intra-abdominalinfection and acute abdomen …percussion tenderness and referred rebound tenderness...

INTRA-ABDOMINAL INFECTION AND ACUTE

ABDOMEN-EPIDEMIOLOGY, DIAGNOSIS AND GENERAL

PRINCIPLES OF SURGICAL MANAGEMENT

Jovanovic Dusan,1

Loncar Zlatibor,1, 2

Doklestic Krstina,1, 2

Karamarkovic Aleksandar1, 2

1Clinic for Emergency Surgery, Clinical Center of Serbia, Belgrade, Serbia

2Faculty of Medicine, University of Belgrade, Serbia

Primljen/Received 01. 02. 2015. god. Prihva}en/Accepted 10. 03. 2015. god.

Abstract: Intra-abdominal infections are multi-factorial and present an complex inflammatory respon-se of the peritoneum to microorganisms followed byexudation in the abdominal cavity and systemic re-sponse Despite advances in management and criticalcare of patients with acute generalized peritonitis dueto hollow viscus perforation, prognosis is still very po-or, with high mortality rate. Early detection and adequ-ate treatment is essential to minimize complications inthe patient with acute abdomen. Prognostic evaluationof complicated IAI by modern scoring systems is im-portant to assess the severity and the prognosis of thedisease. Control of the septic source can be achievedeither by nonoperative or operative means. Nonopera-tive interventional procedures include percutaneousdrainages of abscesses. The management of primaryperitonitis is non-surgical and antibiotic- treatment.The management of secondary peritonitis include sur-gery to control the source of infection, removal of tox-ins, bacteria, and necrotic tissue, antibiotic therapy,supportive therapy and nutrition. “Source control” issine qua non of success and adequate surgical procedu-re involves closure or resection of any openings intothe gastrointestinal tract, resection of inflamed tissueand drainage of all abdominal and pelivic collections.

Key words: Intra-abdominal infection, secondaryperitonitis, source control, surgery.

INTRODUCTION

Intra-abdominal infection (IAI) present an complexinflammatory response of the peritoneum to microorgan-isms followed by exudation in the abdominal cavity andsystemic response (1). Intra-abdominal infection presenta primary, secondary and tertiary peritonitis; in uncompli-cated and complicated forms (1). Acute generalized sec-

ondary peritonitis from gastrointestinal hollow viscusperforation is a potentially life threatening condition. De-spite major advances in diagnosis, management and criti-cal care of patients with secondary peritonitis, prognosisis still very poor, with high mortality rate (1, 2, 3). Sourcecontrol, resuscitation and early antibiotic administrationare crucial (1–4). Intra-abdominal infections are also clas-sified into community-acquired intra-abdominal infecti-ons (CAIAIs) acquired in community and healthcare-ac-quired intra-abdominal infections (HA-IAIs), develop inhospitalized patients (1–4). They are characterized by in-creased mortality because of both underlying patient he-alth status and infection is caused by multi drugs resistantorganisms (4). Uncomplicated IAI involves a one singleorgan and does not proceed to the whole peritoneum,such infections can be successfully treated by surgical re-section alone, or with antibiotics alone (5). In complica-ted IAI the infection spreads from localized peritonitis tothe diffuse peritonitis (1, 2). The treatment of patientswith complicated intra-abdominal infections necessarilyinvolves both: source control and antibiotic therapy (1, 2,6). Both, the anatomic source of infection, and to a greaterdegree the physiological compromise, affect the outco-me. The outcome of IAI depends on the severity of thepatient’s systemic response and his premorbid physiolog-ical reserves, estimated best using the (7).

This review comments on epidemiology, diagno-sis and general principles of surgical management inpatients with acute abdomen.

DEFINITION, CLASSIFICATION,

SCORING

The accepted classification of intra-abdominal in-fection is a division into primary, secondary and terti-ary peritonitis (Table 1) (6).

UDK: 617.55-002; 616.381-002-08

2015; 10(1): 69–78 ID: 214202124

ISSN-1452-662X Review article

Primary peritonitis present the result of the hemato-genous bacterial spread to the peritoneum without lossof integrity of the gastrointestinal tract, secondary peri-tonitis follows a perforation of a hollow organs or cysticstructure and tertiary peritonitis is a recurrent infectionof the peritoneal cavity that follows either primary or se-condary peritonitis (2). Primary peritonitis is rare, and itmainly occurs in early childhood and in cirrhotic adultpatients (2). Secondary peritonitis is an acute peritonealinfection resulting from loss of integrity of the gastroin-testinal tract due to spontaneous or traumatic organ rup-ture (Figure 1) (6). It is the most common form of perito-nitis. Most frequently encountered in clinical practice asa result of perforation of the duodenal ulcer, or by directinvasion from infected gangrenous appendicitis. Ana-stomotic dehiscences are common causes of peritonitisin the postoperative period. Secondary peritonitis withsevere sepsis or septic shock have mortality rates of ap-proximately 30% (4, 6, 8).

Early prognostic evaluation of complicated IAI isimportant to assess the severity and the prognosis of

the disease. Scoring systems can be divided into: disea-se-independent scores for evaluation of serious pati-ents requiring care in the intensive care unit (ICU) suchas Acute Physiology and Chronic Health Evaluation II(APACHE II) scoring system and Simplified AcutePhysiology Score (SAPS II) and peritonitis-specificscores such as Mannheim Peritonitis Index (MPI) (7,9). APCHE-II is applied within 24 hours of admissionof a patient to an ICU: an integer score from 0 to 71 isbased on several measurements; higher scores corre-spond to more severe disease and a higher risk of death(7). The APACHE-II score has been validated prospec-tively in a large number of patients and has been adop-ted by the Surgical Infection Society as the best availa-ble method of risk stratification in IAI (7). AlthoughAPACHE II is considered as a golden standard, valueof this scoring system in peritonitis has been questio-ned because of the APACHE II impossibility to evalua-te interventions, despite the fact that interventionsmight significantly alter many of the physiological va-riables (10, 11, 12).

70 Jovanovic Dusan, Loncar Zlatibor, Doklestic Krstina, Karamarkovic Aleksandar

Figure 1. Secondary peritonitis. a. Perforated liver abscess. b. Fibrin on small bowel loops.

c. Colon perforation. d. Infected pancreatic necrosis.

(Image source: Clinic for Emergency Surgery, Clinical Center of Serbia, Belgrade, Serbia)

The Mannheim Peritonitis Index (MPI) is a speci-fic score, which provides an easy way to handle with cli-nical parameters, allowing the outcome prediction.Long-term survivors have an MPI score of about 20;non-survivors have a score of 33. The MPI is specificfor peritonitis and easy to calculate, even during surgery(11, 12, 13). Billing et al. demonstrated the reliability ofMPI in 2003 patients from 7 centres in Europe (14). Forpatients with a score less than 21 the mean mortality ratewas 2.3%, for score 21–29 mortality was 22.5% and forscore greater than 29 mortality was 59.1%; the sensitiv-ity was 86%, specificity 74% and accuracy 83% in pre-dicting mortality (14). Panhofer et al. proposed the useof both MPI and APACHE II in patients who developedtertiary peritonitis, concluding that combination ofprognostic scores was very useful to detect tertiary peri-tonitis (15). Inui at al. investigated the utility of Char-lson Comorbidity Index and multiple organ dysfunction(MOD) (16). Among patients who failed initial therapy,a non-appendiceal source of infection and a Charlsonscore > or = 2 were determined to be independent riskfactors. Nonappendiceal source of infection and MODscore > or = 4 on postoperative day 7 were independentpredictors for re-intervention (16).

PATHOPHYSIOLOGY

AND HOST RESPONSE

The total area of the peritoneum is approximately1.8 m

2, which is covered by the mesothelial cells mic-

rovilli that measure to 3.0 m in length (2). Peritonealfluid has the properties of lymph, and is secreted by theperitoneal serosa. Diaphragmatic lymphatic channelsact like valves and suck synchronous with respirationperitoneal fluid and any bacteria and pro inflammatorymediators through the thoracic ducts into the venouscirculation. Inspiration decreases intra-thoracic pres-sure relative to intra-abdominal pressure, creating apressure gradient favoring fluid movement out of theabdomen. Entry of pro-inflammatory substances intothe vascular space produces hemodynamic and respira-tory findings of sepsis. Positive-pressure ventilation li-kely attenuates this process. Perforation of the gastro-intestinal tract is the most common cause of acute in-tra-abdominal infection and their highly infectiouscontent flows into the free peritoneal cavity triggers astrong host response (2). The most common causes ofacute abdomen are perforation due to peptic ulcer dise-ase, diverticulitis, appendicitis, malignant lesion, bo-

INTRA-ABDOMINAL INFECTION AND ACUTE ABDOMEN-EPIDEMIOLOGY, DIAGNOSIS AND GENERAL... 71

Table 1. Classification of intraabdominal infections

PRIMARY PERITONITIS Diffuse bacterial peritonitis in theabsence of disruption of intraab-dominal hollow viscera

A. Spontaneous peritonitis in chil-dren

B. Spontaneous peritonitis in adults

C. Peritonitis in patients with CAPD

D. Tuberculous and other granulo-matous peritonitis

SECONDARY PERITONITIS Localized (abscess) or diffuse pe-ritonitis originating from a defectin abdominal viscus

A. Acute perforation peritonitis

1. Gastrointestinal perforation

2. Intestinal ischemia

3. Pelviperitonitis and other forms

B. Postoperative peritonitis

1. Anastomotic leak

2. Accidental perforation and de-vascularization

C. Post-traumatic peritonitis

1. After blunt abdominal trauma

2. After penetrating abdominal tra-uma

TERTIARY PERITONITIS Peritonitislike syndrome occurringlate due to disturbance in the host’simmune response

A. Peritonitis without evidence forpathogens

B. Peritonitis with fungi

C. Peritonitis with low-grade pat-hogenic bacteria

wel wall necrosis after strangulation or incarceratedhernia. The three major intra-peritoneal defense mech-anisms are: mechanical clearance of bacteria vialymphatics, phagocytic killing of bacteria by immunecells, and mechanical sequestration (2). The arm of theperitoneal defense system is to localize bacterial conta-mination. Hyperemia and exudation of fluid follow ac-tivation of immune cells. Several events favor the de-position of fibrin, including activation of mesothelialand macro-phage-mediated procoagulant activity act-ing on fibrinogen in reactive peritoneal fluid, coupledwith loss of plasminogen activator from mesothelialcells. The combined effect is the deposition of fibrino-us exudates. Ileus and fibrin formation accentuate theprocess. Formation of an abscess is one of the benefi-cial functions of fibrin formation encapsulating the in-fection and preventing systemic spread.

DIAGNOSIS

Early detection and adequate treatment is essen-tial to minimize complications in the patient with acuteabdomen (17–21). A physical examination combinedwith abdominal ultrasonography (US) represents theinitial investigation in patients with acute abdominalpain. The abdomen is distended, it is quiet to ausculta-tion, and tender to palpation. Abdominal pain is almostalways the predominant symptom, unless its percep-tion is masked by the administration of analgesics orthe presence of a fresh surgical wound. Rupture of a vi-scus is associated with sudden on-set pain. When fullydeveloped, pain is steady, unrelenting, burning, andaggravated by any motion. Pain is usually most intensein the region of most advanced peritoneal inflamma-tion. Patients can usually localize pain arising from ir-ritation of the parietal peritoneum -peritoneal signs. Itmay be associated with tenderness and involuntarymuscle spasm -guarding. Rebound tenderness can beelicited by gently depressing an area distant from thearea of pathology and letting it bounce back. Direct,percussion tenderness and referred rebound tendernessconfirms the presence of peritoneal irritation. Rigidityof the abdominal muscles is produced after involve-ment of the parietal peritoneum by inflammation butalso by reflex muscle spasm and abdominal hyperten-sion. Reflex spasm may become so severe that it pro-duces board like abdominal rigidity. Rectal and vaginalexaminations are essential to locate the extent of ten-derness and the possible presence of a pelvic mass. An-orexia is always present, nausea is frequent and rarelyaccompanied by vomiting.

Systemic manifestations in complicated IAI areSIRS manifestations: body temperature > 38 °C or < 36 °C,heart rate > 90 beats per minute, respiratory rate > 20

breaths per minute (not ventilated) or PaCO2 < 32mm Hg (ventilated), WBC > 12,000, < 4,000 or >10% immature forms (bands) (18). Bone RC Temper-ature usually ranges between 38 °C and 40 °C; the fe-ver is more spiking in character in younger and healt-hier patients, whereas older or debilitated patientsmay exhibit only a modest febrile response. Tachy-cardia and a diminished palpable peripheral pulse vo-lume are indicative of hypovolemia, hypovolemicshock and sepsis. Respirations are typically rapid andshallow. Hypotension and hypoperfusion signs suchas lactic acidosis, oliguria, and acute alteration ofmental status are indicative of evolution to severesepsis (21). A leukocyte count of more than 25,000 orleukopenia of fewer than 4000/mL3 are both associa-ted with higher mortality. The differential count sho-wing relative lymphopenia and moderate to markedleftward shift, even if the leukocyte count is normal orsubnormal. Procalcitonin (PCT) appeared to be a pa-rameter for early detection of progressing sepsis andvaluable aid in deciding if further relaparotomies we-re necessary after initial operative treatment of an in-tra-abdominal septic focus (19, 22).

Computerized tomography (CT) is the imaging ofchoice for most intra-abdominal processes in he-modynamically stable patient (17, 20, 21). Diagnosticlaparoscopy should be considered in patients without aspecific diagnosis after appropriate imaging and as analternative to active clinical observation which is thecurrent practice in patients with non-specific abdomi-nal pain (17). Plain radiographs of the abdomen mayreveal free air on an upright abdominal or lateral decu-bitus film, a uniform indicator of visceral perforationin the absence of prior intervention (17, 21). The radio-logical picture of intra-abdominal infection otherwisemimics that of paralytic ileus. Radiographs of the chestmay show air beneath the diaphragm if the patient re-mains in an upright position for 5 min or more beforethe film (21).

GENERAL MANAGEMENT

Early treatment of generalized secondary perito-nitis may result in a better outcome and any delay maycorrelate with exponentially increasing mortality (21).Control of the septic source can be achieved either bynonoperative or operative means (21, 23, 24). Nonope-rative interventional procedures include percutaneousdrainages of abscesses. The management of primaryperitonitis, an essentially “non-surgical”, is antibiotic-treatment. The management of secondary peritonitisinclude surgery to control the source of infection, anti-biotic therapy, supportive therapy and nutrition (21,23, 24).


SOURCE CONTROL

“Source control” is sine qua non of success andadequate surgical procedure involves closure or resec-tion of any openings into the gastrointestinal tract, re-section of inflamed tissue and drainage of all fluid col-lections (25). Laparotomy is usually performed thro-ugh a midline incision. Timing and adequacy of sourcecontrol are the most important issues in the manage-ment of intra-abdominal infections, because inadequa-te and late operation may have a negative effect on theoutcome (26, 27, 28). The latter aspect of surgical man-agement is controversial, with recent recommendati-ons focused only on the source of infection as opposedto complete peritoneal debridement. Intensive caremeasures to support tissue oxygenation and maintainorgan function remain important, while awaiting reco-very brought upon trough surgical and antibiotic ther-apy. Antibiotic therapy should be started as early aspossible after diagnosis (26, 27, 28). The trend to conti-nue administration of antibiotics for fixed periods is nolonger justified (28). An important rule towards limit-ing the currently prevailing practices of excessive anti-biotic prescription is the recommendation of the Surgi-cal Infection Society that ’simple’ intra-abdominal in-fection do not require therapeutic postoperative antibi-otics. Antimicrobial regimens effective against com-mon gram-negative and anaerobic enteric pathogensare the mainstay of therapy (26, 27, 28). For patientswith community-acquired intra-abdominal infections,narrower-spectrum antimicrobial agents with a low po-tential for iatrogenic complications are appropriate.Patients with nosocomially-acquired, intra-abdominalinfections are more likely to harbor resistant patho-gens. Inadequate empiric antimicrobial therapy is as-sociated with treatment failure and death. Therefore,broader spectrum antimicrobial regimens are recom-mended for these patients, and to coverage of more re-sistant gram-negative bacilli and anaerobes, use ofagents effective against enterococci, resistant staphy-lococci and Candida should be considered (26, 27, 28).Conditions without such peritoneal inflammatory re-sponse, in which contamination has occurred but infec-tion is not established, or in which the infectious pro-cess remains contained within a diseased, but resecta-ble organ, represent ’simple’ forms of peritonitis like inappedicitis or cholecystitis, not requiring additionalantibiotic therapy for more than 3 to 5 postoperativedays (25–28).

OPERATIVE STRATEGIES

Reduction in mortality is not possible without ef-fective source control (21). The mortality of intraabdo-minal infection was about 90% at the end of the 19th

century, when management was mainly non-operative.Source control done in a single operation reduced mor-tality by more than 50% (21).

The classical, single operation for IAI accomplis-hes the main goal: surgical source control and a one-ti-me removal of toxins, bacteria, and necrotic tissue(21). The single operation is sufficient in the majorityof cases. Only 15% of patients present with advanceddisease that require multiple abdominal re-entries (21,28). The choice of the procedure, and whether the endsof resected bowel are anastomosed, exteriorized, orsimply closed, depends on the anatomical source of in-fection, the degree of peritoneal inflammation and gen-eralized septic response, patient’s comorbidit conditi-ons and physiological reserve. All infectious fluidsshould be aspirated and particulate matter removed byswabbing. Although, cosmetically appealing and pop-ular with surgeons, there is more evidence other thanwashing out bacteria that intraoperative peritoneal la-vage reduces mortality or the incidence of septic com-plications in patients receiving adequate systemic anti-biotics. Drains are still commonly used and misused. Inaddition to the false sense of security and reassurancethey provide, drains can erode into intestine or bloodvessels and promote infective complications. Their useshould be limited to the evacuation of an establishedabscess, to allow escape of potential visceral secretionsas biliary, or pancreatic and to establish a controlled in-testinal fistula when the latter cannot be exteriorized.

Decompression of the abdominal compartmentand intra-abdominal hypertension (IAH) is addressedby the decompression methods, mainly the “leavingthe abdomen open” techniques (28). Adkins Tempo-rary closure of the abdomen may be achieved usingself-adhesive membrane dressings, absorbable mes-hes, nonabsorbable meshes, zippers and vacuum-assi-sted closure (VAC) devices (29, 30). Today Vacu-um-assisted fascial closure (VAC) has become an op-tion for the treatment of open abdomen (29–32). Thesurgical treatment strategies following an initial emer-gency laparotomy may include either a relaparotomy,only when the patient’s condition demands it (“relapa-rotomy on-demand”), or a planned relaparotomy after36–48 hours with temporarily abdomen closure oropen abdomen (33). Wild STAR (Stage AbdominalRepair) permits continuous control of anastomoses andintra-abdominal healing and effective bacterial elimi-nation (34). This is the only method were post-operati-ve complications are diagnosed early before progress-ing to major damages. Additionally, peritoneal fluidlosses can be measured and protein losses replaced byFFP exactly to match the losses. If a patient developsrecurrent peritonitis, a re-intervention is required. Thissituation has been named “relaparotomy on demand.”


It is associated with high mortality rates because the di-agnosis of post-operative peritonitis delayed and pati-ents are operated too late. They often presented withorgan failure and advanced disease that is responsiblefor bad outcome. Ruler et al. published a randomized,clinical trial comparing on-Demand vs Planned Rela-parotomy strategy in patients with severe peritonitis(35). The patients in the on-demand relaparotomy gro-up did not have a significantly lower rate of death ormajor peritonitis-related morbidity compared with theplanned relaparotomy group but did have a substantialreduction in relaparotomies, health care utilization,and medical costs (35).

Source control of appendix perforation

Acute appendicitis is the most common intra-ab-dominal condition requiring emergency surgery. De-layed diagnosis and treatment of appendicitis also maylead to perforation with diffuse peritonitis. Dissemina-ted intra-abdominal infection from appendicitis, howe-ver, is not seen as often today as in the first decades ofthe 20th century, when appendicitis was the major cau-se of severe peritonitis and peritonitis-related mortality(36, 37, 38). Although antibiotics may be used as pri-mary treatment for selected patients with suspected un-complicated appendicitis, appendectomy is still thegold standard therapy for acute appendicitis (36, 37,38). Treatment includes source control by appendec-tomy, rarely in the most severe cases staged abdominalrepair in cases when peritoneal edema has led to abdo-minal compartment syndrome. Studies have demon-strated that antibiotics alone may be useful to treat pati-ents with early, non perforated appendicitis, even ifthere is a risk of recurrence (36, 37, 38). Randomizedclinical trial by Hanson et al. compared antibiotic ther-apy versus appendectomy as primary treatment of acu-te appendicitis (39). Treatment efficacy was 90.8% forantibiotic therapy and 89.2% for surgery. Recurrent ap-pendicitis occurred in 13.9% of patients treated conser-vatively after a median of 1 year (39). The course of ap-pendicitis leading to massive necrosis and life threate-ning infection, often surpassing the omentum’s capabi-lity to contain the infection and form a perityphlic ab-scess and diffuse suppurative peritonitis then results(40, 41). Appendix abscess occurs in 10% of patientswith acute appendicitis (40). There is much contro-versy whether interval appendicectomy is appropriatefor adults with an appendiceal abscess. The traditionalmanagement of appendiceal mass has been initial con-servative treatment followed by interval appendicec-tomy (40). Deakin et al. demonstrated that conservati-ve management approach was successful in the major-ity of patients presenting with an appendix mass (42).

The authors concluded that after initial successful conser-vative management, routine use of interval appendicec-tomy was not justified in asymptomatic patients (42).

Source control

of gastro-duodenal perforation

Gastroduodenal perforations have decreased sig-nificantly in the last years thanks to the widespreadadoption of medical therapies for peptic ulcer diseaseand stress ulcer prophylaxis among critically ill pati-ents. Successful laparoscopic repair of perforated gas-tric and duodenal ulcers has been reported but the tech-nique has yet to be universally accepted (43, 44, 45).This form of peritonitis is initially chemical but in ashort time becomes infected. The proper managementis simple closure. Antibiotic therapy may be given overa very short period in the range of 1 to 3 days becausebacterial numbers are generally small and the sourcecan be closed safely. The high mortality rate of anasto-motic leakage or suture line breakdown after gas-tro-duodenal operations Billroth I and Billroth II resec-tions are explained by the fact that the duodenum is re-troperitoneally fixed and cannot be exteriorized, andthe source of infection often cannot be adequately con-trolled or closed.

Source Control of Colon Perforation

Antibiotics are the standard of care for uncompli-cated diverticulitis (46). Percutaneous drainage is theintervention of choice for simple uniloculated absces-ses (46). It has a success rate of more than 80%, but itmay have a high failure rate in cases of complex multi-loculated or inaccessible abscesses (46). Colon perfo-ration due to diverticulitis or cancer is a common causeof diffuse, fecal peritonitis (Figure 1). Urgent surgeryfor colonic diverticula perforations is indicated in pati-ents with large or/and multiloculated diverticular ab-scesses inaccessible to percutaneous drainage or inwhom clinical symptoms persist after CT guided per-cutaneous drainage, diverticulitis associated with freeperforation and purulent or fecal diffuse peritonitis.This factor, together with the many associated diseasesin the population of elderly patients with colon disease,contributes to the high mortality rate of 37% (46). The-re is still controversy about the optimal surgical mana-gement of peritonitis caused by colonic diverticular di-sease (46, 47). Hartmann’s resection has been the pro-cedure of choice in patients with generalized peritoni-tis and remains a safe technique for emergency colec-tomy in perforated diverticulitis, especially in elderlypatients with multiple co-morbidities. This group ofpatients particularly benefits from staged abdominal


repair for which the overall mortality rate is less than20% (46). Antibiotic therapy needs to cover both facul-tative and obligate anaerobic bacteria and can be dis-continued after five days duration (46). More recently,some reports have suggested that primary resectionand anastomosis is the preferred approach to diverticu-litis, even in the presence of diffuse peritonitis (46, 47).

Peritonitis of Biliary Origin

Because of the delay of diagnosis, biliary peritoni-tis is associated with mortality rates exceeding 30%.Early suspicion is key. Removal of the gallbladder andcommon duct stones represents effective source con-trol (48–54). Early laparoscopic cholecystectomy foracute cholecystitis is safer and shows lower rates ofconversions than delay laparoscopic cholecystectomy(50). Half of the mortality of biliary peritonitis is cau-sed by E. coli and one fourth by clostridium perfrin-

gens, which may cause a fulminate necrotizing infec-tion leading to death within hours (50–54). The lattermay requires immediate re-operation, high doses ofpenicillin (10 million units every 6 hours) IntensiveCare and hyperbaric oxygen. Most cases of acute cho-lecystitis as a complication of Intensive Care are acal-culous and likely represent complications of microva-scular and mucosal dysfunction. This condition, oftenpresents during sepsis originating in the necrotic gall-bladder that becomes infected and must be removed foreffective source control. Despite the evidence, early la-paroscopic cholecystectomy is not the most commontreatment for acute cholecystitis in practise andwrongly it remains common practice to treat acute cho-lecystitis with intravenous antibiotic therapy and inter-val laparoscopic cholecystectomy preferentially (55).

Source Controlof Infected Pancreatic Necrosis

In the acute phase of pancreatitis, antibiotic ther-apy, supporativ therapy and intravenous hydrationaimed at maintaining the patient’s intravascular volu-me and perfusion pressures is the mainstay of treat-ment. Usually during the third week after onset of acu-te pancreatitis, the disease has progressed from initialchemical inflammation to intraabdominal infectionwith high mortality because source control is difficult(Figure 1) (56). Endoscopic retrograde cholangiopan-creatography (ERCP) and sphincterotomy are indica-ted in patients with biliary pancreatitis and impactedgall stones, biliary sepsis, or obstructive jaundice (56).In septic patients with necrotizing pancreatitis, a Fi-ne-needle aspiration (FNA) should be performed fordifferentiation of sterile and infected pancreatic necro-

sis (56). Adequate volume resuscitation and analgesictreatment are the most important treatment of acutepancreatitis. Antibiotic prophylaxis reduces septiccomplications in severe necrotizing pancreatitis andshould be started early, best with 1 gram of imipe-nem/cilastatin every 6 to 8 hours at the onset of acutepancreatitis before infection can be proven. Antibioticsmust be administered for longer periods (56). Surgicaltherapy is indicated in patients with infected pancreaticnecrosis (56, 57). The optimal time point for the surgi-cal intervention is the 3rd to 4th week after onset of thedisease, in that time necrotic tissue will be well demar-cated. The surgical technique of choice is necrosec-tomy with postoperative closed lavage (56, 57, 58).Before closure, large abdominal drains must be placedinto the pancreatic bed to further drain necrotic areasand to collect pancreatic juice preventing further intra-abdominal spread of digestive enzymes. When mostnecroses are removed or overgrown by granulation tis-sue, usually after 8–12 abdominal entries if STAR isdone, and peritoneal edema disappears, the abdomencan be closed fascia-to fascia without meshes. Cho-lecystectomy should be performed to avoid recurrenceof gallstone-associated acute pancreatitis.

Source Control of Small

Bowel Perforation

Most non-traumatic small intestinal perforationsare due to unrecognized bowel strangulation and intes-tinal ischemia (59, 60, 61). Source control includes re-section of the diseased segment and anastomosis (59,60, 61). The high mortality rate of more than 50% canbe reduced by treating advanced cases with the STARoperation that permits inspection of the anastomosis atsubsequent abdominal entries, and diagnose and treatnew necrosis early. In addition, anastomoses can be de-ferred and the bowel simply stapled off at the firstSTAR in deteriorating patients who will not tolerateextensive procedures during sepsis. If small bowel per-forations operated before peritonitis develops it can ha-ve an excellent prognosis. Source control is usually ac-hieved by simple suture closure, rarely by resection ofthe perforated segment and anastomosis.

Source Control

in Postoperative Peritonitis

Postoperative peritonitis is usually due to a leakfrom a suture line (4, 62). Diagnosis is often delay, andpatients, as a rule, are re-explored between the fifth andseventh postoperative day, which contributed to thehigh mortality rate. A suture line leak is easier to repairif it is observed in the colon, small bowel or stomach


compared with leaks of the duodenum or esophagus.Upper gastrointestinal tract disease after an operationallows only a limited therapeutic correction to controlthe source, because these organs are fixed or closely at-tached to the retroperitoneum and the infectious sourcecannot be totally excluded under most circumstances.Resection of the anastomosis or bowel segment is bet-ter than repair. Staged abdominal repair using a tempo-rary abdominal closure device may be of particular be-nefit to this subset of patients with intraabdominal in-fections; we were able to reduce mortality to 24% (62).

Source Control

in Posttraumatic Peritonitis

Peritonitis coused by intestine perforation may de-velop in patients after blunt abdominal trauma (63). Thistype of intraabdominal infection is usually severe becau-se it is masked by other injuries and often recognized late,even when an initial CT was done. This causes delay indiagnosis and most cases present with a diffuse peritonitis(63). General principles of treatment do not differ fromthat of intraabdominal infection (63). Contamination ofthe abdominal cavity seen after penetrating abdominaltrauma is not considered an intraabdominal infection.

In a conclusion, intra-abdominal infections pres-ent an complex inflammatory response of the peritone-um to microorganisms. Despite all advances in mana-gement of patients with secondary peritonitis, progno-sis is still very poor, with high mortality rate. Acute ge-neralized secondary peritonitis is still very interestingfor surgeons and adequate source control is sine quanon of treatment.

Abbreviations

IAI — Intra-abdominal infectionCAIAIs — community-acquired intra-abdominal

infectionsHA-IAIs — healthcare-acquired intra-abdominal

infectionsICU — intensive care unitAPACHE II — Acute Physiology and Chronic

Health Evaluation IISAPS II — Simplified Acute Physiology ScoreMPI — Mannheim Peritonitis IndexMOD — multiple organ dysfunctionVAC — vacuum-assisted closureSTAR — Stage Abdominal Repair


Saètak

INTRA-ABDOMINALNA INFEKCIJA I AKUTNI

ABDOMEN-EPIDEMIOLOGIJA, DIJAGNOZA I OP[TI PRINCIPI

HIRUR[KOG RE[AVANJA

Jovanovi} Du{an,1

Lon~ar Zlatibor,1, 2

Doklesti} Krstina,1, 2

Karamarkovi} Aleksandar1, 2

1Klinika za urgentnu hirurgiju, Klini~ki centar Srbije, Beograd, Srbija

2Medicinski fakultet Univerziteta u Beogradu, Beograd, Srbija

Intra-abdominalne infekcije (IAI) su multifaktorijal-ne i predstavljaju sloèni inflamatorni odgovor peritone-uma na prisustvo patogenih mikroorganizama, sa eksuda-cijom u trbu{nu duplju i sistemskim odgovorom. Uprkosnapretku u zbrinjavanju pacijenata sa akutnim difuznimperitonitisom koji je posledica perforacije {upljeg trbu-{nog organa, prognoza je i dalje veoma lo{a, sa visokomstopom smrtnosti. Rano postavljanje dijagnoze i adekvat-no le~enje su od su{tinskog zna~aja za minimiziranjekomplikacija kod pacijenta sa akutnim abdomenom.Prognosti~ka evaluacija komplikovanih IAI savremenimbodovnim sistemima je va`na zbog procene teìne bolestii prognoze. Kontrola izvora infekcije moè biti ne-hirur-{ka i hirur{ka. Ne-hirur{ke interventne procedure uklju-

~uju drenaù gnojne kolekcije/apscesa. Le~enje sekun-darnog peritonitisa je kompleksno i uklju~uje: hirur{kukontrolu izvora infekcije, uklanjanje nekroti~nog tkiva idetritusa iz trbuha, antibiotsku terapiju, supstitucionu isimptomatsku terapiju, i ishranu. „Kontrola izvora infek-cije“ je sine qua non adekvatnog le~enja, a obuhvata: su-turu mesta perforacije {upljeg organa gastrointestinalnogtrakta, resekciju ishemi~no-nektoti~nog tkiva, uklanjanjeorgana u celini (appendectomia, cholecystectomia), lava-ù trbuha u slu~aju difuznog peritonitisa, kao i drenaùsva ~etri kvadranta, uz plasiranje kontaktnog drena namestu hirur{kog rada.

Klju~ne re~i: Intraabdominalna ifekcija, sekun-darni peritonitis, kontrola izvora, hirurgija.

REFERENCES

1. Malangoni MA, Inui T. Peritonitis — the Western ex-perience. World J Emerg Surg. 2006; 1:25.

2. Menichetti F, Sganga G: Definition and classification ofintra-abdominal infections. J Chemother. 2009; 21(Suppl 1): 3–4.

3. Wacha H, Hau T, Dittmer R, Ohmann C. Risk factorsassociated with intraabdominal infections: a prospective multi-centre study. Peritonitis Study Group. Langenbecks Arch Surg.1999; 384(1): 24–32.

4. Pieracci FM, Barie PS.Management of severe sepsisof abdominal origin. Scand J Surg. 2007; 96(3): 184–196.

5. Giessling U, Petersen S, Freitag M, Kleine-KraneburgH, Ludwig K. Surgical management of severe peritonitis. Zen-tralbl Chir. 2002; 127(7): 594–7.

6. Mulari K, Leppäniemi A. Severe secondary peritonitisfollowing gastrointestinal tract perforation. Scand J Surg. 2004;93(3): 204–8.

7. Giamarellos-Bourboulis EJ, Norrby-Teglund A,Mylona V, et al. Risk assessment in sepsis: a new prognostica-tion rule by APACHE II score and serum soluble urokinase pla-sminogen activator receptor. Crit Care. 2012; 16(4): R149.

8. Mulier S, Penninckx f, Verwaest C, et al. Factors af-fecting mortality in generalized postoperative peritonitis: multi-variate analysis in 96 patients. World J Surg. 2003; 27(4):379–84.

9. Horiuchi A, Watanabe Y, Doi T, et al. Evaluation ofprognostic factors and scoring system in colonic perforation.World J Gastroenterol. 2007; 13(23): 3228–31.

10. Koperna T, Semmler D, Marian F. Risk stratification inemergency surgical patients: is the APACHE II score a reliablemarker of physiological impairment? Arch Surg. 2001; 136(1):55–9.

11. Malik AA, Wani KA, Dar LA, Wani MA, Wani RA,Parray FQ. Mannheim Peritonitis Index and APACHE II — pre-diction of outcome in patients with peritonitis. Ulus TravmaAcil Cerrahi Derg. 2010; 16(1): 27–32.

12. Correia MM, Thuler LCS, Velasco E, Vidal EM, Scha-naider A. Peritonitis Index in oncologic patients. Revista Brasi-leira de Cancerologia. 2001; 47(1): 63–8.

13. Notash AY, Salimi J, Rahimian H, Fesharaki MH, Ab-basi A. Evaluation of Mannheim peritonitis index and multipleorgan failure score in patients with peritonitis. Indian J Gastro-enterol. 2005; 24(5): 197–200.

14. Billing A, Fröhlich D, Schildberg FW. Prediction ofoutcome using the Mannheim peritonitis index in 2003 patients.Peritonitis Study Group. Br J Surg. 1994; 81(2): 209–13.

15. Panhofer P, Izay B, Riedl M, et al. Age, microbiologyand prognostic scores help to differentiate between secondaryand tertiary peritonitis. Langenbecks Arch Surg. 2009; 394(2):265–71.

16. Inui T, Haridas M, Claridge JA, Malangoni MA. Mor-tality for intraabdominal infection is associated with intrinsicrisk factors rather than the source of infection. Surgery. 2009;146(4): 654–61.

17. Emmi V, Sganga G. Diagnosis of intra-abdominal in-fections: Clinical findings and imaging. Infez Med. 2008; 16(Suppl 1): 19–30.

18. Bone RC, Balk RA, Cerra FB et al. Definitions for sep-sis and organ failure and guidelines for the use of innovative the-rapies in sepsis. The ACCP/SCCM Consensus Conference

Committee. American College of Chest Physicians/Society ofCritical Care Medicine. Chest. 1992; 101(6): 1644–55.

19. Novotny AR, Emmanuel K, Hueser N, et al. Procalci-tonin ratio indicates successful surgical treatment of abdominalsepsis. Surgery. 2009; 145(1): 20–6.

20. Foinant M, Lipiecka E, Buc E, et al. Impact of compu-ted tomography on patient’s care in nontraumatic acute abdo-men: 90 patients. J Radiol. 2007; 88(4): 559–66.

21. Grundmann RT, Petersen M, Lippert H, Meyer F. Theacute (surgical) abdomen — epidemiology, diagnosis and gene-ral principles of management. Z Gastroenterol. 2010; 48(6):696–706.

22. Roland SPH, Brunkhorst MF. Sepsis biomarkers andpathogen detection methods-state of the art. Sanamed. 2014;9(1): 49–61.

23. Solomkin JS, Mazuski JE, Baron EJ, et al. Guidelinesfor the selection of anti-infective agents for complicated in-tra-abdominal infections. Clin Infect Dis. 2003; 37(8):997–1005.

24. Suding PN, Orrico RP, Johnson SB, Wilson SE. Con-cordance of inter-rater assessments of surgical methods to achie-ve source control of intra-abdominal infections. Am J Surg.2008; 196(1): 70–3.

25. Blot S, De Waele JJ. Critical issues in the clinical man-agement of complicated intra-abdominal infections. Drugs.2005; 65(12): 1611–20.

26. Mazuski JE, Sawyer RG, Nathens AB, et al. Therapeu-tic Agents Committee of the Surgical Infections Society. TheSurgical Infection Society guidelines on antimicrobial therapyfor intra-abdominal infections: evidence for the recommendati-ons. Surg Infect (Larchmt). 2002; 3(3): 175–233.

27. Mazuski JE. Antimicrobial treatment for intra-abdom-inal infections. Expert Opin Pharmacother. 2007; 8(17):2933–45.

28. Adkins AL, Robbins J, Villalba M, Bendick P, ShanleyCJ. Open abdomen management of intra-abdominal sepsis. AmSurg. 2004; 70(2): 137–40.

29. Barker DE, Kaufman HJ, Smith LA, Ciraulo DL, Ric-hart CL, Burns RP. Vacuum pack technique of temporary abdo-minal closure: A 7-year experience with 112 patients. J trauma.2000; 48(2): 201–6.

30. Miller Pr, Meredith JW, Johnson JC, Chang MC. Pro-spective evaluation of vacuum-assisted fascial closure afteropen abdomen: Planned ventral hernia rate is substantially redu-ced. Ann Surg. 2004; 239(5): 608–14.

31. Perez D, Wildi S, Demartines N, Bramkamp M, Koe-hler C, Clavien PA. Prospective evaluation of vacuum-assistedclosure in abdominal compartment syndrome and severe abdo-minal sepsis. J Am Coll Surg. 2007; 205(4): 586–92.

32. Jansen JO, Loudon MA. Damage control surgery in anon-trauma setting. Br J Surg. 2007; 94(7): 789–90.

33. Wild T, Stortecky S, Stremitzer S, et al. Abdominaldressing — a new standard in therapy of the open abdomen fol-lowing secondary peritonitis?. Zentralbl Chir. 2006; 131 (Suppl1): S111–4.

34. Ozgüç H, Yilmazlar T, Gürlüler E, Ozen Y, Korun N,Zorluo—lu A. Staged abdominal repair in the treatment of in-tra-abdominal infection: analysis of 102 patients. J GastrointestSurg. 2003; 7(5): 646–51.

35. Van Ruler O, Mahler CW, Boer KR, et al. Comparisonof on-demand vs planned relaparotomy strategy in patients with


severe peritonitis: A randomized trial. JAMA. 2007; 298(8):865–72.

36. Mason RJ. Surgery for appendicitis: is it necessary?Surg Infect (Larchmt). 2008; 9(4): 481–8.

37. Eriksson S, Granström L. Randomized controlled trialof appendicectomy versus antibiotic therapy for acute appendi-citis. Br J Surg. 1995; 82(2): 166–9.

38. Styrud J, Eriksson S, Nilsson I,et al. Appendectomyversus antibiotic treatment in acute appendicitis. a prospectivemulticentre randomized controlled trial. World J Surg. 2006;30(6): 1033–7.

39. Hansson J, Körner U, Khorram-Manesh A, Solberg A,Lundholm K. Randomized clinical trial of antibiotic therapyversus appendicectomy as primary treatment of acute appendi-citis in unselected patients. Br J Surg. 2009; 96(5): 473–81.

40. Corfield L.Interval appendicectomy after appendicealmass or abscess in adults: What is “best practice”? Surg Today.2007; 37(1): 1–4.

41. Andersson RE, Petzold MG. Nonsurgical treatment ofappendiceal abscess or phlegmon: A systematic review and me-ta-analysis. Ann Surg. 2007; 246(5): 741–8.

42. Deakin DE, Ahmed I. Interval appendicectomy afterresolution of adult inflammatory appendix mass — is it neces-sary? Surgeon. 2007; 5(1): 45–50.

43. Sauerlenad S, Agresta F, Bergamaschi R, et al. Laparo-scopic for abdominal emergencies: Evidence based guidelinesof the European Association for Endoscopic Surgery. Surg En-dosc. 2006; 20(1): 14–29.

44. Sanabria AE, Morales CH, Villegas MI. Laparoscopicrepair for perforated peptic ulcer disease. Cochrane DatabaseSyst Rev. 2005; 19(4): CD004778.

45. Ergul E, Gozetlik EO. Emergency spontaneous gastricperforations: ulcus versus cancer. Langenbecks Arch Surg.2009; 394(4): 643–6.

46. McCafferty MH, Roth L, Jorden J. Current manage-ment of diverticulitis. Am Surg. 2008; 74(11): 1041–9.

47. Salem L, Flum DR. Primary anastomosis or Hart-mann’s procedure for patients with diverticular peritonitis? Asystematic review. Dis Colon Rectum. 2004; 47(11): 1953–64.

48. Chandra V, Nelson H, Larson DR, Harrington JR. Im-pact of primary resection on the outcome of patients with perfo-rated diverticulitis. Arch Surg. 2004; 139(11): 1221–4.

49. Martín-Pérez J, Delgado-Plasencia L, Bravo-GutiérrezA, et al. Gallstone ileus as a cause of acute abdomen. Importanceof early diagnosis for surgical treatment. Cir Esp. 2013; 91(8):485–9.

50. Lau H, Lo CY, Patil NG, Yuen WK. Early versus de-layed-interval laparoscopic cholecystectomy for acute cho-lecystitis. A meta-analysis. Surg Endosc. 2006; 20(1): 82–7.

51. Papi C, Catarci M, D’Ambrosio L, et al. Timing ofcholecystectomy for acute cholecystitis: A meta-analysis. Am JGastroenterol. 2004; 99(1): 147–55.

52. Gurusamy KS, Samraj K. Early versus delayed laparo-scopic cholecystectomy for acute cholecystitis. Cochrane Data-base Syst Rev. 2006; 18(4): CD005440.

53. Shikata S, Noguchi Y, Fukui T. Early versus delayedcholecystectomy for acute cholecystitis: A meta-analysis of ran-domized controlled trials. Surg Today. 2005; 35(7): 553–60.

54. González-Rodríguez FJ, Paredes-Cotoré JP, Pontón C,et al. Early or delayed laparoscopic cholecystectomy in acutecholecystitis? Conclusions of a controlled trial. Hepatogastroen-terology. 2009; 56(89): 11–6.

55. Casillas RA, Yegiyants S, Collins JC. Early laparosco-pic cholecystectomy is the preferred management of acute cho-lecystitis. Arch Surg. 2008; 143(6): 533–7.

56. Werner J, Büchler MW. Infectious complications innecrotizing pancreatitis. Zentralbl Chir. 2007; 132(5): 433–7.

57. Amano H, Takada T, Isaji S, et al. Therapeutic inter-vention and surgery of acute pancreatitis. J Hepatobiliary Pan-creat Sci. 2010; 17(1): 53–9.

58. Milian J W, Portugal S J, Laynez Ch R, Rodríguez A C,Targarona J, Barreda C L. Necrotic acute pancreatitis in the in-tensive care unit: a comparison between conservative and surgi-cal medical treatment. Rev Gastroenterol Peru. 2010; 30(3):195–200.

59. Ara C, Sogutlu G, Yildiz R, et al. Spontaneous smallbowel perforations due to intestinal tuberculosis should not berepaired by simple closure. J Gastrointest Surg. 2005; 9(4):514–7.

60. Doklesti} K., Karamarkovic A. Ileum perforation dueto accidental chicken bone ingestion — a rare couse of the acuteabdomen. Sanamed. 2012; 7(1): 31–4.

61. Ghosheh B, Salameh JR. Laparoscopic approach toacute small bowel obstruction: review of 1061 cases. Surg En-dosc. 2007; 21(11): 1945–9.

62. Babadzhanov BD, Teshaev OR, Beketov GI. New ap-proaches to the treatment of postoperative peritonitis. VestnKhir Im I I Grek. 2002; 161(4): 25–8.

63. Chichom Mefire A, Weledji PE, Verla VS, Lidwine NM.Diagnostic and therapeutic challenges of isolated small bowel per-forations after blunt abdominal injury in low income settings: anal-ysis of twenty three new cases. Injury. 2014; 45(1): 141–5.


Correspondence to/Autor za korespondencijuDu{an Jovanovi}Clinic for Emergency Surgery,Pasterova 2Clinical Center of Serbia, Belgrade, Serbiae-mail: dr.dusan26ªmail.com

intra-abdominalinfection and acute abdomen …percussion tenderness and referred rebound tenderness...

Documents