- empiric treatment based on pathology
o Peritoneal lavage- culture fluid
TERTIARY o Source control- of pathology; liters of NSS: saline lavage
 Defined as recurrent infection of the peritoneal cavity
after an episode of a primary or secondary peritonitis NON-OPERATIVE TREATMENT
 Occurs when source control, antiBxTx or host immunity are  INDICATIONS
inadequate o Acute Pancreatitis
o Some cases of typhoid peritonitis
MICROBIAL FLORA o Pelvic peritonitis
 Feel an inflammatory mass, vaginal or rectal
 E. coli
 Confirm by aspiration
 Streptococcus fecalis
FROM BOWEL-  Drain pus vaginally/rectally
 Pseudomonas
MIXED FECAL o Pus mainly under diaphragm
 Klebsiella
FLORA o Peritonitis confirmed by aspiration; but patient too ill to
 Proteus
withstand laparotomy. Delay operation until patient
 Anaerobic: Clostridium, Bacteroides
improved
 Chlamydial
GYNECOLOGIC
 Gonococcal
PERITONITIS IN CAPD
 Streptococcal
 CAPD  Continuous Ambulatory Peritoneal Dialysis
 Streptococcal
 Safe cost-effective treatment for ESRD (End Stage Renal
BLOODBORNE  Pneumococcal
Disease)
 Staphylococcal
 Complication of Peritonitis
 Tuberculous
 Microbial Factors:
o Ability to grow in dialysis fluid
CLINICAL FEATURE o Production of extracellular (biofilm)
 Depends on precipitating cause or History
 Severe pain lie still
 Irritation of the diaphragm  shoulder tip
 Vomiting
EARLY  Temperature and pulse rate rises/elevated
 Localized/generalized tenderness extent
 Abdominal wall rigidrebound tenderness
 Abdominal silenthear heart beat and respi
 Direct Rectal Exam (DRE): tenderness on
Pouch of Douglas

 Abdomen: distended, tympanitic, signs of free

fluid
ADVANCE  Toxic: feeble rapid pulse
 Vomiting feculent
 Skin: moist, cold, cyanosed Peritoneal Dialysis

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 Peritonitis

o Complex interplay of opsonisation, phagocytosis and

intercellular killing by peritoneal macrophage,
mesothelials and neutrophils
 BUT Dialyzed peritoneal cavity not a supportive milieu for
operations of cellular and immunologic cellular mechanisms
o Low pH, high osmolarity, IgG, complement
o Correlation between host immunity and incidence of
peritonitis not yet well-established

MICROBIOLOGY
 Staph aureus
 P. aeruginosa

CLINICAL PRESENTATION
 Any 2 criterion to diagnose CAPD-related peritonitis
1. Sign and symptom of peritoneal irritation
 Abdominal Pain
2. Cloudy dialysate effluent with WBC count > 100mm3
3. Positive culture of dialysate fluid
4. Turbid dialysate  by abdominal pain and/or tenderness

DIFFERENTIAL DIAGNOSIS OF A CLOUDY EFFLUENT

 Culture-positive infectious peritonitis
 Infectious peritonitis with sterile cultures
 Chemical peritonitis
 Eosinophilia of the effluent
 Hemoperitoneum
 Malignancy (rare)
 Chylous effluent (rare)
 Specimen taken from “dry” abdomen

MANAGEMENT AND PREVENTION

AMBULATORY BASIS  intraperitoneal antibiotics
HOSPITALIZATION  severely ill
 unable to manage administration
of antibiotics at home
INTRA-PERITONEAL  permits high concentration and
ADMINISTRATION self-delivery by the patient 10-
OF ANTIBIOTICS 14days
PREFERRED
METHOD FOR Rx
DELIVERY

TERMINOLOGIES FOR PERITONITIS

 an episode that occurs within 4 weeks of
2 MAIN ROUTES OF INFECTION RECURRENT completion of treatment of a prior episode
TRANSLUMINAL  from break in sterile technique during but with a different organism
dialysate exchange  an episode that occurs within 4 weeks of
CONTIGUOUS  microorganisms access the completion of treatment of a prior episode
SPREAD peritoneum along tract of PD catheter RELAPSING
with the same organism or 1 sterile
LESSER ROUTES episode
HEMATOGENOUS  from a known distant site of infection  an episode that occurs > 4 weeks after
SPREAD REPEAT completion of treatment of a prior episode
DIRECT  from GI tract with the same organism
CONTAMINATION  failure of effluent to clear after 5 days of
REFRACTORY
appropriate antibiotics
HOST DEFENSE FACTORS CATHETER-  peritonitis in conjuction with an exit-site
 Microorganisms  removed from dialysate cavity by RELATED or tunnel infection with the same
o Fibrin trapping and sequestration of microorganisms PERITONITIS organism or 1 sterile site
operate effectively despite dilution of fibrinogen and
coagulation proteins
o Removal of dialysate serves to  or eliminate inoculum
of contaminating microorganisms

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 Peritonitis

INDICATIONS FOR CATHETER REMOVAL FOR PD- ABDOMINAL ABSCESS

RELATED INFECTIONS  Observe
 Refractory peritonitis  Document
 Relapsing peritonitis  Intervene if deteriorating
 Refractory exit site and tunnel infection o Surgical or percutaneous
 Fungal peritonitis
 Catheter removal may also be considered for:
o Repeat peritonitis
o Mycobactrial peritonitis
o Multiple enteric organisms

ABSCESS IN THE ABDOMEN

CLINICAL PRESENTATION
 s/p (status post) laparotomy 14-21 days
o Temperature does not fall, or it falls & then rises in
spikey pattern w/c shows (+) pus somewhere within
o Patient not well, does not eat, loses weight
o ↑ WBC
o If loops of his gut pass through abscess → may become
obstructed acutely or sub-acutely

LOCALIZED ABSCESS
 Can be a result from: Figure: Intra-abdominal abscess, CT scan (CT scan of the
o Generalized peritonitis – they are one of its major pelvis showing a large intra-abdominal mass)
complications
o Some primary focus of infection – e.g. appendicitis or
SUBPHRENIC ABSCESS
salpingitis (PID)
 Peritonitis – either local or general
o An abdominal injury in which gut was perforated or
o PPU (Perforated Peptic Ulcer)
devitalized
o Typhoid ulcer
o Any laparotomy
o Appendicitis
o Infected CS (Caesarean Section)
o PID (Pelvic Inflammatory Disease)
 Injury to ruptured viscus
 s/p laparotomy with contamination
 Ruptures amebic liver abscess

PELVIC ABSCESS
 From:
o female genital tract
o appendicitis
o generalized peritonitis
 Drainage:
o vaginally (2 routes for female)
o rectally

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