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Intraabdominal Infection

Intraabdominal Infection

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Published by: 2013SecB on Mar 08, 2011
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Peritoneum
A serosal membrane which is composed of a
single layer of flat mesothelial cells
supported by submesothelial connectivetissue.
In this serosal tissue there are fat cells,lymphatics, blood vessels andinflammatory cells like lymphocyte andplasma cells
visceral peritoneum
lines all the organsthat are
intraperitonealparietal peritoneum
lines the anterior,lateral and posteriorwalls of the peritonealcavity
Deepest portion of the peritoneal cavity
o
Pouch of douglas
in women
o
Retrovesical space
in men ( both inthe upright and supine position)Male pelvis the peritoneum iscontinuousFemale pelvis discontinuous at theostia of the oviduct
Through the opening, disease can spreadfrom the extraperitoeal pelvis into theperitoneal cavity. (e.i. pelvic inflammatorydisease)
Ligaments in the abdomen includes(gastrocolic, gastrosplenic, gastrohepaticand hepatoduodenal)
Mesenteries
A double fold of the peritoneum
True Mesentery
o
All connect to the posterior wall
o
Small bowel, transverse mesocolon, sigmoid mesentery (or mesosigmoid)
Specialized mesenteries
o
Do not connect to the posteriorperitoneal wall
o
These are:1.
Greater omentum
- connects thestomach to the colon2.
Lesser omentum
- connects thestomach to the liver3. The
mesoappendix 
- connects theappendix to the ileum
If you remove the intraperitoneal bowel,you can get a good look at the cut surfaceof the mesenteries1. Lesser omentum2. Transverse mesocolon3. Small bowel mesentery4. Sigmoid mesocolon
Peritoneal Circulation
These compartment enable the peritonealcirculation for peritoneal fluid
In the normal abdomen withoutintraperitoneal disease, there is a smallamount of peritoneal fluid thatcontinuously circulates
The movement of the fluid in thiscirculatory pathway is produced by themovement of the diaphragm and peristalsisof bowel
It predominantly flows up the rightparacolic gutter which is deeper and widerthan the left and is partially cleared by thesubphrenic lymphatics
The majority of the peritoneal fluid (90%) iscleared at the subphrenic space by thesubendothelial lymphatics. Theselymphatics are connected at the other sideof the diaphragm.
Peritoneal defense mechanism1. Peritoneal injury
o
Inflammation
loss of mesothelial cells
metastasis of nearby mesothelialcells(3-5 days) repair w/o adhesion
2. Adhesion formation
o
Forms when platelets and fibrin comesin contact w/ exposed basementmembrane
hypoxia
fibroblast invadesthe area
stimulation of a Angiogenesisand collagen synthesis fully developed10 days, maximum of 2-3 days
3. Peritoneal defence against intraabdominal infection
a) Mechanical clearance of bacteria vialymphatics
Cleared through the
stomata
b) Phagocytic killing of bacteria by
immune cells
. These cells from
 
mediator substance, responsible for localand systemic response of our body tointra abdominal infections.
Major cell types
1. Macrophage2. Mesothelial cells3. Capillary endothelial cells4. Recruited neutrophil
Bacteriology of Intra-abdominal Infection
A. Normal bowel floraB. Level of GI perforation
o
Morbidity and mortality varies fromlevel of GIT perforation
o
Proximal bowel
- mostly gm (-)aerobic bacteria
o
Terminal ileum
o
Colon
- richest in gram (-) aerobicand anaerobic bacteriaC. Virulence
o
impairs opsonisation or phagocytosis

abscess formation (fr. B. fragilis PLScapsule)D. Microbial adherence to the peritoneum
o
Bacteria adherent to the peritoneumare resistant to removal by peritoneallavage, in contrast to bacteria inperitoneal fluid.
o
1st 4 hrs
aerobic bacteria, E. coli,etc
o
8hrs
B. fragilisE. Microbial synergya)
aerobic gm(-) bacteria
- lowersoxidation
reduction potential,endotoxin produced suppress local hostdefenceb) B. fragilis- capsular polysaccharideinterferes w/ complement activationand inhibit leukocyte functionF. Host effect on bacterial growth
o
host neurohumoral response toinfection may enhance bacterial growth(NE, cortisol)G. Adjuvant substance
o
adjuvant increases bacterialvirulence or interferes w/ host defence
o
adjuvants: Blood (Hgb, fibrin,platelet), bile salt, urine, pancreaticsecretion, gastric mucin, chyleH. Foreign bodies
o
Macroscopic
Surgical drains
Suture
Laparotomy sponge
Hemostatic pads
Surgical clips
o
Microscopic
Barium sulfate
Clothing fibers
Fecal material
Necrotic tissue
Talcum powder
Diagnosis of Intra
-
abdominal InfectionClinical History

length of time the patient is ill

chills, fever, anorexia, nausea/vomiting,ileus

Pain (OPQRST)
Past Medical History

previous hospitalization

medication

chronic disease
Tests

CBC/ Differential count

Serum electrolyte/Creatinine/Livermetabolite/Amylase

X-raysFPA:a) pneumoperitoneumb) intestinal pneumatosisc) bowel obstructiond) widening of the space between loopse) mass effect- indicative of abscessf) obliterated psoas shadow*if suspecting for an abscess

Ultrasonography and CT scan- diagnosticand therapeutic since it is used in PAD (lessmorbidity and mortality)

peritoneal fluid aspiration for culture
PERITONITIS
Inflammation of the peritoneal cavity orpart of it due to: microorganism, chemicals,irradiation, foreign body injury.
Primary Peritonitis
diffuse bacterialperitonitis in the
absenceof disruption of intra-abdominal hollow viscera
a. Spontaneousperitonitis in adultb. Peritonitis in patientswith CAPDc. Tuberculous and other
granulomatous
peritonitis
Secondary Peritonitis
Localized (abscess) ordiffuse peritonitis
originating from a defect in abdominal viscus
A. Acute perforationperitonitis
1. GI perforation
 
2. Intestinal ischemia3. Pelvic peritonitis andother forms
B. Postoperativeperitonitis
1. Anastomoses
leak 
2. Accidental perforation& devascularisation
C. Post traumaticperitonitis
1. After
blunt 
abdominaltrauma2. After
penetrating
abdominal trauma
Tertiary Peritonitis
Peritonitis like syndromeoccuring late due to dis-turbance in the host im-mune response- Peritonitis withoutevidence forpathogens- Peritonitis w/fungi- Peritonitis w/ lowgrade pathogenicbac-teria
Other forms of peritonitis
1. Aseptic / sterile peritonitis (e.i.chemical PUD)2. Drug related peritonitis (e.i. NH anderythromycin estolate)3. Periodic peritonitis: familial disease(Jews, Arabs, Armenians) Tx:colchicines4. Lead peritonitis5. Hyperlipidemic peritonitis6. Porphyric peritonitis7. Talcum peritonitis (hypersensitivityresponse)8. Foreign body peritonitis
INTRA ABDOMINAL ABSCESS
accumulation of pus in the intra peritonealspace as defence to excessive tissue injuryand bacteria to terminate peritonealinfection1. Associated w/ primary peritonitis2. Associated w/ secondary peritonitis
MANAGEMENT OF INTRA ABDOMINALINFECTION
if source is controlled w/ early surgicalintervention, peritonitis responds tovigorous antibiotics & supportive therapy
failure to resolve

continuous peritonealsoiling

death
PRE-OP PREPARATION
1. Intravascular volume loading
low dose dopamine

improve renal bloodflow2. High oxygen concentration untilintravascular volume is restored3. Assess respiratory function (ABG)- if functionis impaired
ventilatory support is needed
o
PaCO2 of 50 mmHg or greater
o
PaO2 below 60 mmHg
hypoxemia
o
shallow rapid respirations, musclefatigue or use of accessory muscleof respiration4. Administration of broad spectrum antibiotic5. NGT to evacuate the stomach and preventvomiting6. NPO7. Relieve pain ONCE DECISION to operate hasbeen made (morphine IV 1-3 mg q 20-30 min)8. Monitor V/S biochemical & hemodynamicdata
urine output monitoring- foley catheter
renal failure in peritonitis due to1. Hypovolemic shock2. Septic shock3. Increased intra abdominal pressure4. Nephrotoxic drugs (e.i. aminoglycoside-mycin!)
OPERATIVE MANAGEMENTCleaning of the Abdominal Cavity
1. Immediate evacuation of all purulentcollection
resection/closure of all perforated bowel
primary anastomosis is not recommendedin purulent peritonitis due to anastomoticleaks
radical debridement2. Intra operative high volume lavage
to wash out pus, feces & necrotic material:end point is clear fluid aspirated
8-12 L3. Primary closure of abdominal incision isdifficult or even unwise
increase intra-abdominal pressure
compression of mesenteric and renalveins -> renal failure and bowel necrosis
fascial prosthesis (Marlex silastic)
isused if one plans to do re laparotomy.Removed once abdominal & visceraledema is resolved and decision to close theabdominal wall definitely.
Closed Catheter/needle Aspiration
Percutaneous drainage of an intra-abdominal abscess is usually successful if the following criterias are met

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