Peritoneum • A serosal membrane which is composed of

a single layer of flat mesothelial cells supported by submesothelial connective tissue. In this serosal tissue there are fat cells, lymphatics, blood vessels and inflammatory cells like lymphocyte and plasma cells

visceral peritoneum parietal peritoneum

lines all the organs that are intraperitoneal lines the anterior, lateral and posterior walls of the peritoneal cavity Peritoneal Circulation • These compartment enable the peritoneal circulation for peritoneal fluid • In the normal abdomen without intraperitoneal disease, there is a small amount of peritoneal fluid that continuously circulates • The movement of the fluid in this circulatory pathway is produced by the movement of the diaphragm and peristalsis of bowel • It predominantly flows up the right paracolic gutter which is deeper and wider than the left and is partially cleared by the subphrenic lymphatics

Deepest portion of the peritoneal cavity o Pouch of douglas in women o Retrovesical space in men ( both in the upright and supine position) the peritoneum is continuous discontinuous at the ostia of the oviduct

Male pelvis Female pelvis

Through the opening, disease can spread from the extraperitoeal pelvis into the peritoneal cavity. (e.i. pelvic inflammatory disease) Ligaments in the abdomen includes (gastrocolic, gastrosplenic, gastrohepatic and 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 posterior peritoneal wall o These are: 1. Greater omentum- connects the stomach to the colon 2. Lesser omentum- connects the stomach to the liver 3. The mesoappendix- connects the appendix to the ileum • If you remove the intraperitoneal bowel, you can get a good look at the cut surface of the mesenteries 1. Lesser omentum 2. Transverse mesocolon 3. Small bowel mesentery 4. Sigmoid mesocolon

The majority of the peritoneal fluid (90%) is cleared at the subphrenic space by the subendothelial lymphatics. These lymphatics are connected at the other side of the diaphragm.

Peritoneal defense mechanism 1. Peritoneal injury o Inflammationloss of mesothelial cells metastasis of nearby mesothelial cells(3-5 days) repair w/o adhesion 2. Adhesion formation o Forms when platelets and fibrin comes in contact w/ exposed basement membrane hypoxia fibroblast invades the area stimulation of a Angiogenesis and collagen synthesis fully developed 10 days, maximum of 2-3 days 3. Peritoneal defence against intra abdominal infection a) Mechanical clearance of bacteria via lymphatics

 Cleared through the stomata b) Phagocytic killing of bacteria by immune cells. These cells from

mediator substance, responsible for local and systemic response of our body to intra abdominal infections. Major cell types 1. Macrophage 2. Mesothelial cells 3. Capillary endothelial cells 4. Recruited neutrophil Bacteriology of Intra-abdominal Infection A. Normal bowel flora B. Level of GI perforation o Morbidity and mortality varies from level of GIT perforation o Proximal bowel- mostly gm (-) aerobic bacteria o Terminal ileum o Colon- richest in gram (-) aerobic and anaerobic bacteria C. Virulence o impairs opsonisation or phagocytosis abscess formation (fr. B. fragilis PLS capsule) D. Microbial adherence to the peritoneum o Bacteria adherent to the peritoneum are resistant to removal by peritoneal lavage, in contrast to bacteria in peritoneal fluid. o 1st 4 hrs aerobic bacteria, E. coli, etc o 8hrs B. fragilis E. Microbial synergy a) aerobic gm(-) bacteria - lowers oxidation reduction potential, endotoxin produced suppress local host defence b) B. fragilis- capsular polysaccharide interferes w/ complement activation and inhibit leukocyte function F. Host effect on bacterial growth o host neurohumoral response to infection may enhance bacterial growth (NE, cortisol) G. Adjuvant substance o adjuvant increases bacterial virulence or interferes w/ host defence o adjuvants: Blood (Hgb, fibrin, platelet), bile salt, urine, pancreatic secretion, gastric mucin, chyle H. 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 Infection Clinical 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/Liver metabolite/Amylase X-rays FPA: a) pneumoperitoneum b) intestinal pneumatosis c) bowel obstruction d) widening of the space between loops e) mass effect- indicative of abscess f) obliterated psoas shadow *if suspecting for an abscess Ultrasonography and CT scan- diagnostic and therapeutic since it is used in PAD (less morbidity and mortality) peritoneal fluid aspiration for culture PERITONITIS

Inflammation of the peritoneal cavity or part of it due to: microorganism, chemicals, irradiation, foreign body injury. diffuse bacterial peritonitis in the absence of disruption of intraabdominal hollow viscera a. Spontaneous peritonitis in adult b. Peritonitis in patients with CAPD c. Tuberculous and other granulomatous peritonitis Localized (abscess) or diffuse peritonitis originating from a defect in abdominal viscus A. Acute perforation peritonitis 1. GI perforation

Primary Peritonitis

Secondary Peritonitis

Tertiary Peritonitis

2. Intestinal ischemia 3. Pelvic peritonitis and other forms B. Postoperative peritonitis 1. Anastomoses leak 2. Accidental perforation & devascularisation C. Post traumatic peritonitis 1. After blunt abdominal trauma 2. After penetrating abdominal trauma Peritonitis like syndrome occuring late due to disturbance in the host immune response Peritonitis without evidence for pathogens Peritonitis w/ fungi Peritonitis w/ low grade pathogenic bacteria

1. Intravascular volume loading

Other forms of peritonitis 1. Aseptic / sterile peritonitis (e.i. chemical PUD) 2. Drug related peritonitis (e.i. NH and erythromycin estolate) 3. Periodic peritonitis: familial disease (Jews, Arabs, Armenians) Tx: colchicines 4. Lead peritonitis 5. Hyperlipidemic peritonitis 6. Porphyric peritonitis 7. Talcum peritonitis (hypersensitivity response) 8. Foreign body peritonitis INTRA ABDOMINAL ABSCESS • accumulation of pus in the intra peritoneal space as defence to excessive tissue injury and bacteria to terminate peritoneal infection 1. Associated w/ primary peritonitis 2. Associated w/ secondary peritonitis MANAGEMENT OF INTRA ABDOMINAL INFECTION • if source is controlled w/ early surgical intervention, peritonitis responds to vigorous antibiotics & supportive therapy

low dose dopamine improve renal blood flow 2. High oxygen concentration until intravascular volume is restored 3. Assess respiratory function (ABG)- if function is impaired • ventilatory support is needed o PaCO2 of 50 mmHg or greater o PaO2 below 60 mmHghypoxemia o shallow rapid respirations, muscle fatigue or use of accessory muscle of respiration 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 • renal failure in peritonitis due to 1. Hypovolemic shock 2. Septic shock 3. Increased intra abdominal pressure 4. Nephrotoxic drugs (e.i. aminoglycosidemycin!) OPERATIVE MANAGEMENT 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 anastomotic leaks • radical debridement 2. Intra operative high volume lavage • to wash out pus, feces & necrotic material: end point is clear fluid aspirated • 8-12 L 3. Primary closure of abdominal incision is difficult or even unwise

• •

increase intra-abdominal pressure compression of mesenteric and renal veins -> renal failure and bowel necrosis fascial prosthesis (Marlex silastic) is used if one plans to do re laparotomy. Removed once abdominal & visceral edema is resolved and decision to close the abdominal wall definitely.

failure to resolve continuous peritoneal soiling death

PRE-OP PREPARATION

Closed Catheter/needle Aspiration • Percutaneous drainage of an intraabdominal abscess is usually successful if the following criterias are met

1. unilocular fluid collection 2. a safe percutaneous route of access is available 3. joined evaluation by surgeon & radiologist 4. with immediate operative back up available • Catheter are removed when the criteria for abscess resolution are met - resolution of symptoms and indicator of infection (leukocytosis) - decrease in daily drainage, less than 10 ml & from purulent to serous - radiology verify abscess resolution and closure of communication

1. Fluid that is too viscous for drainage or the presence of phlegmon and necrotic debris 2. Multiloculated collection & multiple abscesses 3. Fistulous communication as in drainage of necrotic tumor mistaken for an abscess 4. Immunocompromised patients Open Surgical Drainage • failure of percutaneous drainage • inability to safely drain percutaneously • presence of pancreatic or carcinomatosis abscess • associated w/ a high output bowel fistula • involvement of lesser sac

Factors that cause Percutaneous Aspiration Drainage Failure • multiple isolated inter-loop abscesses • abscess suspected clinically but cannot be localized by CT/ultrasonography Types of Intra-Abdominal Abscess Left Subphrenic Abscess Notes Most common variety of upper abdominal abscess after peritonitis or leakage from a viscus Splenectomy/pancre atitis (L) subhepatic/subphre nic abscess complication of the disease of stomach, duodenum and pancreas. Most common cause is pancreatic abscess Secondary to rupture of hepatic abscess and post operative complication of gastric and duodenal surgery due to 1. gastric procedure 2. biliary surgery 3. appendicitis 4. colonic surgery multiple abscesses/ loculation between loops of bowel, mesentery, abdominal wall & omentum, rarely involved the upper Signs/Symptoms Costal tenderness of the left (+) Kehr sign (+) left pleural effusion Limitation of diaphragmatic motion mid epigastric tenderness -ultrasound/CT scan

Lesser Sac Abscess

Treatment drained posteriorly through the bed of the 12th rib extraperitoneal approach (lateral extraserous route) -approach directly at the upper abdominal incision -drains are placed at dependent area -sump suction drains

Diagnostic

Right Subphrenic Abscess

-pain upper abdomen (Kehr sign)/lower chest -limitation of right diaphragmatic motion -air fluid level : right upper quadrant pain and tenderness No reliable S/Sx has preceding signs of peritonitis w/ incomplete resolution trans peritoneal exploration Ultrasound/CT scan

Right Subhepatic abscess (Morrison,s pouch) Interloop Abscess

CT scan most reliable diagnostic tool

Pelvic Abscesses

Retroperitoneal Abscess

abdomen, involves the pelvis (gravity) due to a. Ruptured colonic diverticulitis b. PID c. Ruptured appendicitis -drainage into the pelvis during resolution of generalized peritonitis Due to: a. Pancreatitis b. Primary/ secondary infection of the kidney/ureter/colon c. Osteomyelitis d. Trauma

poorly localized dull lower abdominal pain -irritation of bladder (urgency/frequenc y), rectum (diarrhea/tenesm us) fever/ tenderness over the involved site

- pelvic drainage (rectum/vagina) - drainage should be delayed until formation of the pyogenic membrane that excluded the space -extraperitoneal approach -percutaneous catheter by CT scan/ultrasound

Ultrasound/CT scan -tender mass on rectal/vaginal exam

: CT scan

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