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‫بسم‬
‫هللا‬
‫الرحمن‬
‫الرحيم‬
‫صدق‬
‫هللا‬
‫العظيم‬
‫قالوا‬
‫سبحانك‬
‫ال‬
‫علم‬
‫لنا‬
‫إال‬
‫ما‬
‫علمتنا‬
‫إنك‬
‫أنت‬
‫العليم‬
‫الحكيم‬
‫سورة‬
‫البقرة‬
‫اآلية‬
:
32
INTRA-ABDOMINAL
INFECTION
Hamed Rashad
Professor Of Surgery Banha University
Introduction
• Doctors should be broud of themselves
• Surgeons have a special mission
• Who is the good surgeon
Introduction
• The only thing left to the patient is the scar ?
• The longer the incision the bigger the surgeon
• The metabolic response to surgery and trauma
a- Inevitable catabolic phase
b- Turning point phase
c- Anabolic phase
d- Late anabolic Fat gain phase
5
Definition of Peritoneum
• The peritoneum is the largest serous membrane of the body
lining the abdominal cavity
Structure
• Consists of a closed sac, containing a small amount of
serous fluid, within the abdominal cavity.
Two layers
• The parietal layer - lines the abdominal wall
• Visceral layer – covers the organs (viscera) in the
abdominal and pelvic cavities
Anatomy
•Parietal peritoneum lines the anterior abdominal wall
•The two layers are actually in contact - friction prevented by
the presence of serous fluid secreted by the peritoneal cells
•Peritoneal cavity is only a potential cavity
•In women there is the communication of the peritoneal
cavity to the external atmosphere through the openings of the
fallopian tubes (at fimbrial ends)
•In males the peritoneal cavity is completely closed.
Functions of the Peritoneum
• Pain perception ( Parietal peritoneum )
• Visceral lubrication
• Fluid and particulate absorption
• Inflammatory and immune response
• Fibrinolytic activity
Intra abdominal infection
• Intraperitoneal = All intraabdominal organ
• Extraperitoneal = Duodenum - pancreas -
kidneys
Intra abdominal infection
Infection :
• Invasion of microorganisms to the healthy
tissue produces an inflammatory reaction
• Sepsis:
 Infection, (with local manifestations) plus
– >2 SIRS Criteria.
– Temp > 38oC or < 36oC
– HR > 90 bpm
– RR > 20 bpm or PaCO2 < 32 mmHg
– WBC > 12 x 109/L, < 4 x 109/L or >10% band form
Intra abdominal infection
• Severe Sepsis:
 Sepsis associated with hypotension,
hypoperfusion, and/or organ-dysfunction
 The hypotension can be corrected with fluid
replacement
• Septic shock: sepsis with hypotension
despite adequate fluid resuscitation
Intra abdominal infection
• Definition :
Bacterial inflammation that affect the visceral as
well as the parietal peritoneum and may diffuse
to neighboring tissues.
 Peritonitis
 Intraabdominal abscess
Highlight of intraabdominal infection
•Intra abdominal infections are still an
extremely difficult problem in surgery
– High incidence: ± 8 % of total hospital
mortality
– High mortality rate :
• < 20th century : 80-90
• > 1974: Recently 13 – 43 %
• Published epidemiologic data suggest that sepsis
causes one-third to half of in-hospital mortality in the
USA.
Intraabdominal infection
Classification
• Uncomplicated IAIs
The infectious process involves only a single
organ and does not proceed to the peritoneum
• Complicated IAIs
Infections that spread beyond the hollow
viscus of origin into the peritoneal space and
are associated with abscess formation or
peritonitis
Complicated intraabdominal infection
cIAIs
• cIAIs is an important cause of mortality and
morbidity if poorly managed
• A recent multicenter observational study
conducted on 132 medical institutions
worldwide enrolled 4553 patients with
cIAIs . The overall mortality was 9.2%
intraabdominal infection
• The infection may be in the retroperitoneal
space or in the peritoneal cavity and can
arise as a result of surgery
• Organs are retroperitoneal if they have
peritoneum on their anterior side only
- Duodenum
- Pancreas
- kidney
Commener Causes for
intraabdominal sepsis
• Infarcted tissue
(strangulated bowel,
intestinal ischaemia
following arterial embolus or
venous thrombosis
  Intestinal perforation
especially colonic origin
(faecal peritonitis)
  Biliary infection with
obstructed jaundice
  Pancreatitis; in predicted
severe disease (on Ranson or
Imrie criteria)
Complicated IAI Peritonitis
 Peritonitis is inflammation of the peritoneum, the serous
membrane lining the abdominal cavity and covering the
viscera that may be:
1- Primary (spontaneous bacterial peritonitis)
2- Secondary - Occurs as a result of spillage of gut
organisms through a hole in the gut wall
3- Tertiary - Peritonitis in a critically ill patient which
persists or recurs 48 hours after adequate treatment
Other Forms of Peritonitis
1. Aseptic / sterile peritonitis Ex. Chemical  peptic
ulcer
2. Drug-related peritonitis: isoniazid and erythromycin
estolate
3. Periodic peritonitis: familial dse (Jews, Arabs,
Armenians) Meditranian Tx: colchicine
4. Lead peritonitis
5. Hyperlipidemic peritonitis
6. Porphyrin peritonitis
7. Talc peritonitis (hypersensitivity response)
8. Foreign body peritonitis
Common Pathogens
Aerobic gm-ve bacteria
• E col
• Kledsiella
• Pseudomonas aeruginosa
• Extended-spectrum B-lactamase producing
enterobacteriaceae
Common Pathogens
Aerobic gm+ve bacteria
- Enterococcus faecalis
- Staph aureus
- Strepococci
Anaerobic bacteria
- Bacteroids
Diagnosis : Symptoms
• Acute spontaneous abdominal pain
exacerbated by movement or breathing
• Abdominal distension - fever – nausea –
vomiting – dyspnea – hypotension
• Irregular intestine (constipation/diarrhea
Clinical manifestations of PP
Fever (>37.8°C [100°F]) is the most common presenting sign,
50 to 80%, and may be present without abdominal signs or
symptoms.
Tenderness Rebound tenderness and paralytic ileus
may be present.
Symptoms and signs of the cause
Signs of toxemia or septicemia
Patients risk factors
Any cause for general ill health
• Immunological or
• Acquired
Specific Factors Affecting Operative
Risk
1. Cardiovascular
2. Respiratory
3. Genitourinary
4. Nutritional Status
5. Obesity
6. Diabetes
7. Jaundice
8. Coagulation Status
9. Immunological Status
10. Drugs
11. Pregnancy
12. Elderly patients
Specific Factors Affecting Operative
Risk
26
•Generalized :
• 1-Primary peritonitis 2-Secondary
bacterial peritonitis
•3-tertiaty
•Localized (abscess)
• - pelvic – subphrenic – peritoneal
(supracolic gutter –
• infracolic gutter)
Acute peritonitis
GENERALIZED PERITONITIS
Secondary peritonitis (rupture
vicus)
1. Intraperitoneal:
• - Biliary tree source
• - GIT source
• - Female genital
2. Retroperitoneal
• - Pancreas
• - UT
3. Localized abscess:
• lesser sac, liver, subphrenic, pelvic, spleen, periappedicular
,Paracoilc
• Retroperitoneal,
4. Trauma
Causes of
infection
The effect of infection on the entire organ
•Total surface area of the peritoneum: 2 m²
•Inflamatory edema expanding the peritoneum to a
thickness of 5 mm results in fluid loss of 5 – 8 L
from the entire organ to the peritoneal cavity. This
leads to an initial Hypovolemic shock, followed by
dehydration, and finally, toxin-induced shock and
death of the patient
Damage to vital organ
•Heart :
–Dehydration, tachycardia, hypotension, reduction of
circulation time and cardiac output and venous return
with increased peripheral resistance ( blood pooling ),
hypoxia, shock
•Lung :
–Disturbance of pulmonary distribution with atrial
venous shunting, increase in pulmonary resistance,
alveolar cell destruction, an increase of oxygen transfer
distance, hypoxia, acute respiratory distress. Atelectasis
due to increased intra-abdominal pressure
Damage to vital organ
•Kidney:
–Reduced perfusion in the presence of hypovolemia,
increased intra-abdominal pressure and augmented
buildup of toxic metabolites, hypoxic and toxic damage
to renal epithelia, increase in urea nitrogen and
creatinine, renal insufficiency
•Intestines :
–Local hypoxia, increased sympathetic activity,
disproportionate bacterial growth, translocation,bowel
distention, reduction of perfusion and influx of toxin
into the circulation, increase of intra-abdominal
pressure with negative effects on renal and pulmonary
function
diagnoses:
• Blood Test
• Samples of fluid from the abdomen
• CT Scan
• Chest X-rays
• Peritoneal lavage.
Perforated Ulcer
Perforated Ulcer
• Diagnosis: upright CXR
• Air under the diaphragm
Plain x-ray abdomen ileus
CT Peritonitis
a, b. A 65-year-old man with hepatitis induced liver cirrhosis, fever, and
abdominal pain. Axial contrast-enhanced MDCT image (a) and schematic
drawing (b) show smooth, uniform thickening of the peritoneum (arrows)
due to spontaneous bacterial peritonitis.
Axial MDCT image shows free intraperitoneal air
(asterisks), ascites, smooth pelvic peritoneal thickening
(arrows), and bowel wall thickening (open arrows)
indicative of peritonitis caused by intestinal perforation.
Axial contrast-enhanced MDCT image shows a right tubo-
ovarian abscess (black arrows) with fluid collections
surrounded by smoothly thickened and enhanced peritoneum
(white arrows).
Initial Diagnostic Evaluation
1. Routine history, physical examination, and
laboratory studies will identify most patients
with suspected intra-abdominal infection for
whom further evaluation and management are
warranted (A-II).
Initial Diagnostic Evaluation
3. Further diagnostic imaging is unnecessary in
patients with obvious signs of diffuse peritonitis and
in whom immediate surgical intervention is to be
performed (B-III).
4. In adult patients not undergoing immediate
laparotomy, computed tomography (CT) scan is the
imaging modality of choice to determine the presence
of intra-abdominal infection and its source (A-II).
Microbiologic Evaluation
5. Blood cultures do not provide additional clinically
relevant information for patients with community-
acquired intraabdominal infection and are therefore
not routinely recommended for such patients (B-III).
Treatment Approach
• Hospitalization is recommended.
• Antibiotics are prescribed to control the
infection & intravenous therapy (IV) is
used to restore hydration.
• Surgery is often necessary to remove the
source of infection.
Medical Management
Fluid and electrolyte replacement.
Massive antibiotic therapy is usually
initiated early in the treatment of peritonitis.
Analgesics, Antiemetics are prescribed
Intestinal intubation and suction assist in
relieving abdominal distention and in
promoting intestinal function.
3 pilars for optimal therapy Of IAI
The more you optimize the patient,
The better the post-op recovery
Early cases are opened early
Late cases are opened late
Preoperative critical care
1. Fluid resuscitation
2. Administration of antibiotics and oxygen
3. Nasogastric intubation
4. Urinary catheterization
5. Monitoring of vital signs and
biochemical and hemodynamic data
Preoperative evaluation
• Vital signs: temperature, blood pressure,
pulse rate, and respiratory rate are
continuously recorded
• Preoperative biochemical evaluation: Wbc,
serum levels of electrolytes, creatinine,
glucose, bilirubin, alkaline phosphatase, and
urinalysis
Preoperative evaluation
• Nasogastric intubation is performed to
evacuate the stomach, prevent further
vomiting, and reduce the accumulation of
additional air in the paralyzed bowel
• Urinary catheterization is used to record
initial bladder urine volume and to monitor
subsequent urinary output.
Fluid resuscitation
• Anesthesia can cause Myocardial
depression and vasodilatation
• Rehydration can increase a patient’s
tolerance to anesthesia and surgical stress
Fluid Resuscitation guidelines
5. Patients should undergo rapid restoration of intravascular
volume and additional measures as needed to promote
physiological stability (A-II).
6. For patients with septic shock, such resuscitation should
begin immediately when hypotension is identified (A-II).
7. For patients without evidence of volume depletion,
intravenous fluid therapy should begin when the diagnosis of
intra-abdominal infection is first suspected (B-III).
Clinical sign 0f extracellular fluid deficit
Mild Moderate severe
CNS Sleepy
Apatic
Delayed respons
Hypoactivit
↓tendon reflex
Distal acral
anaesthesia
Stupor,coma
Cardiovasc Tachicardia Tachycardia
Orthostatic
hypotension
Collapsed vein
Tiny pulse
Sianosis
Hipotension,shock
Acral :cold
Pulseless
Tissue Mouth mucosa :
dry
↓Turgor
↓ ↓ Toungue
↓ ↓ turgor
↓ ↓ ↓ turgor
Urine Yellowish ↓ and yellowih Oliguria
Deficit 3=5 % BW 6-8 % BW 10 % BW
Antibiotics
Empiric antibiotic therapy for established
secondary bacterial peritonitis plays an
important supplemental role.
• The choice of antibiotics depends on :
– The expected organism
– The estimate of the antibiotic susceptibility of the
expected organism ( community Vs hospital-acquired
infection )
– The extent of contamination
– The hemodynamic stability of the patient
Antibiotics
• Mild to moderate IAI
– 2 nd generation cephalosporin with
activity against anaerobes (
cefotetan,cefoxitin)
– Semisynthetic penicillin in combination
with ß lactamase inhibitor ( Ticarcilin-
clavulanic acid,ampicillin-sulbactam,or
piperacillin-tazobactam )
Antibiotics
Severe IAI
– Aminoglycoside +metronidazole or
clindamycin
– 3 rd gen cephalosporin +
metronidazole/clindamycin
– Semisynthetic penicilin Imipenem + ß
lactamase inhibitor
– Fluoroquinolone + anti anaerobe
– Levofloxacin or trofloxacin
Timing of Initiation of Antimicrobial Therapy
8. Antimicrobial therapy should be initiated once a patient
receives a diagnosis of an intra-abdominal infection or once
such an infection is considered likely. For patients with septic
shock, antibiotics should be administered as soon as possible
(A-III).
9. For patients without septic shock, antimicrobial therapy
should be started in the emergency department (B-III).
10. Satisfactory antimicrobial drug levels should be
maintained during a source control intervention, which may
necessitate additional administration of antimicrobials just
before initiation of the procedure (A-I).
Pain management
• Once a decision to operate has been made,
pain should be relieved with potent narcotics.
• Morphine 1-3 mg repeated every 20-30
minutes
Blood glucose level
• Aggressive perioperative insulin with the use
of insulin drip to maintain glucose levels
between 80 -110 mg/dL was associated with
decreased mortality in surgical critically ill
patients.
Hyper/Hypothermia
• Patients with hyper/hypothermia should have
their temperature corrected toward normal
before operation.
• Acetaminophen or cooling mattress is often
effective in reducing fever
• A warming mattress should be used for
hypothermic patient
Management of Intra-abdominal
Infection
• If source is controlled w/ early surgical
intervention, peritonitis responds to vigorous
antibiotics & supportive therapy.
• Failure to solved ---> continuous peritoneal
soiling ----> death
Parts of treatment:
A. Pre-operative preparation:
4. Administration of Broad Spectrum Antibiotic
5. NGT to evacuate the stomach and prevent vomiting
6. NPO
7. Relieve pain ONCE DECISION to operate has been
made: - Morphine IV 1-3 mg q 20-30 min
8. Monitor V/S, biochemical & hemodynamic data:
• Urine output monitoring – foley catheter
Management of Intra-abdominal
Infection
Management of Intra-abdominal Infection
B. Cleaning of the Abdominal Cavity:
1. Immediate evacuation of all purulent collection
• Resection/closure of all perforated bowel
• Primary anastomosis is not recommended in purulent
peritonitis due to an anastomotic leak
• Radical debridement
2. Intra-operative high volume lavage:
• To wash out pus, feces & necrotic material; endpoint
is clear fluid aspirated
• 8 – 12 L
Management of Intra-abdominal Infection
C - Primary closure of abdominal incision is difficult or
even unwise
– Increase intra-abdominal pressure ---> compression
of mesenteric & renal vein ---> renal failure & bowel
necrosis
– Fascial Prosthesis (Marlex Silastic) is used if one
plans to do a re-laparotomy. Removed once
abdominal & visceral edema resolved, and the
decision to close abd. wall definitely.
THANK YOU

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Intra-Abdominal infection the lect #.ppt

  • 3. Introduction • Doctors should be broud of themselves • Surgeons have a special mission • Who is the good surgeon
  • 4. Introduction • The only thing left to the patient is the scar ? • The longer the incision the bigger the surgeon • The metabolic response to surgery and trauma a- Inevitable catabolic phase b- Turning point phase c- Anabolic phase d- Late anabolic Fat gain phase
  • 5. 5 Definition of Peritoneum • The peritoneum is the largest serous membrane of the body lining the abdominal cavity Structure • Consists of a closed sac, containing a small amount of serous fluid, within the abdominal cavity. Two layers • The parietal layer - lines the abdominal wall • Visceral layer – covers the organs (viscera) in the abdominal and pelvic cavities
  • 6. Anatomy •Parietal peritoneum lines the anterior abdominal wall •The two layers are actually in contact - friction prevented by the presence of serous fluid secreted by the peritoneal cells •Peritoneal cavity is only a potential cavity •In women there is the communication of the peritoneal cavity to the external atmosphere through the openings of the fallopian tubes (at fimbrial ends) •In males the peritoneal cavity is completely closed.
  • 7. Functions of the Peritoneum • Pain perception ( Parietal peritoneum ) • Visceral lubrication • Fluid and particulate absorption • Inflammatory and immune response • Fibrinolytic activity
  • 8. Intra abdominal infection • Intraperitoneal = All intraabdominal organ • Extraperitoneal = Duodenum - pancreas - kidneys
  • 9. Intra abdominal infection Infection : • Invasion of microorganisms to the healthy tissue produces an inflammatory reaction • Sepsis:  Infection, (with local manifestations) plus – >2 SIRS Criteria. – Temp > 38oC or < 36oC – HR > 90 bpm – RR > 20 bpm or PaCO2 < 32 mmHg – WBC > 12 x 109/L, < 4 x 109/L or >10% band form
  • 10. Intra abdominal infection • Severe Sepsis:  Sepsis associated with hypotension, hypoperfusion, and/or organ-dysfunction  The hypotension can be corrected with fluid replacement • Septic shock: sepsis with hypotension despite adequate fluid resuscitation
  • 11. Intra abdominal infection • Definition : Bacterial inflammation that affect the visceral as well as the parietal peritoneum and may diffuse to neighboring tissues.  Peritonitis  Intraabdominal abscess
  • 12. Highlight of intraabdominal infection •Intra abdominal infections are still an extremely difficult problem in surgery – High incidence: ± 8 % of total hospital mortality – High mortality rate : • < 20th century : 80-90 • > 1974: Recently 13 – 43 % • Published epidemiologic data suggest that sepsis causes one-third to half of in-hospital mortality in the USA.
  • 13. Intraabdominal infection Classification • Uncomplicated IAIs The infectious process involves only a single organ and does not proceed to the peritoneum • Complicated IAIs Infections that spread beyond the hollow viscus of origin into the peritoneal space and are associated with abscess formation or peritonitis
  • 14. Complicated intraabdominal infection cIAIs • cIAIs is an important cause of mortality and morbidity if poorly managed • A recent multicenter observational study conducted on 132 medical institutions worldwide enrolled 4553 patients with cIAIs . The overall mortality was 9.2%
  • 15. intraabdominal infection • The infection may be in the retroperitoneal space or in the peritoneal cavity and can arise as a result of surgery • Organs are retroperitoneal if they have peritoneum on their anterior side only - Duodenum - Pancreas - kidney
  • 16. Commener Causes for intraabdominal sepsis • Infarcted tissue (strangulated bowel, intestinal ischaemia following arterial embolus or venous thrombosis   Intestinal perforation especially colonic origin (faecal peritonitis)   Biliary infection with obstructed jaundice   Pancreatitis; in predicted severe disease (on Ranson or Imrie criteria)
  • 17. Complicated IAI Peritonitis  Peritonitis is inflammation of the peritoneum, the serous membrane lining the abdominal cavity and covering the viscera that may be: 1- Primary (spontaneous bacterial peritonitis) 2- Secondary - Occurs as a result of spillage of gut organisms through a hole in the gut wall 3- Tertiary - Peritonitis in a critically ill patient which persists or recurs 48 hours after adequate treatment
  • 18. Other Forms of Peritonitis 1. Aseptic / sterile peritonitis Ex. Chemical  peptic ulcer 2. Drug-related peritonitis: isoniazid and erythromycin estolate 3. Periodic peritonitis: familial dse (Jews, Arabs, Armenians) Meditranian Tx: colchicine 4. Lead peritonitis 5. Hyperlipidemic peritonitis 6. Porphyrin peritonitis 7. Talc peritonitis (hypersensitivity response) 8. Foreign body peritonitis
  • 19. Common Pathogens Aerobic gm-ve bacteria • E col • Kledsiella • Pseudomonas aeruginosa • Extended-spectrum B-lactamase producing enterobacteriaceae
  • 20. Common Pathogens Aerobic gm+ve bacteria - Enterococcus faecalis - Staph aureus - Strepococci Anaerobic bacteria - Bacteroids
  • 21. Diagnosis : Symptoms • Acute spontaneous abdominal pain exacerbated by movement or breathing • Abdominal distension - fever – nausea – vomiting – dyspnea – hypotension • Irregular intestine (constipation/diarrhea
  • 22. Clinical manifestations of PP Fever (>37.8°C [100°F]) is the most common presenting sign, 50 to 80%, and may be present without abdominal signs or symptoms. Tenderness Rebound tenderness and paralytic ileus may be present. Symptoms and signs of the cause Signs of toxemia or septicemia
  • 23. Patients risk factors Any cause for general ill health • Immunological or • Acquired
  • 24. Specific Factors Affecting Operative Risk 1. Cardiovascular 2. Respiratory 3. Genitourinary 4. Nutritional Status 5. Obesity 6. Diabetes 7. Jaundice 8. Coagulation Status 9. Immunological Status 10. Drugs 11. Pregnancy 12. Elderly patients
  • 25. Specific Factors Affecting Operative Risk
  • 26. 26 •Generalized : • 1-Primary peritonitis 2-Secondary bacterial peritonitis •3-tertiaty •Localized (abscess) • - pelvic – subphrenic – peritoneal (supracolic gutter – • infracolic gutter) Acute peritonitis
  • 28. Secondary peritonitis (rupture vicus) 1. Intraperitoneal: • - Biliary tree source • - GIT source • - Female genital 2. Retroperitoneal • - Pancreas • - UT 3. Localized abscess: • lesser sac, liver, subphrenic, pelvic, spleen, periappedicular ,Paracoilc • Retroperitoneal, 4. Trauma
  • 30.
  • 31. The effect of infection on the entire organ •Total surface area of the peritoneum: 2 m² •Inflamatory edema expanding the peritoneum to a thickness of 5 mm results in fluid loss of 5 – 8 L from the entire organ to the peritoneal cavity. This leads to an initial Hypovolemic shock, followed by dehydration, and finally, toxin-induced shock and death of the patient
  • 32. Damage to vital organ •Heart : –Dehydration, tachycardia, hypotension, reduction of circulation time and cardiac output and venous return with increased peripheral resistance ( blood pooling ), hypoxia, shock •Lung : –Disturbance of pulmonary distribution with atrial venous shunting, increase in pulmonary resistance, alveolar cell destruction, an increase of oxygen transfer distance, hypoxia, acute respiratory distress. Atelectasis due to increased intra-abdominal pressure
  • 33. Damage to vital organ •Kidney: –Reduced perfusion in the presence of hypovolemia, increased intra-abdominal pressure and augmented buildup of toxic metabolites, hypoxic and toxic damage to renal epithelia, increase in urea nitrogen and creatinine, renal insufficiency •Intestines : –Local hypoxia, increased sympathetic activity, disproportionate bacterial growth, translocation,bowel distention, reduction of perfusion and influx of toxin into the circulation, increase of intra-abdominal pressure with negative effects on renal and pulmonary function
  • 34. diagnoses: • Blood Test • Samples of fluid from the abdomen • CT Scan • Chest X-rays • Peritoneal lavage.
  • 36. Perforated Ulcer • Diagnosis: upright CXR • Air under the diaphragm
  • 39. a, b. A 65-year-old man with hepatitis induced liver cirrhosis, fever, and abdominal pain. Axial contrast-enhanced MDCT image (a) and schematic drawing (b) show smooth, uniform thickening of the peritoneum (arrows) due to spontaneous bacterial peritonitis.
  • 40. Axial MDCT image shows free intraperitoneal air (asterisks), ascites, smooth pelvic peritoneal thickening (arrows), and bowel wall thickening (open arrows) indicative of peritonitis caused by intestinal perforation.
  • 41. Axial contrast-enhanced MDCT image shows a right tubo- ovarian abscess (black arrows) with fluid collections surrounded by smoothly thickened and enhanced peritoneum (white arrows).
  • 42. Initial Diagnostic Evaluation 1. Routine history, physical examination, and laboratory studies will identify most patients with suspected intra-abdominal infection for whom further evaluation and management are warranted (A-II).
  • 43. Initial Diagnostic Evaluation 3. Further diagnostic imaging is unnecessary in patients with obvious signs of diffuse peritonitis and in whom immediate surgical intervention is to be performed (B-III). 4. In adult patients not undergoing immediate laparotomy, computed tomography (CT) scan is the imaging modality of choice to determine the presence of intra-abdominal infection and its source (A-II).
  • 44. Microbiologic Evaluation 5. Blood cultures do not provide additional clinically relevant information for patients with community- acquired intraabdominal infection and are therefore not routinely recommended for such patients (B-III).
  • 45. Treatment Approach • Hospitalization is recommended. • Antibiotics are prescribed to control the infection & intravenous therapy (IV) is used to restore hydration. • Surgery is often necessary to remove the source of infection.
  • 46. Medical Management Fluid and electrolyte replacement. Massive antibiotic therapy is usually initiated early in the treatment of peritonitis. Analgesics, Antiemetics are prescribed Intestinal intubation and suction assist in relieving abdominal distention and in promoting intestinal function.
  • 47. 3 pilars for optimal therapy Of IAI
  • 48. The more you optimize the patient, The better the post-op recovery Early cases are opened early Late cases are opened late
  • 49. Preoperative critical care 1. Fluid resuscitation 2. Administration of antibiotics and oxygen 3. Nasogastric intubation 4. Urinary catheterization 5. Monitoring of vital signs and biochemical and hemodynamic data
  • 50. Preoperative evaluation • Vital signs: temperature, blood pressure, pulse rate, and respiratory rate are continuously recorded • Preoperative biochemical evaluation: Wbc, serum levels of electrolytes, creatinine, glucose, bilirubin, alkaline phosphatase, and urinalysis
  • 51. Preoperative evaluation • Nasogastric intubation is performed to evacuate the stomach, prevent further vomiting, and reduce the accumulation of additional air in the paralyzed bowel • Urinary catheterization is used to record initial bladder urine volume and to monitor subsequent urinary output.
  • 52. Fluid resuscitation • Anesthesia can cause Myocardial depression and vasodilatation • Rehydration can increase a patient’s tolerance to anesthesia and surgical stress
  • 53. Fluid Resuscitation guidelines 5. Patients should undergo rapid restoration of intravascular volume and additional measures as needed to promote physiological stability (A-II). 6. For patients with septic shock, such resuscitation should begin immediately when hypotension is identified (A-II). 7. For patients without evidence of volume depletion, intravenous fluid therapy should begin when the diagnosis of intra-abdominal infection is first suspected (B-III).
  • 54. Clinical sign 0f extracellular fluid deficit Mild Moderate severe CNS Sleepy Apatic Delayed respons Hypoactivit ↓tendon reflex Distal acral anaesthesia Stupor,coma Cardiovasc Tachicardia Tachycardia Orthostatic hypotension Collapsed vein Tiny pulse Sianosis Hipotension,shock Acral :cold Pulseless Tissue Mouth mucosa : dry ↓Turgor ↓ ↓ Toungue ↓ ↓ turgor ↓ ↓ ↓ turgor Urine Yellowish ↓ and yellowih Oliguria Deficit 3=5 % BW 6-8 % BW 10 % BW
  • 55. Antibiotics Empiric antibiotic therapy for established secondary bacterial peritonitis plays an important supplemental role. • The choice of antibiotics depends on : – The expected organism – The estimate of the antibiotic susceptibility of the expected organism ( community Vs hospital-acquired infection ) – The extent of contamination – The hemodynamic stability of the patient
  • 56. Antibiotics • Mild to moderate IAI – 2 nd generation cephalosporin with activity against anaerobes ( cefotetan,cefoxitin) – Semisynthetic penicillin in combination with ß lactamase inhibitor ( Ticarcilin- clavulanic acid,ampicillin-sulbactam,or piperacillin-tazobactam )
  • 57. Antibiotics Severe IAI – Aminoglycoside +metronidazole or clindamycin – 3 rd gen cephalosporin + metronidazole/clindamycin – Semisynthetic penicilin Imipenem + ß lactamase inhibitor – Fluoroquinolone + anti anaerobe – Levofloxacin or trofloxacin
  • 58. Timing of Initiation of Antimicrobial Therapy 8. Antimicrobial therapy should be initiated once a patient receives a diagnosis of an intra-abdominal infection or once such an infection is considered likely. For patients with septic shock, antibiotics should be administered as soon as possible (A-III). 9. For patients without septic shock, antimicrobial therapy should be started in the emergency department (B-III). 10. Satisfactory antimicrobial drug levels should be maintained during a source control intervention, which may necessitate additional administration of antimicrobials just before initiation of the procedure (A-I).
  • 59. Pain management • Once a decision to operate has been made, pain should be relieved with potent narcotics. • Morphine 1-3 mg repeated every 20-30 minutes
  • 60. Blood glucose level • Aggressive perioperative insulin with the use of insulin drip to maintain glucose levels between 80 -110 mg/dL was associated with decreased mortality in surgical critically ill patients.
  • 61. Hyper/Hypothermia • Patients with hyper/hypothermia should have their temperature corrected toward normal before operation. • Acetaminophen or cooling mattress is often effective in reducing fever • A warming mattress should be used for hypothermic patient
  • 62. Management of Intra-abdominal Infection • If source is controlled w/ early surgical intervention, peritonitis responds to vigorous antibiotics & supportive therapy. • Failure to solved ---> continuous peritoneal soiling ----> death
  • 63. Parts of treatment: A. Pre-operative preparation: 4. Administration of Broad Spectrum Antibiotic 5. NGT to evacuate the stomach and prevent vomiting 6. NPO 7. Relieve pain ONCE DECISION to operate has been made: - Morphine IV 1-3 mg q 20-30 min 8. Monitor V/S, biochemical & hemodynamic data: • Urine output monitoring – foley catheter Management of Intra-abdominal Infection
  • 64. Management of Intra-abdominal Infection B. Cleaning of the Abdominal Cavity: 1. Immediate evacuation of all purulent collection • Resection/closure of all perforated bowel • Primary anastomosis is not recommended in purulent peritonitis due to an anastomotic leak • Radical debridement 2. Intra-operative high volume lavage: • To wash out pus, feces & necrotic material; endpoint is clear fluid aspirated • 8 – 12 L
  • 65. Management of Intra-abdominal Infection C - Primary closure of abdominal incision is difficult or even unwise – Increase intra-abdominal pressure ---> compression of mesenteric & renal vein ---> renal failure & bowel necrosis – Fascial Prosthesis (Marlex Silastic) is used if one plans to do a re-laparotomy. Removed once abdominal & visceral edema resolved, and the decision to close abd. wall definitely.
  • 66.