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A N N A L S OF SURGERY Vol. 224, No. 1, 10-18 © 1996


Vol. 224, No. 1, 10-18

© 1996 Lippincott-Raven Publishers

Management of Secondary Peritonitis

Dietmar H. Wittmann, M.D., Ph.D., F.A.C.S., Moshe Schein, M.D., F.C.S. (S.A.),

and Robert E. Condon, M.D., F.A.C.S.

From the Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin


The authors review current definition, classification, scoring, microbiology, inflammatory response, and goals of management of secondary peritonitis.

Summary Background Data

Despite improved diagnostic modalities, potentantibiotics, modern intensive care, and

aggressive surgical treatment, up to one third of patients still die of severe secondary peritonitis.

Against the background of current understanding of the local and systemic inflammatory

response associated with peritonitis, there is growing controversy concerning the optimal antibiotic and operative therapy, intensified by lack of properly conducted randomized studies. In this overview the authors attempt to outline controversies, suggest a practical clinical approach, and highlight issues necessitating furtherresearch.


The authors reviewthe literatureand reporttheirexperience.


The emerging concepts concerning antibiotic treatment suggest that less-in terms of the number of drugs and the duration of treatment-is better. The classical single operation for peritonitis, which obliterates the source of infection and purges the peritoneal cavity, may be inadequate for severe forms

of peritonitis; for the latter, more aggressive surgical techniques are necessary to decompress increased

intra-abdominal pressure and prevent or treat persistent and recurrent infection. The widespread

acceptance of the more aggressive and demanding surgical methods has been hampered by the lack

of randomized trials and reportedly high associated morbidity rates.


Sepsis represents the host's systemic inflammatory response to bacterial peritonitis. To improve results, both the initiator and the biologic consequences of the peritoneal infective-inflammatory process should be addressed. The initiator may be better controlled in severe forms of peritonitis by aggressive surgical methods, whereas the search for methods to abort its systemic consequences is continuing.

overview is to present the "state of the art" in the man-

intestinal perforation and those resulting from injuries agement of secondary peritonitis, to emphasize persist-

ing controversies, and to identify the gaps in our knowl-

edge that require further study.



Peritonitis and intra-abdominal infection are not syn-

onymous. Peritonitis denotes inflammation of the peri-

Intra-abdominal infections after spontaneous gastro-

or complicating abdominal operations, still represent the

"bread and butter" for surgeons. The purpose of this

Address reprint requests to Dietmar H. Wittmann, M.D., Ph.D.,

F.A.C.S., Department of Surgery, Medical College

of Wisconsin,

9200 W. Wisconsin Avenue, Milwaukee, WI 53226.

Accepted for publication August 10, 1995.


Vol. 224.9No. 1

Management of Secondary Peritonitis


toneum from any cause. It may be regarded as the local- ized equivalent of the systemic inflammatory response seen after any trigger of inflammation,",2 which recently

has been described as systemic inflammatory response syndrome.3 Intra-abdominal infection denotes peritoni- tis caused by bacteria (e.g., a local inflammatory process initiated by bacteria and their toxins). It may be regarded

as the localized equivalent of systemic sepsis (Fig. 1). In-

tra-abdominal abscess is an intra-abdominal infection

thathas been confined within the abdominal cavity. Be-

cause the vast majority ofclinically significant peritonitis is caused by bacteria, both terms are used interchange- ably. Intra-abdominal infection is defined as an in-

flammatory response of the peritoneum to micro-organ- isms and their toxins, which results in purulent exudate in the abdominal cavity. Conditions without such peri- toneal inflammatory response, in which contamination

has occurred but infection is not established (e.g., early

traumatic bowel perforation), or in which the infectious process remains contained within a diseased, but resect- able, organ (e.g., gallbladder or appendix), represent "simple" forms of peritonitis, easily cured by an opera-

tion and not requiring prolonged additional antibiotic



Many attempts have been made to classify peritonitis

in general, and secondary peritonitis in particular, which

include a large variety of different pathologic conditions



Figure 1. Relation between systemic inflammatory response syndrome

and sepsis vs. peritonitisand intra-abdominal infection.


1. Primary peritonitis Diffuse bacterial peritonitis

in the absence of

disruption of intra- abdominal hollow viscera 11. Secondary peritonitis

Localized (abscess) or diffuseperitonitis originating from a defect in abdominal viscus

Ill. Tertiary peritonitis Peritonitislike syndrome occurring late due to disturbance in the

host's immune


A. Spontaneous peritonitis in children

B. Spontaneous peritonitis in adults

C. Peritonitis in patients with CAPD

D. Tuberculous and other granulomatous peritonitis

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


C. Post-traumatic peritonitis

1. After blunt abdominal trauma

2. After penetrating abdominal trauma

A. Peritonitis without evidence for


B. Peritonitis with fungi

C. Peritonitis with low-grade

pathogenic bacteria

CAPD = continued ambulatory peritoneal dialysis.

ranging in severity from a local problem such as gangre-

nous appendicitis to a devastating disease such as diffuse

postoperative peritonitis due to a dehiscence of a gastro-

duodenal anastomosis.5-8 A simplified version is pre- sented in Table 1. It differentiates between the relatively

rare forms of primary peritonitis, which usually respond

to medical treatment, and tertiary peritonitis, which does

not respond to any treatment, from the commonly oc-

curring secondary peritonitis that mandates surgical in-



The multifaceted nature of abdominal surgical infec-

tions makes it difficult to precisely define the disease and

to assess its severity and therapeutic progress. Both the

anatomic source ofinfection, and to a greater degree, the physiologic compromise it inflicts, affects the out- come.9 " The mortality of intra-abdominal infection is related mainly to the severity of the patient's systemic response and his premorbid physiologic reserves, esti-

mated best using the Acute Physiology and Chronic

Health Evaluation II (APACHE-II) scoring system (Fig.

2).6,12The APACHE-II score hasbeen validatedprospec-

tively in a large number ofpatients and has been adopted

by the Surgical Infection Society as the best available

12 Wittmann, Schein, and Condon









60%c Lo R+













0 2



8 10 121416 1820 2224 26 283032 3436 38


Figure 2. Mortality of intra-abdominal infections in 924 APACHE

tified cases. Log R + (1

R) =-4.333

(APACHE 11 X 0.226).


method of risk stratification in intra-abdominal infec-

tion .


The micro-organisms associated with secondarv and

tertiary peritonitis are summarized in Table 2. Typically.

primary peritonitis is a monomicrobial, aerobic infec-

tion. The presence of obligate anaerobes, or a mixed

flora. suggests secondary peritonitis. The latter- repre-

sents a polymicrobial infection after a spontaneous or traumatic breach in a micro-organism-containing vis- cus. or because of a postoperative breakdown of intesti- nal anastomosis. The number and types of bacteria in-

crease progressively down the gastrointestinal tract.

Proximally, it contains a sparse aerobe (coliforms) and

oral anaerobe flora (< 104), with the stomach and duo-

denum normallv sterile. However, diseases of the stom-

ach (e.g., carcinoma. gastric outlet obstruction) or acid-

reducing drugs may result in its colonization. 14 Distally,

the colon contains the largest concentration of bacte-

ria-in I g of stool, up to 10 - obligate anaerobes and 10' facultative anaerobes (formerly aerobes). After a perfo-

ration of the colon, more than 400 different species of

Ann. Surg. -July 1996

bacteria invade the peritoneal cavity. Only a few are in-

volved in the ensuing infection (Table 3).5"6 Postopera-

tive state, administration of systemic and luminal anti-

biotics, and the invasive environment of the intensive

care unit may drastically modify patients ecology, result-

ing in colonization of the foregut with peculiar micro-

organisms (e.g, fungi, coagulase-negative staphylococci and gram-negative bacteria of low pathogenicity). These

are the organisms that may be found in tertiary peritoni-

tis, in intensive care unit infections, and in multiple-or-

gan failure.'7

Biphasic Infection

A series of experimental studies in rodents has clarified

the bacteriology of secondary peritonitis, emphasizing

the key process of bacterial simplification and nsver-

gil.'5 From the initial plethora of contaminating bac- teria, the inoculum is spontaneously reduced to include only a few organisms that survive well outside their nat-

ural environment: endotoxin-generating facultative an- aerobes such as Esclerichici coli, responsible for the

acute peritonitis phase with positive blood cultures, and

obligate anaerobes, such as Bacteroides.s fagilis, for late abscess formation. These bacteria act in sIvncegr: both are necessary to produce an abscess, and the obligate an-

aerobe can increase the lethality of an otherwise nonle- thal inoculum of the facultative micro-organism.


The outcome of peritonitis depends on the results of a

struggle between two main forces: the patient's systemic

and peritoneal defenses on one hand and the volume,

nature, and duration of the contamination on the other.

The exact events that follow the invasion of the perito-

neal cavity with bacteria and adjuvants of infection (e.g, blood, bile, barium sulfate) and, subsequently, its trans- lymphatic systemic spread, are subjects of excellent re-


Secondary peritonitis

All forms including infected pancreatic necroses

Tertiary peritonitis Microorganisms do not cause tertiary peritonitis


Gram-negative and gram-positive facultative and

obligate anaerobic bacteria; predominant are

Escherichia co/i and Bacteriodes fragilis

Fungi, Pseudomonas spp.- Entrococcus spp.-

gram-negative of low pathogenicity

Recommended Therapy

Third generation cephalosporins/ metronidazole combination or penicillin/ beta-lactamase inhibitor combinations or imipenem/cilastatin or ciprofloxacin/

clindamycin combination

Antibiotics no help

Vol. 224 - No. 1

Management of Secondary Peritonitis





No. of Isolates













Escherichia co/i










Kluyvera ascorbata


Koserella trabulsii


Morganella morganii


Providencia alcalifaciens


Cedecea lapagei














* No antibiotics had been administered for at least 3 days before specimen collec-

tion. For bacteriological methods. see: Krepel CJ, Gohr CM, Edmiston CE, Condon

RE. Surgial sepsis constancy of antibiotic susceptibility of causative organisms.

Surgery 1995, 17:505-509.

views.'9-'2 The microorganisms and their products (e.g, endotoxins) stimulate the host's cellular defenses to acti- vate a myriad of inflammatory mediators that are re- sponsible for the sepsis (e.g, systemic response to infec-


The recent explosion in molecular biology has in-

creased our understanding of the cytokine-mediated in-

flammatory response in peritonitis. During peritonitis,

cytokines (tumor necrosis factor-a, interleukin-l, in-

terleukin-6, elastase, and others) are measurable in the

systemic circulation,-2 and in much greater concentra-

tions in the peritoneal exudate22; the magnitude of the

phenomena negatively correlates with outcome. Bacte-

rial peritonitis appears to induce an intense compart-

mentalized inflammatory process. The largest part of peritoneal cytokines probably derive from macrophages

exposed to endotoxin liberated from infecting bacteria. Other potential sources are direct translocation of cyto- kines through the intestinal barrier-23 or production by tissues traumatized duringthe operative trauma forperi-

tonitis.24 The compartmentalization of the cytokine cas-

cades in peritonitis corroborates the concept that circu-

lating concentrations of cytokines may be misleading

and not reflect their tissue concentration or biological ac-

tivity. Local estimation of cytokines in the peritoneal ex-

udate may thus better reflect the severity of an initially local process (i.e, peritonitis). Certain levels of peritoneal

cytokines, at a particular point in time, stimulate the peritoneal defenses against infection. In different (higher?) levels and certain phases (late?) peritoneal cy-

tokines possess an adverse, end-organ damaging effect.2'

Timely therapeutic intervention is crucial to abort the

ensuing, self-perpetuating "mediator disease" (systemic

inflammatory response syndrome) before the overpro-

duced "terminal" mediator nitric oxide (NO) com-

pletely asphyxiates cells by blocking the Krebs-cycle, in-

flicting advanced injury at the cellular and microvascular

level, leading to sequential multiple-organ failure and



The management of primary peritonitis, an essentially

"nonsurgical," antibiotic-treated disease is referred to

elsewhere.<67 Goals of management of secondary perito-

nitis are summarized in Table 4.2x The sine qlua non of

success is timely surgical intervention to stop delivery of

bacteria and adjuvants into the peritoneal cavity. All

other measures are of little use if the operation does not

successfullyabort the infectivesource and quantitatively reduce the inoculum of micro-organisms and adjuvants

of infection so that they can be effectively handled by the patient's defenses, supported by antibiotic therapy. As yet, effective "antimediator" therapy to modulate the lo-

cal and systemic inflammatory repercussions of perito-

nitis is not available. Consequently, intensive measures

to support tissue oxygenation and maintain organ func- tion are necessary while awaiting recovery brought on

trough antibiotic and surgical therapy.


1. Supportive measures

A. To combat hypovolemia and shock and maintain adequate tissue oxygenation

B. To treat bacteria, not eliminated by surgery, with antibiotics

C. To support failing organ systems

D. To provide adequate nutrition

II.Operative treatment

Principle 1 (Repair)

Control the source of infection Principle 2 (Purge)

Evacuate bacterial inoculum, pus, and adluvants (peritoneal 'toilet'')

Principle 3 (Decompress)

Treat abdominal compartment syndrome

Principle 4 (Control)

Prevent or treat persistent and recurrent infection or verify both repair and purge

14 Wittmann, Schein, and Condon

Antibiotic Therapy

Advances in bacteriology and the introduction, during the 1960s and 1970s, of antibiotics (e.g., aminoglyco- sides, cephalosporins) with limited activity against obli-

gate anaerobes have refocused the attention on the an-

aerobic nature of secondary peritonitis. This prompted the aforementioned experimental studies that identified

E. coli and B. ftagi/is as the main target organisms for

therapy. The current practice of early empirical admin- istration of antibiotics targeted against these bacteria is

well established.42" However, issues concerning the choice and timing of drugs, the need for operative cul- tures, and the duration of postoperative administration are controversial.

Unfortunately,the numerous prospective randomized

studies concerned with antibiotic management of"peri- tonitis" do not provide the information they promise be-

cause thle patientswhose illnessesare most severe usually are excluded by study design. Many trials are "diluted" witlh low mor-tality-penetrating trauma cases that repre- senit contamination ratherthan infection. Consequently, the aver-age mortality rate in the antibiotics studies re- viewed by Solomkin et al.3") was only 3.5%. This sharply

contrasts with the 32% and 29% mortality rates of 569

and 924 cases, respectively, which consistently are asso-

ciated with severe intra-abdominal infections.63'

Nevertheless, and despite of the numerous options ad- vertised, antibiotic therapy for secondary peritonitis is sim-

ple. The emerging concepts suggest that less, in terms of the

number of drugs and the duration of treatment, is better.32 To hit the primary endotoxin-producing target organism

E. coli, an antibiotic that kills all strains and thus does not induce resistance, is required. Third-generation cephalo-

sporins such as cefotaxime sodium, ceftizoxime sodium, cefmenoxime hydrochloride, and ceftriaxonesodium meet

this requirement. In 104 studies, none of 10,478 strains of

E. coli tested had a minimal inhibitory concentration in

excess of the concentrations sustained over 12 hours in the

peritoneum with a 2-g dose of cefotaxime sodium.2933 The

once popular "triple" regimen of the 1970s (ampicillin, an aminoglycoside, and metronidazole or clindamycin) has become obsolete. Aminoglycosides are significantly more nephrotoxic than third-generation cephalosporins, are in- efficient in the low pH level of the infected peritoneal envi- ronment,34 and are no longer the first choice of antibiotics in the initial treatment of intra-abdominal infection.2932 The enterococctus, which frequently is isolated in experi- mental and clinical peritonitis, is almost (may transfer re-

sistant genes to other bacteria) clinically insignificant ex- cept for its role as a cofactor for B. fragilis in the formation of abscesses.'8 Thus, it does not require coverage with am- picillin if the obligate anaerobes (e.g., Bfragilis) are ade- quately covered by metronidazole or clindamycin.

A few low-mortality35,36 or retrospective studies37 sug-

Ann. Surg.*-July 1996

gest that monotherapy with a single broad-spectrum an- tibiotic that includes full activity against E. coli may be equal or superior to polytherapy with multiple drug com-

binations. We are not convinced by studies that claim


aerobes represent an effective monotherapy. Half of the patients in one series35 have been cured of infection with

antibiotics to which even their aerobic bacteria were re- sistant. This suggests that in many instances, operation

alone may be curative, a well-known reality in the pre-

antimicrobial era, when the mortality rate was reduced from 90% to 40% by introducing operative manage-


Because monotherapy has not been studied ade-

quately in patients with established peritonitis from an intestinal or postoperative source, and because many of

the 3-Lactam antibiotics are not fully effective against

obligate anaerobes in the peritoneal cavity,29 we advo-

cate the addition of metronidazole to an effective, non-

toxic, antiaerobic agent. The active compound of cilas-

tatin-imipenem is an effective sole agent for severe intra-

abdominal infection.39 It should be reserved, however, as a "second-line" agent forthe nosocomially altered spec-

trum of postoperative peritonitis. Our general recom-

mendations are summarized in Table 2. The value of obtaining routine intraoperative perito-

neal cultures has become questionable because the re-

sults rarely influence clinical decisions29.36.37.40and usu- ally are available only when therapy is no longer neces-


The trend to continue administration ofantibiotics for

fixed periods4' 42 is no longer justified. Recommenda-

tions ofthe Surgical Infection Society that the conditions representing "simple" (simple cholecystitis, appendici- tis, etc.) intra-abdominal infection, or contamination

only (early operated-on spontaneous or traumatic gas-

trointestinal lesions) do not require prolonged therapeu- tic postoperative antibiotics4 is an important step toward

limiting the currently prevailing practices of excessive

antibiotic prescription.4344 Further changes in the cur-

rent practices are being examined to possibly minimize

postoperative administration by intraoperative stratifi- cation ofthe extent of infection, tailoring the duration of therapy to operative findings.45 It still is widely be-

lieved-and practiced-that anti-infectiveagentsshould

be continued until temperature and leukocyte count are within normal limits, but there is no evidence that con- tinuing therapy aborts the potentially developing infec- tivecomplications. Surgeonswho stopped antibioticsac- cording to a protocol, despite continued fever, did not observe an excessive rate ofinfectious complications; the

pyrexia resolved spontaneously in the vast majority of

the patients.45 Microbiological studies in patients un- dergoing relaparotomies for diffuse peritonitis demon-

strated that the peritoneal cavity becomes almost sterile

Vol. 224 - No. 1

Management of Secondary Peritonitis


after a few days.46 Thus, it appears that at a certain stage,

infection is cured; however, the fever, fueled by ongoing,

usually self-limited hypercytokinemia, persists. We be- lieve that the persistence of postoperative pyrexia or other clinical and laboratory signs of infection is not an

indication to continue, restart, or change antibiotics. In- stead, while awaiting a spontaneous remittance, a search

should be conducted for a treatable extra-abdominal and

especially intraperitoneal cause. Further studies are nec-

essary to better define the exact point in time in which

the transition from infection to "inflammation-only"

occurs and beyond which antibioticsare obsolete.

An unresolved issue remains the clinical significance

of antibiotic-induced endotoxemia. Several studies sug-

gest that some antibiotics possess greater endotoxin-lib-

erating abilities and cytokine production.47 This phe-

nomenon has been claimed to be of clinical importance in patients with sepsis,48 but its relevance was never ex- amined in the setup of peritonitis. If evidence were pro- duced that intraperitoneal killing of bacteria with antibi-

otics excessively triggers the cascades of inflammation,

then there would be a case for withholding the drugs until the source of infection is dealt with, and the pus is evac-

uated operatively.

Operative Therapy

The classical, single operation forintra-abdominal in- fection (principles 1 and 2, Table 3) was established dur- ing the early decades of this century and reduced overall

mortality from 90% (19th century) to approximately

40% in 1926.38 Principle 1 eliminates the source of infec- tion; frequently, it involves a simple procedure, such as

appendectomy or omentopexy of a perforated peptic ul-

cer. Occasionally, major resections to remove the infec-

tive focus are indicated, such as gastrectomy or colec- tomy, for perforated gastric carcinoma or colonic diver-

ticulitis, respectively. Generally, the choice of the

procedure, and whether the ends of resected bowel are anastomosed, exteriorized, or simply closed depends on

the anatomic source ofinfection, the degree ofperitoneal

inflammation and generalized septic response, and the patient's premorbid reserves. No formula is available,

but the prevailing trend has been to minimize the imme-

diate risk of complications by avoiding any intestinal su-

ture lines in the presence of severe peritonitis.3:

Principle 2 purges the infected abdominal cavity. All

infectious fluids should be aspirated, and particulate

matter should be removed by swabbing. Although cos- metically appealing and popular with surgeons, there is

no evidence that intraoperative peritoneal lavage reduces

mortality or the incidence of septic complications in pa-

tients receiving adequate systemic antibiotics.49'50 Peri-

toneal irrigation with antibiotics is not advantageous be-

cause bacteria need to be exposed to the antibiotic for


Critical patient's condition (hemodynamic instability) precluding definitive repair Excessive peritoneal edema (abdominal compartment syndrome:

pulmonary, cardiac, renal, or hepatic dysfunction, and decreased visceral perfusion) preventing abdominal closure without undue tension, intra-abdominal pressure > 15 mmHg Massive abdominal wall loss Impossibility to eliminate or to control the source of infection Incomplete debridement of necrotic tissue

Uncertainty of viability of remaining bowel Uncontrolled bleeding (the need for "packing")

hours to be effective. The addition of antiseptics may produce toxic effects.49 Intraperitoneal instillation of heparin has decreased mortality in a few experimental

studies, but clinical trials are lacking.5' The concept of

radical debridement of the peritoneal cavity did not withstand the test of a prospective randomized study52 because aggressive debridement caused excessive bleed-

ing from the denuded peritoneum and endangered the integrity ofthe friable intestine. The role ofpostoperative peritoneal lavage is at best questionable53 because the ba- sic question remains whether it is possible to irrigate the whole abdominal cavity; do we irrigate the abdomen or only the drain tract?54 Despite the dictum that it is im-

possible to effectively drain the free peritoneal cavity, drains still are commonly used and misused. In addition

to the false sense of security and reassurance they pro- vide, drains can erode into intestine or blood vessels and

promote infective complications.54 Their use should be

limited to the evacuation of an established abscess, to

allow escape of potential visceral secretions (e.g., biliary, pancreatic) and to establish a controlled intestinal fistula

when the latter cannot be exteriorized.754

Despite gradual improvement in critical care and an-

timicrobial therapy, the mortality rate of intra-abdomi- nal infection remained unacceptably high until the

1980s. True progress may have been hidden because in

later decades, more patients with advanced types of in- tra-abdominal infection (e.g., postoperative peritonitis) were treated actively. Nevertheless, it became clear that

if the initial standard operation fails, persisting or recur- rent intra-abdominal infection sometimes is overlooked or the diagnosis is delayed.55 Waiting for the appearance

of signs of persisting infection or organ failure as the in-

dication for re-exploration ("on demand") of the abdo-

men often proved futile.56 To improve results, methods to affect principles 3 and 4 (Table 3) had to be addressed.

The 1980s witnessed the evolution of two therapeutic

concepts: open management (laparostomy) 57.58 and

"planned" relaparotomies.5960 Planned relaparotomy addresses principle 4: multiple operative interventions

16 Wittmann, Schein, and Condon

are planned before or during (but not after) the first pro- cedure for peritonitis. The commitment is made to re- turn to the abdominal cavity to re-explore, evacuate, de-

bride, or resect, until those disease processes indicating

the need for serial relaparotomies are resolved. More-

over, planned relaparotomy allows verification of the in-

tegrity of anastomoses, fashioned at the first operation, or their eventual construction during subsequent relapa- rotomy,61 62 as opposed to the routine avoidance of su- ture-lines advocated by the single operation propo-


Open management addresses principle 3 and facili-

tates frequent re-exploration. It serves to decompress the high intra-abdominal pressure caused by peritoneal

edema associated w'ttl inflammation and fluid resuscita-

tion, thus obviating the deleterious systemic conse-

quences of the abdominal compartment syndrome.64

Early results of these methods were promising, particu- larly in the management of infected pancreatic necrosis, but were less favorable in cases of postoperative peritoni-

tis.65 Simple open management was plagued by intestinal fistulas and abdominal-wall defects,66 problems that were almost eliminated by introduction of temporary ab-

dominal closure devices such as the artificial burr or

mesh-zipper techniques.6'67 Staged abdominal repair as a conceptual operative approach combines the advan- tages of planned relaparotomy and of open management with a minimal rate of complications.6 Using the indica- tions presented in Table 4, approximately 10% to 15% of all patients undergoing intra-abdominal infection sur- gery will qualify for this management policy.6'68 A pro-

spective nonrandomized attempt to compare "closed"

and "open" abdomen techniques did not demonstrate

an advantage of the latter.69 Recent nonrandomized se-

ries failed to to demonstrate the benefits of planned re-

laparotomies.7" However, another prospective study

showed the staged abdominal repair approach to be su-

perior to conventional operative therapy when patients at equal mortality risk were compared.68 It has been shown in trauma cases that repeated operations per- formed in patients in whom the inflammatory response is already "switched-on" by the traumatic event (and their macrophages thus primed) may act as a "second hit," escalating the and precipitating multiorgan dys-

function.7" The "second hit" issue in the setup of reoper-

ative therapy for peritonitis should be clarified; namely, what should be the interval between relaparotomies to avoid adding wood to the inflammatory fire? A 24-hour interval is supported by collected clinical experience and

by bacteriological studies. Bacteria regrow to their initial

inoculum 24 hours after peritoneal irrigation.72

A prospective, randomized, multicenter study (re- cently approved by the Surgical Infection Society) will be

necessary to further document the value of the demand-

ing. potentially harmful, and costly management modal-

Ann. Surg.*-July1996

ities required to address principles 3 and 428.61.68.73,74 However, we believe these techniques to be beneficial if initiated early, in well-selected patients, for specific indi- cations (Table 5), performed by a team of dedicated surgeons. Conversely, indiscriminate use at "the end of

the operative list," often by ever-changing members of

juniorstaff, represents a recipe fordisasters.70

Management of Intra-Abdominal Abscess

Erroneously, the term intra-abdominal abscess has been used as a synonym for peritonitis. This is not true because abscesses develop from effective host defenses and represent a relatively successful outcome of perito- nitis. Abscesses may be visceral and nonvisceral, intra-

or extraperitoneal. Nonvisceral abscesses arise after res-

olution of diffuse peritonitis in which a loculated area of infection and suppuration is "walled off" and persists, or

after a perforation of a viscus (or an intestinal anastomo-

sis) that is effectively localized by peritoneal defenses.7