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 lines all the organs that are intraperitoneal

parietal peritoneum lines the anterior, lateral and posterior walls of the peritoneal cavity

Deepest portion of the peritoneal cavity o Pouch of douglas in women o Retrovesical space in men ( both in the upright and supine position)

Male pelvis the peritoneum is continuous

Female pelvis discontinuous at the ostia of the oviduct

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

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

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 mechanism1. Peritoneal injury

o Inflammationloss 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 InfectionA. 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 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/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.

Primary Peritonitis diffuse bacterial peritonitis in the absence of disruption of intra-abdominal hollow viscera a. Spontaneous peritonitis in adult b. Peritonitis in patients with CAPD c. Tuberculous and other granulomatous peritonitis

Secondary Peritonitis Localized (abscess) or diffuse peritonitis originating from a defect in abdominal viscus A. Acute perforation peritonitis 1. GI perforation 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

Tertiary Peritonitis Peritonitis like syndromeoccuring late due to dis-turbance in the host im-

mune response- Peritonitis withoutevidence for pathogens- Peritonitis w/ fungi- Peritonitis w/ lowgrade pathogenic bac-teria

Other forms of peritonitis1. 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: colchicines4. Lead peritonitis5. Hyperlipidemic peritonitis6. Porphyric peritonitis7. 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

failure to resolve continuous peritoneal soiling death

PRE-OP PREPARATION 1. Intravascular volume loading 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 mmHghypoxemia 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. aminoglycoside-mycin!)

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.

Closed Catheter/needle Aspiration Percutaneous drainage of an intra-abdominal 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

Factors that cause Percutaneous Aspiration Drainage Failure 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

multiple isolated inter-loop abscesses

abscess suspected clinically but cannot be localized by CT/ultrasonography

Types of Intra-Abdominal Abscess

Notes Signs/Symptoms Treatment DiagnosticLeft Subphrenic Abscess

Most common variety of upper abdominal abscess after peritonitis or leakage from a viscus Splenectomy/pancreatitis

Costal tenderness of the left (+) Kehr sign (+) left pleural effusion Limitation of diaphragmatic motion

drained posteriorly through the bed of the 12th rib extraperitoneal approach (lateral extraserous route)

Lesser Sac Abscess (L) subhepatic/subphrenic abscess complication of the disease of stomach, duodenum and pancreas. Most common cause is pancreatic abscess

mid epigastric tenderness-ultrasound/CT scan

-approach directly at the upper abdominal incision-drains are placed at dependent area -sump suction drains

Right Subphrenic Abscess

Secondary to rupture of hepatic abscess and post operative complication of gastric and duodenal surgery

-pain upper abdomen (Kehr sign)/lower chest -limitation of right diaphragmatic motion-air fluid level

Right Subhepatic abscess (Morrison,s pouch)

due to 1. gastric procedure 2. biliary surgery 3. appendicitis 4. colonic surgery

: right upper quadrant pain and tenderness

Ultrasound/CT scan

Interloop Abscess multiple abscesses/ loculation between loops of bowel, mesentery, abdominal wall & omentum, rarely involved the upper abdomen, involves the pelvis (gravity)

No reliable S/Sx has preceding signs of peritonitis w/ incomplete resolution

trans peritoneal exploration

CT scan most reliable diagnostic tool

Pelvic Abscesses due to a. Ruptured colonic diverticulitis b. PID c. Ruptured appendicitis-drainage into the pelvis during resolution of generalized peritonitis

poorly localized dull lower abdominal pain-irritation of bladder (urgency/frequency), rectum (diarrhea/tenesmus)

- pelvic drainage(rectum/vagina)- drainage should bedelayed until formation of the pyogenic membrane that excluded the space

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

Retroperitoneal Abscess

Due to:a. Pancreatitis b. Primary/ secondary infection of the kidney/ureter/colon c. Osteomyelitis d. Trauma

fever/ tenderness over the involved site

-extraperitoneal approach-percutaneous catheter by CT scan/ultrasound

: CT scan