PERITONITIS AND INTRAABDOMINAL INFECTION ASSOCIATE ...

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PERITONITIS AND INTRAABDOMINAL INFECTION PROFESSOR TURGUT IPEK Peritonitis means inflamation of the peritoneum or part of it. Secondary peritonitis is defined as the presence of purulent exudate in the abdominal cavity derived from an enteric source.

Transcript of PERITONITIS AND INTRAABDOMINAL INFECTION ASSOCIATE ...

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PERITONITIS AND INTRAABDOMINAL INFECTIONPROFESSOR TURGUT IPEK

• Peritonitis means inflamation of the peritoneum or part of it.

• Secondary peritonitis is defined as the presence of purulent exudate in the abdominal cavity derived from an enteric source.

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• The same terms are occasionally used to define different pathologicconditions.

• Perforation/Abcess/Fistula.• Following perforation of a hollow visceral organ bacteria leak into

surrounding tissue.• Host defense mechanisms confine this leakage to form an abscess.• This abscess may rupture into another hollow viscus or the skin and

thus form a fistula.• If the abscess perforates in the free peritoneal cavity, diffuse peritonitis

results.• Bacteremia.• The presence of bacteria in blood cultures without systemic signs of

infection.

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• Septicemia.• The presence of bacteria in blood cultures originating from

an infectious focus with a systemic host response, in otherwords, signs of systemic infection.

• Sepsis.• Asystemic infection originating from a focus, with the

inability to obtain positive blood cultures.• Septic Shock.• Sepsis with either high cardiac output and low systemic

vascular resistance (hyperdynamic phase) or low cardiacoutput (hypodynamic phase).

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• Sepsis Syndrome.• The clinical signs and symptoms of sepsis without

a septic focus and without bacteria isolated fromthe bloodstream. This term is synonymous withtertiary peritonitis.

• Organ Failure.• The sequential dysfunction of various organs,

usually starting with lung, kidney, heart, orintestinal tract.

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• ANATOMY OF THE PERITONEUM• The peritoneum is formed by a single layer of mesothelial

cells together with an underlying supporting layer of highly vascularized loose connective tissue.

• The total area of the peritoneum is approximately 1.8 m2, which is almost equal to the body surface area of the skin.

• Peritoneum covers all of the intestinal organs and theabdominal wall, diaphragm, retroperitoneum, and pelvis.

• Peritoneal fluid has the properties of lymph.• It is secreted everywhere by the peritoneal serosa and is

absorbed primarily through the diaphragm, 80 percentreaching the central circulation via the thoracic lymphatics.

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• Innervation.• The parietal peritoneum is innervated by both somatic and

visceral afferent nerves and is quite sensitive, respondingto various stimuli somewhat as does the skin.

• In contrast to the parietal peritoneum, the visceralperitoneum receives afferent innervation only from theautomatic nervous system and is relatively insensitive.

• Visceral afferent nerves respond primarily to traction ordistention, but less well to pressure, and are not capable of mediating pain and temperature sensation.

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• PHYSIOLOGY OF THE PERITONEUM• General Response to Injury• Following injury, histamine and other permeability factors

are released from peritoneal mast cells, increasing vascularpermeability of the peritoneum with exudation of protien-rich plasma containing fibrinogen into the peritonealcavity.

• A myriad of inflammatory cells and cytokines, autocoids, and other chemical moieties participate in this process.

• Trapping of fluid within the peritoneum and peritonealcavity as well as within the bowel lumen considerablyincreases intraabdominal pressure.

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• Increased intraabdominal pressure not onlynegatively influences pulmonary, cardiac, andrenal function, but also has deleterious effects on hepatic and intestinal or splanhnic perfusion.

• These secondary system impairments potentiatethe development of acute respiratory distresssyndrome (ARDS), multiple organ failure, anddeath.

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• Inflammation and Host Defenses• Any noxious stimulus, such as bacterial endo- or

exotoxins or trauma, might initiate the series of events captured under the term hostinflammatory response.

• It consists of soluble and cellular components.• The soluble components include

immunoglobulins, the complement system, thecontact activation system, leukotrienes, inflammatort autacoids, and acute phase cytokines.

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• Cellular components of inflammation include macrophagesand phagocytic cells, mast cells and basophils, platelets, endothelial cells, lymphocytes, and leukocytes.

• The terminal pathway of all events of inflammationcompletes bacterial killing, eliminates foreign material, and restores normal physiology and anatomy.

• Bacterial killing, or cytotoxicity, may be achieved via suchfactors as free oxygen radicals, nitric oxide, cytotoxiclymphocytes, bactericcidal permeability-increasing (BPI) proteins, cathepepsins, lactopherin, lysozymes, proteases, lipidhydrolases, and nucleases. The clinical picture of sepsis, ARDS, and multiple organ failure are intermediatestages that clinically parallel sequential cell death.

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• CLINICAL MANIFESTATIONS OF PERITONITIS LEADING TO SEPTIC SHOCK

• Clinical findings include a disturbed sensorium, tachypnea, tachycardia, hypotension, fever, oliguria, and heart failure.

• Two distinct phases of septic shock areencountered clinically, an early hyperdynamic anda late hypodynamic phase.

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• CLINICAL PRESENTATION OF PERITONITIS• Signs and Symptoms• Abdominal pain is almost always the predominant

symptom.• A good example of the effects of the dual mechanism of

pain perception is the chain of events in the developmentof acute appendicitis.

• Initially, inflammation of the appendix is projected viaautonomic nerve fibers to the region of umblicus andepigastrium with symptoms of diffuse epigastric pain, nause, and, sometimes, vomiting.

• The character of pain changes as the disease progresses.

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• As the somatic pathways of paraappendiceal peritoneumand adjacent structures become involved, the patientexperiences migration of pain from the epigastrium andumblicus to the right lower abdomen, an increase in theperceived intensity of pain, and then localization toMcBurney’s point.

• Anorexia is almost always present; nausea may be accompanied later by vomiting.

• Fever usually ranges between 38 and 41°C.• Tachycardia and a diminished palpable peripheral pulse

volume indicate hypovolemia.• Abdominal distention is due to concomitant ileus.

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• Tenderness is present over the entire extent of theperitoneum involved in the inflammatory process.

• Rigidity of the abdominal muscles is produced byvoluntary guarding initially and also by reflex musclespasm.

• Laboratory and Other Tests• Leukocytosis is common in acute intraabdominal infection.• Slayt• A leukocyte count of more than 25000 or leukopenia of

fewer than 4000/mL3 are both associated with highermortality.

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• The radiologic picture of intraabdominal infection mimicsthat of paralytic ileus.

• A lateral abdominal view might reveal superimposedcalcifications of the pancreas, indicating pancreatitis.

• Free air may be visible on an upright abdominal or lateraldecubitus film if a ruptured hollow viscus is the cause of peritonitis.

• Computed tomography (CT) is not required in the initialworkup of acute peritonitis and may only delay neededoperative management.

• CT and ultrasound, however, are very helpful in thediagnosis of an intraabdominal abscess.

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• PRIMARY BACTERIAL PERITONITIS• Spontaneous Peritonitis• Primary peritonitis refers to inflammation of the peritoneum from a

suspected extraperitoneal source, often via hematogenous spread.• It occurs in children and in adults, and can be a life-threatening illness,

particularly in patients with cirrhosis.• Spontaneous bacterial peritonitis is now more common in adults than

in children and shows no differential sex incidence.• Children with nephrosis, formerly the group most commonly affected,

have been replaced by adults with cirrhosis or systemic lupus.• E.coli is the most common isolated microorganism.

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• In children, the bacteria responsible for primary peritonitis arehemolytic streptococci and pneumococci.

• The route by which bacteria are transmitted to the peritoneal cavity is not known.

• The mortality risk is of the order of 48 to 70 percent in cirrhotic adultsbut is lower in nephrotic children.

• Clinical Manifestations.• Most patients complain of some abdominal pain and distention;

vomiting, lethargy, and fever are more prominent in children.• Diarrhea is usual in neonates but seldom seen in adults.• Leukocytosis usually is present.• Free air usually is not seen on abdominal radiographs.

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• Diagnosis• A peritoneal tap is the most useful diagnostic test.• A PMN cell count greater than 250/mm3 is considered

positive.• Treatment• Antibiotic therapy should be started and the patient

initially managed nonoperatively.• Usually, a cephalosporin or ampicillin-sulbactam is

appropriate since 90 percent of the organisms causingspontaneous peritonitis are sensitive to these antibiotics.

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• Peritonitis Related to Peritoneal Dialysis• Peritonitis is the dominant complication of continuous ambulatory

peritoneal dialysis (CAPD) in patients with end-stage renal disease.• Catheter-related infection is the most common mechanism.• Two-thirds of patients with positive cultures have a gram-positive

coccus as the causative organism, usually Staphylococcus aureus or S. Epidermidis.

• Anaerobes rarely are recovered.• The diagnosis is established when any of the following is present:• positive culture from the peritoneal fluid;• a cloudy dialysate effluent; and• clinical signs of peritonitis.• The initial treatment of dialysis-related peritonitis is administration of

antibiotics and heparin in the dialysate.

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• Tuberculous Peritonitis• Tuberculous peritonitis, formerly frequently fatal as a manifestation of

uncontrolled generalized tuberculosis.• Clinical Manifestations• Clinically, tuberculous peritonitis is insidious, presenting with fever,

anorexia, weakness, and weight loss.In the past, the disease has beenclassified into moist and dry phases.The “moist” phase refers to theearly, subacute stage with fever, ascites, abdominal pain, andweakness.Ascites is progressive and may become massive.The “dry”form presents later without ascites, following resolution during whichdense adhesions are formed.

• Diagnosis• A peritoneal fluid tap will show mostly lymphocytes.• The laparoscopic appearance of tuberculous peritonitis is

characteristic.• Treatment• Treatment is administration of antituberculous drugs.

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• SECONDARY BACTERIAL PERITONITIS• Perforation Peritonitis• Perforation peritonitis is the most common form of acute intraabdominal

infection.• Perforation of the Stomach and Duodenum.• İnfection after peptic ulcer perforation presents acutely.• The proper management is simple closure of the perforation.• Small Bowel Perforation• Intraabdominal infection after small bowel ğerforation falls into two major

catogeries.• In the first, bowel obstruction is present.• In the second form, bowel wall necrosis due to inflammation or inadequate

vascular supply leads to perforation.• The mortality rate can be more than 50 percent.

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• Typhoid Perforation• Typhoid perforation is usually seen in the third week of

infection with Salmonella typhi.• Typhoid bacilli are though to penetrate the Peyer’s patches

of the intestinal wall, mainly in the distal ileum.• These collections of lymphoid cells hypertrophy, leading

to hemorrhage and then perforation.• Trimethoprim-sulfamethoxazol is the treatment of choice

for uncomplicated typhoid, but in patients with peritonitis, cefataxime plus metranidazole is a better treatmentregimen.

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• Peritonitis Following Appendicitis• If the appendix has perforated, however, the

disease may become life-threatening, especiallywhen the omentum is not able to contain theinfection and diffuse suppurative peritonitisresults.

• Treatment is more likely to be succesful once theappendix is removed and the source of infection is thus controlled.

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• Colon Perforation• About 22 percent of cases of peritonitis have their

anatomic origin in the colon.• More than half of these are due to inflammatory disease

such as diverticulitis and colitis.• Colon perforation following diverticulitis is more common

but less serious since diverticulitis itself institutes localhost defenses.

• Carcinoma of the colon, if the ileocecal valve is component, may lead to diffuse fecal peritonitis as a resultof rupture of the cecum or ascending colon.

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• Amebic Perforation• Entamoeba histolytica infection of the intestine usually

causes a dysentery-like illness, but sometimes liver abscessor perforation of the large bowel occurs.

• Liver abscess also can perforate secondarily and causediffuse peritonitis.

• Peritonitis Following Pancreatitis• Translocation of bacteria is possibly the mechanism of

progress from the initial chemical inflammation of pancreatitis to retro-and intraabdominal peripancreaticinfections.

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• Peritonitis of Genitourinary Origin• A variety of conditions originating from the genitourinary tract can

cause peritonitis.• Ruptured perinephric abscess and ruptured chronic cystitis after

radiation therapy for female reproductive tract cancer are examples.• Pelvic peritonitis due to sexually transmitted infection is seen in young

women.• Postoperative Peritonitis• Postoperative peritonitis is usually due to a leak from a suture line and

is typically discovered only after some delay, as a rule between thefifth and seventh postoperative day.

• Delay contributes to a high mortality rate.

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• Peritonitis after Trauma• Peritonitis may develop after blunt trauma in

patients who have unrecognized intraabdominalinjuries such as a ruptured mesentery with loss of the vascular supply to the small or large bowel, ora frank bowel perforation.

• Patients suffering penetrating trauma, eithergunshot wound or stab wound, usually areoperated on and the wound repaired or controlledimmediately; these injuries lead to peritonitis onlywhen a leak occurs following the initial repair.

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• OTHER FORMS OF PERITONITIS• Aseptic/Sterile Peritonitis• This form of peritonitis develops whenever irritant material

gains entry to the peritoneal cavity.• The soilage initially is sterile, or nearly so, which

distinguishes chemical peritonitis at onset fromsuppurative peritonitis.

• Foreign-Body Peritonitis• Foreign bodies may be deposited in the peritoneal cavity

during operations (sponge or instrument inadvertantly leftbehind) or might result from penetrating injuries orperforation of the intestines following ingestion.

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• Periodic Peritonitis• Recurrent episodes of abdominal pain, fever, and

leukocytosis occur in certain population groups in andaround the Levant, notably in Armenians, Jews and Arabs.

• The disease appears to be familial.• Colchicine is effective in preventing recurrent attacks.• Drug-Related Peritonitis• Administration of isoniazid and of erythromycin estolate

have been reported to cause acute abdominal symptomsmimicking peritonitis but not development of trueperitonitis.

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• Lead Peritonitis• Lead peritonitis has the same clinical picture as acute

intermittent porphyria.• It is associated with lead intoxication (occuring in painters,

smelter workers, pica in children) and a careful history willlead to the correct diagnosis.

• Hyperlipidemic Peritonitis• Abdominal pain mimicking peritonitis may be seen in

patients with type1 and type 5 hyperlipoproteinemia, a group of heterogenous disorders resulting from increasedconcentration of chylomicrons or very-low-densitylipoproteins in the blood.

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• Porphyric Peritonitis• Porphyric peritonitis is a condition of perceived abdominal pain rather

than an inflammation of the peritoneum.• Intraabdominal infection can be ruled out by the demonstration of

porphobilinogen in the Watson-Schwartz test.• Talcum Peritonitis• Peritoneal inflammation, exudation and formation of pseudotumors

(chronic inflammatory omental tumors), and formation of dense adhesions may follow contamination of the peritoneal cavity by glovelubricants (talcum, lycopodium, mineral oil, cornstarch, rice starch) orby cellulose fibers from disposible gauze pads, drapes, and gowns.

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• TERTIARY PERITONITIS• This state has been called the nonbacterial sepsis

syndrome or the systemic inflammatory responsesyndrome, or, following treatment of intraabdominal infection, tertiary peritonitis.

• The clinical picture is one mimicking occultsepsis, as manifested by a hyperdynamiccardiovascular state, low-grade fever, and general hypermetabolism.

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• INTRAABDOMINAL ABSCESS• Abscess Formation• In a developing abscess, bacteria continue to divide and to

produce toxins and enzymes that, together with theproteolytic enzymes of dying phagocytes,liquify theabscess contents and increase osmotic pressure.

• Oxygen and nutrients diffuse poorly through the abscesscapsule, thus promoting anaerobic glycolysis, whichfinally results in an anaerobic environment with highpressure, low pH, low oxygen, and high carbon dioxidelevels.

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• Clinical Features and Diagnosis• An intraabdominal abscess may be seen with either

primary and secondary peritonitis.• Left Subphrenic Abscess• Formerly uncommon, these are now the most common

variety of upper abdominal abscess residual afterperitonitis or leaking from a viscus.

• Lesser Sac Abscess• Technically, this is a variety of left subhepatic-subphrenic

abscess, since the lesser peritoneal sac anatomically is a portion of the left subhepatic space.

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• Right Subphrenic Abscess• Abscess within this space are most frequently secondary to rupture of a

hepatic abscess or less frequently to operation on the stomach orduodenum.

• Right Subhepatic Abscess• The most posterior (deepest) part of this space is called Morison’s

pouch.• A gastric procedure, especially an emergency operation for

complications of ulcer disease, is the most common antecedent event.• Interloop (Midabdominal) Abscess• These are often multiple abscess that arise as loculations between

loops of bowel, mesentery, abdominal wall, and omentum.

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• Pelvic Abscess• This form of abscess most often follows a ruptured colonic

diverticulum, pelvic inflammatory disease, rupturedappendix, or drainage into the pelvis during resolution of generalized peritonitis.

• Pancreatic Abscess• Acute necrotizing pancreatitis is the antecedent cause of

pancreatic abscess in the majority of cases.• Secondary infection of a pancreatic pseudocyst and

abdominal trauma with pancreatic injury are otherimportant causes.

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• Retroperitoneal Abscess• Abscess within the retroperitoneal spaces are not

common.• An abscess located in the upper retroperitoneum is

usually secondary to infection of the pancreas.• Retroperitoneal abscess in other locations may be

caused by primary or secondary infections of thekidneys, ureters, or colon, or osteomyelitis of thespine or after trauma.

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• Management• Percutaneous drainage• Percutaneous needle aspiration and closed catheter drainage, using CT

and ultrasound guidance, is preferred to operative drainage of mostintraabdominal abscess.

• Percutaneous drainage of an intraabdominal abscess is usuallysuccessful if the following criteria are met:

• there is a well-established, unilocular fluid collection;• a safe percutaneous route of access is available; this often means

location of the abscess adjacent to the body wall;• joint evaluation by a surgeon and a radiologist is done so that correct

judgments and decisions are made; and• there is immediate operative backup available in case of failure or

complications.

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• Open Surgical Drainage• The indications for open surgical drainage are failure of percutaneous

drainage, inability to safely drain percutaneously, the presence of a pancreatic or carcinomatous abscess, an association with a bowelfistula, the involvement of the lesser sac, or the presence of multiple, isolated interloop abscesses.

• Antibiotic Therapy in Conjunction with Abscess Management• Antibiotic therapy should be initiated before percutaneous or operative

abscess drainage, guided by the sensitivity studies obtained fromprevious intraoperative specimens and antibiotics already used in treatment of the antecedent abdominal infection.

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• NONOPERATIVE MANAGEMENT OF PERITONITIS

• Preoperative Preparation• The essential features of preoperative treatment of

peritonitis involve fluid resuscitation, antibiotics, oxygen and, if needed, ventilator support, nasogastric intubation, urinary catheterization, andpossibly early hemofiltration, and monitoring of vital signs and biochemical and hemodynamicdata.

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• Fluid Resuscitation• Extensive inflammation of the peritoneal membrane causes fluid to

shift into the peritoneal cavity and the interstitial space.• Large volumes of fluid may be necessary to restore the intravascular

volume and to maintain a satisfactory urine output.• Oxygen and Ventilator Support• Oxygen is administred to overcome the mild hypoxemia commonly

present in peritonitis as a result of the increased metabolic demand of infection, some degree of intrapulmonary shunting, and the mechanicalimpairment of pulmonary ventilation by the distended, tender abdomen.

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• Intubation, Catheterization, and HemodynamicMonitoring

• Vital signs (temperature, blood pressure, pulse, respirations) are continuously recorded.

• Preoperative biochemical evaluation should includemeasurement of serum electrolytes, creatinine, glucose, bilirubin, and alkaline phosphatase, and a urinalysis.

• Epidural/Peridural Analgesia• Peridural analgesia is very helpful in patients with

peritonitis to reduce their requirement for parenteralanalgesics.

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• Renal Support• Monitoring of renal function is essential and requires early corrective

measures.• Narcotics• Analgesic drugs should not be administered to patients with suspected

peritonitis, or any other acute abdominal process, until a firm diagnosis has been made or, at least, a decision to operate has been made.

• Vasoactive Drugs• Administration of drugs with predominant alpha-adrenergic effects is

sometimes of value in the treatment of the hyperdynamic phase of sepsissecondary to peritonitis.

• Steroids• Steroids are not currently recommended in the management of bacterial

peritonitis.• Fever• A temperature above 38.5°C can be associated with difficulty in

administration of anesthesia.• Administration of salicylates often will be effective in reducing fever.

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• OPERATIVE TREATMENT OF SUPPURATIVE PERITONITIS• Cleaning the Abdminal Cavity• Intraoperative High-Volume Lavage• This treatment involves extensive intraoperative lavage of the entire

abdominal cavity.• Initially, 1 to 5 L of physiologic saline or Ringer’s solution is placed

into the abdominal cavity, the viscera are manipulated so that the fluidreaches all parts of the abdominal cavity to wash out pus, feces, andnecrotic material, and then the fluid is suctioned away.

• This procedure is repeated until the suctioned fluid runs repetitivelyclear.

• Usually, a total of 8 to 12 L is used in adults.

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• Radical Debridement• Radical debridement is a poorly defined technique because

it is almost impossible, witout causing too much bleeding, to radically debride all necrotic tissue in intraabdominalinfections, including intraabdominal abscesses.

• Continuous Postoperative Irrigation• In this method, four to six Tenckhoff catheters are placed

in the abdominal cavity and irrigation fluid is infusedthrough them for an hour.

• The process is then reversed to drain the abdominal cavity, and then the cycle is repeated.

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• Open Abdomen and Staged Abdominal Repair• This concept of planned relaparotomies later fused with the

open-abdomen technique when the requirement fortension-free abdominal wound closure became evident.

• The new concept, termed stages abdominal repair, usesnew devices for closure such as a zipper with larger seams(Ethizip), Marlex mesh with a zipper, or an artificial burrdevice.

• Relaparotomies are performed at 24-h intervals in theoperating room.

• Once all problems are solved, the abdominal cavity is closed definitively.

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Acute appendicitis• Incidence• Acute appendicitis is the most common acute surgical

condition of the abdomen. The disease occurs at all ages but is most frequent in the second and third decades of life.

• Etiology and Pathogenesis• Obstruction of the lumen is the domuniant factor in the

production of acute appendicitis. Fecaliths are usual cause of appendiceal obstruction. Less common are hyperthropyof lymhoid tissue;inspissated barium from previous X-ray studies;vegetable and fruit ; seeds; and intestinal worms;particularly ascarids.

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• Bacteriology• A variety of anaerobs, aerobs, or facultative

bacteria have been cultured from peritoneal fluid, abcess contents, and appendiceal tissue in patients with gangrenaous or perforated appendicitis.

• Bacteriodes fragilis and Escherichia coli were isolated from almost all specimens. Other frequent isolates were Peptostreptococcus (80 percent), Pseudomanas (40 percent), B.splanchnicus (40 percent) and Lactobacillus (37 Percent).

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• Clinical Manifestations• Symptoms:Abdominal pain is the prime symptom of cause

appendicitis.Classically the pain initially is diffusely centered in the lower epigastrium or umblical area, is moderately severe and is steady-sometimes with intermitent cramping superimposed. After a period varying from 1 to 12 h, but usually within 4 to 6 h, the pain localizes in the right lower quadrant.

• Variations in the anatomic location of the appendix account for many of the variatioms in the principal locus of the somatic phase of the pain. For ezample a long appendix with the inflamed tip in the left lower quadrant causes pain in that area;a retroceacal appendix may cause principally flank or back pain ; a pelvic appendix may cause testicular pain presumably from irritation of the spermatic artery and ureter.

• Anorexia naerly always accompanies appendicitis.Vomiting occurs in about 75 percent of patients.

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• Signs• Temparaature elevation is rarely more than 1 C.• Tenderness is often maximal at or near the point described by Mc Burney as

being `1located exactly between an inch and ahalf and two inches from the anterior spinous process of the ileum on a straight line drawn from that processto the umblicus``

• Rovsing`s sign-pain in the right lower quadrant when palpatory pressure is exerted in the left lower quadrant- aaaalso indicaates yhe site of the peritoneal irritation.

• As the examining finger exertspressure on the peritoneum of the cul-de-sac of Douglas, pain is felt in the suprapubic areaas wel as locally.

• The psoas sign indicates an irritative focus in proximity to that muscle. The test is performed by having patients lie on their left side; the examiner then slowly extends the right thigh, thus strecthing the iliopsoas muscle.

• Similarly, a positive obturator sign of hypogastric pain on streching the obturator internus indicates irritaion at the locus. The test is performed by passive internal rotation of the flexed right thigh with the patient supine.

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• Labarotory Findings• Moderate leukocytosis, from about 10.000 to

18.000/mm3.Pain films of the abdomen in acute appenddicitis often reveal a distended loop or two of small bowel in the right lower quadrant less often a distended cecum.

• Laparoscpoy• Laparoscopy can be used to distinguish

gynecologic disease and ileitis from appendicitis . If the diagnosis of appendicitis is made laparoscopic appendectomy can be performed.

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• Differential Diagnosis.• Acute mesenteric adenitis• Acute gastroenteritis• Disease of the male• including torsions of the testis and acute epididymitis.• Meckel`s diverticulitis• Intussuception• Regional enteritis• Perforated peptic ulcer• Diverticulitis or Perforating Carcinoma Of the Cecum or of That Portion of the

Sigmoid That lies on the Right Side.• Epiploic appendagitis• Urinary tract infection• Uretral stone• Primary peritonitis• Henoch-Schonlein Purpura• Yersinosis

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• Gynecologic Disorders; pelvic inflammaorydisease ,ruptured graafian follicul, twisted ovarian cyst or tumor, endometriosis and ruptured ectopicpregnacy.

• Other diseases;: Closed loop intestinal obstruction, mesenteric vascular occlusuion, pleuritis of the right lower chest acute cholecysstitis acute pancreatitis hamatoma of the abdominal wall.

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• Appendicitis in the Young• Diagnosis accuracy for acute appendicitis is

considerably lower than in adults.• The disease progresses more rapidly than in adults

–gangrene and rupture occur earlier in the course of acute appendicitis in children. The rupture rate varies from 15 to 50 precent in reported series.

• Rupture of gangrenous appendicitis is more frequently followed by diffuse peritoinits and distant intraabdominal abcesses than in adults.

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• Appendicicitis in the Elderly.• Less than 10 percent of patients operated on

for acute appendiciis are over sixty years of age but morethan 50 percent of all deaths from appendicitis are in this age group. This is attributable to delay of definitive treatment greater frequency of progressive uncontrolled infection and a high incidence of concomitant disease.

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• Appendicitis During Pregnancy• Diagnosis is difficult. Symptoms of appendicitis

such as abdominal pain and nausea are also common in pregnancy. Displacement of the appendix by the gravid uterus changes the location of the somatic componentof abdominal pain and the point of maximal tenderness to a higher and more lateral position. Leukocytosis of pregnancy ,where white cell counts as high as 15.000/mm3 are normal,compromises the value of this test.Laporoscopy can be used in atypical cases and may laparotomy unnecessary.

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• Appendicitis in Patients with AIDS/HIV Infection• Most immunodeficient patients have no WBC elevation

preoperatively. Diagnostic laporoscopy is helpful in establishing or ruling out the diagnosis.

• Treatment:• There is but one treatment for acute appendicitis and

complications. To attempt to treat appendicitis with antibiotics is misguided because it ignores the obstructive causaation of appendicitis and is to be condemned. Thus the only question to be resolved is -when the timing of surgical intervention.

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• References– Wittmann DH, Walker AP, Condon RE

Peritonitis and Intraabdominal Infection. Principles of Surgery ed. Schwartz SI McGrawHill 1994, 1449-1483.

– Condon RE, Telford GL Appendicitis. Textbook of Surgery, ed:Sabiston DC. W.B. Saunders Philadelphia 1991,884-898.