INTRA-ABDOMINAL
INFECTIONS
Dr. Sameh Ahmad Muhamad abdelghany
Lecturer Of Clinical Pharmacology
Mansura Faculty of medicine
2
Infections
INTRODUCTION
TYPES
RISK FACTORS
Diagnosis
Treatment
CONTENTS
3
OBJECTIVES
 Describe pathogenesis & clinical
characteristics of intra-abdominal
infections
 Identify most likely etiologic organism(s)
 Review appropriate drug therapy
Definition
5
INTRA-ABDOMINAL INFECTIONS
 Infections contained within the peritoneum or
retroperitoneal space.
 Peritoneal cavity contains:
 Stomach
 Jejunum, Ileum
 Appendix
 Large intestine (colon)
 Liver, gallbladder and spleen
 Retroperitoneal space:
 Duodenum
 Pancreas
 Kidneys
6
INTRA-ABDOMINAL
INFECTIONS
 Peritonitis
 Intra-abdominal Abscess
 Appendicitis
 Diverticulitis
 Antibiotic-Associated Diarrhea
 Food Poisoning/Traveler’s Diarrhea
 Helicobacter pylori
 Pelvic Inflammatory Disease
 Viral
 Parasitic
7
Anatomy of GIT
8
GIT Microflora
 Stomach:
o Helicobacter pylori
o Streptococci
o Lactobacilli
 Upper Intestine:
 Aerobes
o Streptococci (Enterococci)
o Staphylococci
o Lactobacilli
o E. coli, Klebsiella
 Anaerobes
o Bacteroides
9
GIT Microflora
 Ileum:
 Aerobes:
o Streptococci
o Staphylococci
o Escherichia coli,Klebsiella
o Enterobacter
 Anaerobes:
o Bacteroides
o Clostridium
10
GIT Microflora
 Colon:
 Anaerobes:
o Bacteroides
o Peptostreptococci
o Clostridium
o Bifidobacteria
 Aerobes:
o Escherichia coli, Klebsiella
o Enterobacter
o Streptococci (Enterococci)
o Staphylococci
11
GIT Microflora
Intra-abdominal infections result in
2 major clinical manifestations
I. Early or diffuse infection results in
localized or generalized peritonitis.
II. Late and localized infections produces
an intra-abdominal abscess.
PERITONITIS
13
Peritonitis
 Inflammation of the serous
lining of the peritoneal
cavity due to:
o Microorganisms
o Chemicals
o Irradiation
o Foreign body injury
14
Peritonitis
 TYPES
I. Primary (Spontaneous Bacterial
Peritonitis)
II. Secondary
III. Tertiary
15
Primary Peritonitis
 Relatively infrequent
 25% of patients with alcoholic cirrhosis
 60% of all patients on chronic ambulatory
peritoneal dialysis (CAPD) will have at least
one episode in 1st year.
 Average incidence in CAPD patients is 1.3 to
1.4 episodes/yr.
 Catheter connecting abdominal cavity to
exterior body is a major risk factor
16
Primary Peritonitis
 No focus of disease is evident
 Arises without a breach in the peritoneal
cavity or GIT
 Bacteria transported from blood stream to
peritoneal cavity (Cirrhosis, CAPD)
 Usually monomicrobial
17
Primary Peritonitis
 Usually occurs in people who have an
accumulation of fluid in their
abdomens (ascites).
 The fluid that accumulates creates a
good environment for the growth of
bacteria.
18
Primary Peritonitis
 Common Bacteria:
 Escherichia coli
 Streptococci
 Enterococci
 Klebsiella
 Staphylococci (CAPD patients)
 Pseudomonas aeruginosa
 Bacteroides sp.
19
Secondary Peritonitis
 Caused by the entry of bacteria or enzymes
into the peritoneum from the gastrointestinal
or biliary tract.
 This can be caused due to :
i. an ulcer eating its way through stomach
wall
ii. intestine when there is a rupture of the
appendix
iii. a ruptured diverticulum.
20
Secondary Peritonitis
 Also, it can occur due to burst or injury to
an internal organ which bleeds into the
internal cavity.
o Community acquired or nosocomial
o Usually polymicrobial
21
Tertairy Peritonitis
 Peritonitis in a critically ill patient
which persists or recurs at least 48 h
after apparently adequate
management of primary or
secondary peritonitis
22
Risky of Peritonitis
Peritonitis is very
serious & can be
life threatening if
not treated
properly!!!
RISK
FACTORS
24
Risk Factors
Risk factors for Primary
Peritonitis:
 Liver disease (cirrhosis)
 Fluid in the abdomen
 Weakened immune system
 Pelvic inflammatory disease
25
Risk Factors
 Risk factors for secondary peritonitis
include:
 Appendicitis (inflammation of the
appendix)
 Stomach ulcers, Twisted intestine,
Pancreatitis
 Inflammatory bowel disease
 Injury caused by an operation.
 Peritoneal dialysis, Trauma.
DIAGNOSIS
27
CLINICAL PICTURE
 Abdominal pain
 Anorexia, Nausea/Vomiting
 Loss of Appetite
 Fever (38-40 ºC)
 Abdominal distention and tenderness
 Hypoactive or faint bowl sounds
 Leukocytosis
28
CLINICAL PICTURE
 Shallow Breaths
 Low BP
 Limited Urine Production
 Inability to pass gas or feces
29
CLINICAL PICTURE
 An acutely ill patient tends to lie
“very” still because any movement
causes excruciating pain.
 They will lie with there knees bent
to decrease strain on the tender
peritoneum.
30
Physical Examination
 Detect any swelling & tenderness in
the area as well as signs of fluid has
collected in the area.
 Listen to the bowel sounds & check
for difficulty breathing
 Low blood pressure
 signs of dehydration.
31
Physical Examination
 The abdomen may be rigid and
boardlike
 Accumulations of fluid will be
notable in primary due to ascites.
32
Peritonitis
33
INVESTIGATIONS
a) Blood Test
b) Samples of fluid from the abdomen
c) CT Scan
d) Chest X-rays
e) Peritoneal lavage
34
INVESTIGATIONS
 Peritoneal Fluid Analysis
 Normally:
 20 to 50 mL transudate
 Peritoneal membrane measures approx. 1.7 metres
square
 WBC < 300 cells/mm3
 Protein: <3 g/dL
 Bacterial peritonitis:
 300 to 500mL inflow/hr resulting in hypovolemia.
 WBC > 300 cells/mm3
 Gram stain + for bacteria
35
INVESTIGATIONS
 Microbiology
 Blood cultures often –ve
 Peritoneal fluid used (paracentesis)
 Health care associated intra-abdominal
infection usually due to nosocomial
organisms particular to the site of the
operation and specific hospital and unit
36
Prognosis
 Untreated peritonitis is poor, usually
resulting in death.
 With Tx, prognosis is variable, dependent
on the underlying causes.
37
Peritonitis
38
Peritonitis
INTRA-ABDOMINAL
ANBCESS
40
Intra – abdominal Abscess
 Result from chronic inflammation and often
occur without generalized peritonitis.
 Located within peritoneal cavity or visceral
organs.
 May range from a few milliliters to a liter in
volume.
 Often have a fibrinous capsule and take days to
yrs to form.
 Appendicitis is the most common cause.
 Ultrasound or CT scan may be used for
evaluation
41
Intra – abdominal Abscess
 Common Bacteria:
 E. coli
 Klebsiella
 Enterococci
 B. fragilis
 Clostridium
42
CLINICAL PICTURE
 Symptoms less dramatic than peritonitis
 +/- pain
 +/- fever
 +/- abdominal distention
43
Complication
 Ruptured abscess
o Spread of bacteria + toxins into
peritoneum - peritonitis
o Spread of bacteria + toxins into systemic
circulation – sepsis, multi-organ failure,
death
44
INVESTIGATIONS
 Labs:
 Leukocytosis
 +/- positive blood cultures
 +/-hyperglycemia
 Ultrasound, GI contrast study, or CT
scan may be used for evaluation
45
Intra – abdominal Abscess
TREATMENT
47
Treatment of
Intra-abdominal Infections
 Combination of modalities:
A. Surgical:
 Prompt drainage of abscess (secondary
peritonitis) and/or debridement,
 Resection of perforated colon, small
intestine, ulcers
 Repair of trauma.
48
Treatment of
Intra-abdominal Infections
B. Support of Vital functions:
 Blood pressure/fluid replacement,
 Monitor heart rate
 Monitor urine out put (0.5 ml/kg/hr)
C. Appropriate antimicrobial therapy
49
Antibiotic Therapy
 Empiric Antibiotic Therapy MUST include
aerobic/anaerobic coverage
 Aerobic and Anaerobic activity
o Ampicillin/sulbactam (Unasyn) (enterococci)
o Piperacillin/tazobactam (Zosyn) (enterococci)
o Cefotetan (Cefotetan)
o Cefoxitin (Mefoxin)
o Imipenem/cilastin (Primaxin)
o Meropenem (Merrem)
o Moxifloxacin (Avelox)
50
Antibiotic Therapy
 Empiric Antibiotic Therapy MUST include
aerobic/anaerobic coverage
 Anaerobic activity
o Chloramphenicol( also includes aerobic Gram
+/-)
o Clindamycin (also includes aerobic Gram +)
o Metronidazole (anaerobic coverage only)
51
Antibiotic Therapy
 Empiric Antibiotic Therapy MUST include
aerobic/anaerobic coverage
 Aerobic activity
i. Aminoglycosides:
o gentamicin, tobramycin (Gram negatives only)
ii. Beta-lactams:
o Cefotaxime (Claforan)
o Ceftriaxone (Rocephin)
o Aztreonam (Azactam) (Gram negative only)
iii. Quinolones:
o Ciprofloxacin (Cipro) (Mostly Gram negative)
o Levofloxacin (Levaquin) (Gram +/- and some anaerobic
coverage)
iv. Vancomycin/Linezolid (Enterococci, MRSA)
52
Antibiotic Therapy
 Factors involved in selection:
 Severity of infection, suspected infecting organism(s)
and resistance patterns, efficacy, toxicity (renal
dysfunction),allergies.
 Evaluating response:
 Improvement in 2 to 3 days
 Switch for oral antibiotic therapy
 Failure to improve:
 Resistant organisms
 Recurrent surgical infections
 Other infections: (urinary tract infections, pneumonia)
APPENDECITIS
54
Appendicitis
 Highest incidence 10-19y/o
 Male > female
 Pathophysiology:
o Relationship to onset of signs
 0-24h after signs onset: obstruction within
appendix , inflammation & occlusion of
vascular & lymphatic flow, bacterial
overgrowth then necrosis.
 >48h after signs onset: perforation,
abscess/peritonitis
55
Appendicitis
56
CLINICAL PICTURE
 Early sign:
 dull, non-localized pain
 Indigestion
 bowel irregularity
 flatulence
57
CLINICAL PICTURE
 Later signs:
 pain/tenderness more localized
 N/V
 Fever > 39 degrees celcius
 leukocytes >15000
 perforation likely
58
Management
 Treatment :Both surgical & Antibiotics
 Acute, non-perforated appendicitis
 cefazolin + metronidazole
 Perforated appendicitis
o Anti-anaerobic cephalosporin (e.g. Cefotetan,
Cefoxitin, Piperacillin/tazobactam,
Ampicillin/sulbactam, Imipenem
o Combination therapy: Aminoglycoside +/-
Clindamycin or Metronidazole
 Antibiotics are started before surgery, continued
for 7- 10 days.
Antibiotic
Associated Diarrhea
60
Antibiotic Associated Diarrhea
 Antibiotic therapy (broad spectrum
agents:
 Clindamycin
 Ampicillin
 3rd generation cephalosporins
61
Pseudomembranous Colitis
 Clostridium difficile: toxin mediated
disease
 Toxin A (major) and B (minor):
o cause inflammation, necrosis, loss of fluid
electrolytes
 Associated with broad spectrum
antibiotics
62
Pseudomembranous Colitis
 Patients may develop diarrhea after 3 or
more days of hospitalization or within 2
months of antibiotic therapy.
 3 to 5% of adults are carriers of C.
difficile
 Recurrence in 7 to 20% of patients.
63
Pseudomembranous Colitis
 Treatment
 FIRST LINE:
 Metronidazole (Treatment of Choice)
o 250mg PO QID or 500mg PO/IV TID x 10-14 days
 ALTERNATIVE: (if pregnant, not responding to
metronidazole or recurrences)
 Vancomycin
o 125mg PO QID x 10-14 days +/- rifampin 600mg PO
BID
 Always stop the drug responsible for causing the
infection as soon as possible!
64
Pseudomembranous Colitis
65
thanksF o r W a t c h i n g

Intra-abdominal infections

  • 1.
    INTRA-ABDOMINAL INFECTIONS Dr. Sameh AhmadMuhamad abdelghany Lecturer Of Clinical Pharmacology Mansura Faculty of medicine
  • 2.
  • 3.
    3 OBJECTIVES  Describe pathogenesis& clinical characteristics of intra-abdominal infections  Identify most likely etiologic organism(s)  Review appropriate drug therapy
  • 4.
  • 5.
    5 INTRA-ABDOMINAL INFECTIONS  Infectionscontained within the peritoneum or retroperitoneal space.  Peritoneal cavity contains:  Stomach  Jejunum, Ileum  Appendix  Large intestine (colon)  Liver, gallbladder and spleen  Retroperitoneal space:  Duodenum  Pancreas  Kidneys
  • 6.
    6 INTRA-ABDOMINAL INFECTIONS  Peritonitis  Intra-abdominalAbscess  Appendicitis  Diverticulitis  Antibiotic-Associated Diarrhea  Food Poisoning/Traveler’s Diarrhea  Helicobacter pylori  Pelvic Inflammatory Disease  Viral  Parasitic
  • 7.
  • 8.
    8 GIT Microflora  Stomach: oHelicobacter pylori o Streptococci o Lactobacilli  Upper Intestine:  Aerobes o Streptococci (Enterococci) o Staphylococci o Lactobacilli o E. coli, Klebsiella  Anaerobes o Bacteroides
  • 9.
    9 GIT Microflora  Ileum: Aerobes: o Streptococci o Staphylococci o Escherichia coli,Klebsiella o Enterobacter  Anaerobes: o Bacteroides o Clostridium
  • 10.
    10 GIT Microflora  Colon: Anaerobes: o Bacteroides o Peptostreptococci o Clostridium o Bifidobacteria  Aerobes: o Escherichia coli, Klebsiella o Enterobacter o Streptococci (Enterococci) o Staphylococci
  • 11.
    11 GIT Microflora Intra-abdominal infectionsresult in 2 major clinical manifestations I. Early or diffuse infection results in localized or generalized peritonitis. II. Late and localized infections produces an intra-abdominal abscess.
  • 12.
  • 13.
    13 Peritonitis  Inflammation ofthe serous lining of the peritoneal cavity due to: o Microorganisms o Chemicals o Irradiation o Foreign body injury
  • 14.
    14 Peritonitis  TYPES I. Primary(Spontaneous Bacterial Peritonitis) II. Secondary III. Tertiary
  • 15.
    15 Primary Peritonitis  Relativelyinfrequent  25% of patients with alcoholic cirrhosis  60% of all patients on chronic ambulatory peritoneal dialysis (CAPD) will have at least one episode in 1st year.  Average incidence in CAPD patients is 1.3 to 1.4 episodes/yr.  Catheter connecting abdominal cavity to exterior body is a major risk factor
  • 16.
    16 Primary Peritonitis  Nofocus of disease is evident  Arises without a breach in the peritoneal cavity or GIT  Bacteria transported from blood stream to peritoneal cavity (Cirrhosis, CAPD)  Usually monomicrobial
  • 17.
    17 Primary Peritonitis  Usuallyoccurs in people who have an accumulation of fluid in their abdomens (ascites).  The fluid that accumulates creates a good environment for the growth of bacteria.
  • 18.
    18 Primary Peritonitis  CommonBacteria:  Escherichia coli  Streptococci  Enterococci  Klebsiella  Staphylococci (CAPD patients)  Pseudomonas aeruginosa  Bacteroides sp.
  • 19.
    19 Secondary Peritonitis  Causedby the entry of bacteria or enzymes into the peritoneum from the gastrointestinal or biliary tract.  This can be caused due to : i. an ulcer eating its way through stomach wall ii. intestine when there is a rupture of the appendix iii. a ruptured diverticulum.
  • 20.
    20 Secondary Peritonitis  Also,it can occur due to burst or injury to an internal organ which bleeds into the internal cavity. o Community acquired or nosocomial o Usually polymicrobial
  • 21.
    21 Tertairy Peritonitis  Peritonitisin a critically ill patient which persists or recurs at least 48 h after apparently adequate management of primary or secondary peritonitis
  • 22.
    22 Risky of Peritonitis Peritonitisis very serious & can be life threatening if not treated properly!!!
  • 23.
  • 24.
    24 Risk Factors Risk factorsfor Primary Peritonitis:  Liver disease (cirrhosis)  Fluid in the abdomen  Weakened immune system  Pelvic inflammatory disease
  • 25.
    25 Risk Factors  Riskfactors for secondary peritonitis include:  Appendicitis (inflammation of the appendix)  Stomach ulcers, Twisted intestine, Pancreatitis  Inflammatory bowel disease  Injury caused by an operation.  Peritoneal dialysis, Trauma.
  • 26.
  • 27.
    27 CLINICAL PICTURE  Abdominalpain  Anorexia, Nausea/Vomiting  Loss of Appetite  Fever (38-40 ºC)  Abdominal distention and tenderness  Hypoactive or faint bowl sounds  Leukocytosis
  • 28.
    28 CLINICAL PICTURE  ShallowBreaths  Low BP  Limited Urine Production  Inability to pass gas or feces
  • 29.
    29 CLINICAL PICTURE  Anacutely ill patient tends to lie “very” still because any movement causes excruciating pain.  They will lie with there knees bent to decrease strain on the tender peritoneum.
  • 30.
    30 Physical Examination  Detectany swelling & tenderness in the area as well as signs of fluid has collected in the area.  Listen to the bowel sounds & check for difficulty breathing  Low blood pressure  signs of dehydration.
  • 31.
    31 Physical Examination  Theabdomen may be rigid and boardlike  Accumulations of fluid will be notable in primary due to ascites.
  • 32.
  • 33.
    33 INVESTIGATIONS a) Blood Test b)Samples of fluid from the abdomen c) CT Scan d) Chest X-rays e) Peritoneal lavage
  • 34.
    34 INVESTIGATIONS  Peritoneal FluidAnalysis  Normally:  20 to 50 mL transudate  Peritoneal membrane measures approx. 1.7 metres square  WBC < 300 cells/mm3  Protein: <3 g/dL  Bacterial peritonitis:  300 to 500mL inflow/hr resulting in hypovolemia.  WBC > 300 cells/mm3  Gram stain + for bacteria
  • 35.
    35 INVESTIGATIONS  Microbiology  Bloodcultures often –ve  Peritoneal fluid used (paracentesis)  Health care associated intra-abdominal infection usually due to nosocomial organisms particular to the site of the operation and specific hospital and unit
  • 36.
    36 Prognosis  Untreated peritonitisis poor, usually resulting in death.  With Tx, prognosis is variable, dependent on the underlying causes.
  • 37.
  • 38.
  • 39.
  • 40.
    40 Intra – abdominalAbscess  Result from chronic inflammation and often occur without generalized peritonitis.  Located within peritoneal cavity or visceral organs.  May range from a few milliliters to a liter in volume.  Often have a fibrinous capsule and take days to yrs to form.  Appendicitis is the most common cause.  Ultrasound or CT scan may be used for evaluation
  • 41.
    41 Intra – abdominalAbscess  Common Bacteria:  E. coli  Klebsiella  Enterococci  B. fragilis  Clostridium
  • 42.
    42 CLINICAL PICTURE  Symptomsless dramatic than peritonitis  +/- pain  +/- fever  +/- abdominal distention
  • 43.
    43 Complication  Ruptured abscess oSpread of bacteria + toxins into peritoneum - peritonitis o Spread of bacteria + toxins into systemic circulation – sepsis, multi-organ failure, death
  • 44.
    44 INVESTIGATIONS  Labs:  Leukocytosis +/- positive blood cultures  +/-hyperglycemia  Ultrasound, GI contrast study, or CT scan may be used for evaluation
  • 45.
  • 46.
  • 47.
    47 Treatment of Intra-abdominal Infections Combination of modalities: A. Surgical:  Prompt drainage of abscess (secondary peritonitis) and/or debridement,  Resection of perforated colon, small intestine, ulcers  Repair of trauma.
  • 48.
    48 Treatment of Intra-abdominal Infections B.Support of Vital functions:  Blood pressure/fluid replacement,  Monitor heart rate  Monitor urine out put (0.5 ml/kg/hr) C. Appropriate antimicrobial therapy
  • 49.
    49 Antibiotic Therapy  EmpiricAntibiotic Therapy MUST include aerobic/anaerobic coverage  Aerobic and Anaerobic activity o Ampicillin/sulbactam (Unasyn) (enterococci) o Piperacillin/tazobactam (Zosyn) (enterococci) o Cefotetan (Cefotetan) o Cefoxitin (Mefoxin) o Imipenem/cilastin (Primaxin) o Meropenem (Merrem) o Moxifloxacin (Avelox)
  • 50.
    50 Antibiotic Therapy  EmpiricAntibiotic Therapy MUST include aerobic/anaerobic coverage  Anaerobic activity o Chloramphenicol( also includes aerobic Gram +/-) o Clindamycin (also includes aerobic Gram +) o Metronidazole (anaerobic coverage only)
  • 51.
    51 Antibiotic Therapy  EmpiricAntibiotic Therapy MUST include aerobic/anaerobic coverage  Aerobic activity i. Aminoglycosides: o gentamicin, tobramycin (Gram negatives only) ii. Beta-lactams: o Cefotaxime (Claforan) o Ceftriaxone (Rocephin) o Aztreonam (Azactam) (Gram negative only) iii. Quinolones: o Ciprofloxacin (Cipro) (Mostly Gram negative) o Levofloxacin (Levaquin) (Gram +/- and some anaerobic coverage) iv. Vancomycin/Linezolid (Enterococci, MRSA)
  • 52.
    52 Antibiotic Therapy  Factorsinvolved in selection:  Severity of infection, suspected infecting organism(s) and resistance patterns, efficacy, toxicity (renal dysfunction),allergies.  Evaluating response:  Improvement in 2 to 3 days  Switch for oral antibiotic therapy  Failure to improve:  Resistant organisms  Recurrent surgical infections  Other infections: (urinary tract infections, pneumonia)
  • 53.
  • 54.
    54 Appendicitis  Highest incidence10-19y/o  Male > female  Pathophysiology: o Relationship to onset of signs  0-24h after signs onset: obstruction within appendix , inflammation & occlusion of vascular & lymphatic flow, bacterial overgrowth then necrosis.  >48h after signs onset: perforation, abscess/peritonitis
  • 55.
  • 56.
    56 CLINICAL PICTURE  Earlysign:  dull, non-localized pain  Indigestion  bowel irregularity  flatulence
  • 57.
    57 CLINICAL PICTURE  Latersigns:  pain/tenderness more localized  N/V  Fever > 39 degrees celcius  leukocytes >15000  perforation likely
  • 58.
    58 Management  Treatment :Bothsurgical & Antibiotics  Acute, non-perforated appendicitis  cefazolin + metronidazole  Perforated appendicitis o Anti-anaerobic cephalosporin (e.g. Cefotetan, Cefoxitin, Piperacillin/tazobactam, Ampicillin/sulbactam, Imipenem o Combination therapy: Aminoglycoside +/- Clindamycin or Metronidazole  Antibiotics are started before surgery, continued for 7- 10 days.
  • 59.
  • 60.
    60 Antibiotic Associated Diarrhea Antibiotic therapy (broad spectrum agents:  Clindamycin  Ampicillin  3rd generation cephalosporins
  • 61.
    61 Pseudomembranous Colitis  Clostridiumdifficile: toxin mediated disease  Toxin A (major) and B (minor): o cause inflammation, necrosis, loss of fluid electrolytes  Associated with broad spectrum antibiotics
  • 62.
    62 Pseudomembranous Colitis  Patientsmay develop diarrhea after 3 or more days of hospitalization or within 2 months of antibiotic therapy.  3 to 5% of adults are carriers of C. difficile  Recurrence in 7 to 20% of patients.
  • 63.
    63 Pseudomembranous Colitis  Treatment FIRST LINE:  Metronidazole (Treatment of Choice) o 250mg PO QID or 500mg PO/IV TID x 10-14 days  ALTERNATIVE: (if pregnant, not responding to metronidazole or recurrences)  Vancomycin o 125mg PO QID x 10-14 days +/- rifampin 600mg PO BID  Always stop the drug responsible for causing the infection as soon as possible!
  • 64.
  • 65.
    65 thanksF o rW a t c h i n g