Contamination and Infection, Principles of Treatment
Moshe Schein · Roger Saadia
In peritonitis – source control is above all.
“The mechanical control of the source of infection, while itself nonbiologic,
determines the extent of the host biologic response to the disease.” (Ronald V. Maier)
The finding of inflammation, bowel contents or pus, localized or dispersed throughout the peritoneal cavity is common at emergency laparotomy. How is this scenario best handled? This chapter will discuss general aspects of the surgical treatment.
Nomenclature
Peritonitisand intra-abdominal infection are not synonymous. The former may result from sterile inflammation of the peritoneum, like the chemical peritoni- tis seen following a very recent perforation of a peptic ulcer or acute pancreatitis.
Intra-abdominal infection implies inflammation of the peritoneum caused by micro- organisms. Because, in clinical practice, the vast majority of cases of peritonitis are bacterial, these two terms are used interchangeably.
As a reminder:
Primary peritonitisis caused by micro-organisms which originate from a source outside the abdomen. In young girls, it is usually a Streptococcus gaining access via the genital tract; in cirrhotics, E. coli is thought to be a blood-borne agent infecting the ascites; and in patients receiving peritoneal dialysis, Staphylococcus migrates from the skin along the dialysis catheter. Primary peritonitis in patients without a predisposing factor, such as ascites or dialysis catheter, is extremely rare.
It is usually diagnosed during a laparotomy for an “acute abdomen” when odorless pus is found without an apparent source. The diagnosis is reached by exclusion (after a thorough abdominal exploration), and is confirmed by a Gram-stain and culture, which document a solitary organism. In patients with a known predispos- ing factor (e.g. ascites associated with chronic liver disease), primary peritonitis should be suspected and diagnosed by paracentesis, thus avoiding an operation – as an exploratory laparotomy in an advanced cirrhotic patient often represents an autopsy in vivo. Initial antibiotic treatment is empiric, until results of bacteriologi- cal sensitivities become available.
Secondary peritonitisimplies that the source of infection is a disrupted or inflamed abdominal viscus. This entity is “bread and butter” for you, the general surgeon.
Tertiary peritonitis(> Chap. 48).
Intra-abdominal infection (IAI)is defined as an inflammatory response of the peritoneum to micro-organisms and their toxins that results in a purulent ex- udate in the abdominal cavity.
Abdominal contaminationrepresents conditions without a significant peritoneal inflammatory response: soiling has occurred but infection is not estab- lished yet (e.g. early traumatic bowel perforation).
Resectable IAIrepresents infectious processes that are contained within a diseased but resectable organ (e.g. gangrenous appendicitis). These conditions are easily eradicated by an operation and consequently do not require prolonged post- operative antibiotic therapy.
Non-resectable IAIare infections that have spread beyond the confines of the source organ. In perforated appendicitis, for instance, you may resect the ap- pendix but residual peritoneal infection persists, requiring extended antibiotic cov- erage.
Abdominal sepsisis still a term used very commonly, yet it is confusing.
According to modern consensus usage “sepsis” means systemic inflammatory response syndrome (SIRS) plus a source of infection (> Chap. 48). The use of
“sepsis”, in the abdominal context, would not take into account the important initial local inflammation within the peritoneal cavity. This peritoneal response is analog- ous, at a local level, with SIRS at the systemic level, because it represents, likewise, a non-specific inflammatory response of the host to a variety of noxious stimuli,not necessarily infectious. Strictly speaking, therefore, local contamination, infection and sepsis refer to different processes. Yet, they may co-exist in the same patient, developing simultaneously or consecutively. The soiling of the peritoneal cavity with feces may result in one or another pathological entity,belonging to a continuum of local and systemic conditions ranging from local contamination to septic shock.
Untreated or neglected abdominal contamination progresses to intra-abdominal infection, which is invariably associated with a systemic inflammatory response.
More significantly, abdominal inflammation or indeed the systemic response (fever, leukocytosis) may even persist after the intra-peritoneal infection has been eradicated.
This is not just a matter of semantics or hair-splitting. It has clinical relevance in determining management.
Abdominal contamination is controlled by the local peritoneal defense mechanisms, assisted by operative peritoneal toilet and prophylactic antibiotics.
Resectable infection is managed by the resection of the contained focus of infection, supplemented with a short peri-operative course of antibiotics.
Infection, which is not entirely “resectable”, requires surgical control of its source and, in this situation, therapeutic antibiotics are continued postoperatively
(> Chaps. 7 and 42).
Management
The outcome of intra-abdominal infection (IAI) depends on the virulence of infection, the patient’s pre-morbid reserves, and his current physiological com- promise. Your goal here is to assist the patient’s own local and systemic defenses.
The philosophy of managementis simple – comprising two steps: source control, followed by damage control.
Source control
The key to success is timely surgical intervention to stop delivery of bacteria and adjuvants of inflammation (bile, blood, fecal fiber, barium) into the peritoneal cavity. All other measures are of little use if the operation does not successfully eradicate the infective source and reduce the inoculum to an amount that can be handled effectively by the patient’s defenses, supported by antibiotic therapy. This is not controversial – all the rest may be.
Source controlfrequently involves a simple procedure such as appendectomy
(> Chap. 28) or closure of a perforated ulcer (> Chap. 17). Occasionally, a major
resection to remove the infective focus is indicated, such as gastrectomy or col- ectomy for perforated gastric carcinoma (> Chap. 17) or colonic diverticulitis
(> Chap. 26), respectively. Generally, the choice of the procedure, and whether the
ends of resected bowel are anastomosed or exteriorized (creation of a stoma), depends on the anatomical source of infection, the degree of peritoneal inflam- mation and SIRS, and the patient’s pre-morbid reserves, as will be discussed in the individual chapters.
Damage control
This comprises maneuvers aimed at cleaning the peritoneal cavity, so-called peritoneal toilet. What should this entail?
Contaminants and infectious fluids should be aspirated and particulate matter removed by swabbing or mopping the peritoneal surfaces with moist laparotomy pads. Although cosmetically appealing and popular with surgeons, there is no scientific evidence that intra-operative peritoneal lavage reduces mortality or infective complications in patients receiving adequate systemic antibiotics. Also peritoneal irrigation with antibiotics is not advantageous, and the local addition of antiseptics may produce toxic effects. You may want to “irrigate copiously” (a term popular among American surgeons) as much as you wish, but know that beyond wetting your own underwear and shoes, you do not accomplish much. Should you choose to remain a dedicated irrigator, remember to suck out all the lavage fluid before you close; there is evidence that leaving saline or Ringer’s solution behind interferes with peritoneal defenses by “diluting the macrophages”.
Bacteria swim perhaps better than macrophages!
The concept of radical debridement of the peritoneal cavity,by removing every bit of fibrin, which covers the peritoneal surfaces and viscera, did not withstand the test of a prospective randomized study, since aggressive debridement causes excessive bleeding from the denuded peritoneum and endangers the integrity of the friable intestine.
Despite the dictum that it is impossible to effectively drain the free peritone- al cavity, drains are still commonly used and misused. Their use should be limited to the evacuation of an “established” abscess (when the ensuing cavity would not collapse or cannot be filled with omentum or adjacent structures), to allow escape of potential visceral secretions (e.g., biliary, pancreatic) and, rarely, to establish a controlled intestinal fistula when the latter cannot be exteriorized. To prevent erosion of intestine use soft drains, for the shortest duration possible, keeping them away from bowel. In general, active-suction drainage may be better than the passive, and infective complications can be reduced using “closed “systems.Drains provide a false sense of security and reassurance;we have all seen the moribund post- operative patient with an abdomen “crying” to be re-explored while his surgeon is strongly denying any possibility of intra-peritoneal catastrophe because the tiny drains he inserted, in each abdominal quadrant, are “dry” and non-productive. This is particularly true of drains inserted to deal with post-op hemorrhage (> Chap.50);
it is perfectly possible to have a drain producing no more than a few milliliters of blood yet sitting in an abdomen full of clot.Drains inserted close to an anastomo- sis “just in case it leaks” are more likely to cause anastomotic problems than to deal with them.
The role of postoperative peritoneal lavage, through tube drains left in place for this purpose, is at best questionable. Is it really possible to irrigate the whole abdominal cavity? In our experience tubes or drains are rapidly “walled-off ” by adhesions and adjacent tissues. You’ll be irrigating nothing more than the drains’
tracks (> Fig. 12.1).
Aggressive Modalities of Management
“In doubtful cases do not wait too long Before exploring, for it is quite wrong To act upon the slogan Wait and See,
When looking may provide the remedy” (Zachary Cope, 1881–1974)
Most of your IAI patients will respond to the combination of adequate source control with competent supportive management and appropriate antibiotic administration. Most but not all – a few will need more. During the 1980s it became clear that if the initial standard operation fails, persisting or recurrent IAI some- times is overlooked or the diagnosis is delayed. Waiting for signs of persisting infection or organ failure as the indication for re-exploration (“on demand”) of the abdomen often proves futile. To improve results, two new concepts of aggressive management had to be addressed: to repeat or ascertain source control and to extend damage control:
Planned re-laparotomycontinues the process of source control – repeated op- erative interventions are planned before the first “index” procedure for peritonitis is completed. The commitment is made to return to the abdominal cavity to re- explore, evacuate, debride or resect as needed, until the disease processes are resolved (> Chap. 46).
Open management (laparostomy)is an addition to damage control, it facili- tates frequent re-explorations. It also serves to decompress the high intra-abdomi-
Fig. 12.1. “Which of the drains is draining?”
nal pressure caused by peritoneal edema associated with inflammation, infection and fluid resuscitation, thus obviating the deleterious local and systemic con- sequences of the abdominal compartment syndrome (> Chaps. 36 and 46).
Early results of these methods were promising, particularly in the manage- ment of infected pancreatic necrosis but were less favorable in cases of post- operative peritonitis, perhaps because the sickest patients were included. Intes- tinal fistulas plagued simple open management – problems that were significantly reduced by introduction of temporary abdominal closure (TAC) techniques as explained in > Chap. 46. Our indications to utilize these modalities are shown in
> Table 12.1.
In our experience, less than a fifth (remember, we promised not to use per- centages) of all patients operated upon for IAI will qualify for such management modalities. Note, however that such aggressive treatment methods carry their own list of complications (in surgery you pay for anything you do…). The possibility has been raised that re-laparotomies constitute a “second hit” in patients in whom the inflammatory response is already “switched-on” – thus escalating the systemic inflammatory response syndrome (SIRS) (> Chap.48).To solve this controversy,pro- spective randomized studies are necessary but extremely difficult,if not impossible, to organize. We believe, however, that these techniques are beneficial if initiated early, in well-selected patients, for specific indications, and performed by a team of dedicated surgeons. Conversely, indiscriminate use, at “the end of the operative list”, often by ever changing members of the junior staff, is a recipe for disaster (> Chap. 46).
Table 12.1. Indications for laparostomy/planned re-laparotomy
∑ Critical patient condition (hemodynamic instability) precluding appropriate source control at the first operation, thus calling for “abbreviated laparotomy”
or “damage control” strategy
∑ Excessive peritoneal (visceral) swelling preventing tension free abdominal closure (Abdominal Compartment Syndrome; > Chap. 36)
∑ Massive abdominal wall loss
∑ Inability to eliminate or to control the source of infection
∑ Incomplete debridement of necrotic tissue
∑ Uncertain viability of remaining bowel (> Chap. 23)
∑ Uncontrolled bleeding (the need for “packing”)
Intra-abdominal Abscess
Many surgical texts still, erroneously, use the term intra-abdominal abscess as a synonym with peritonitis. This is not true as abscesses develop due to effective host defenses and represent a relatively successful outcome of peritonitis. The mainstay of treatment is drainage, but by which route? This is discussed in detail in
> Chap. 44.
Need for Peritoneal Cultures
The expensive ritual of obtaining routine intra-operative peritoneal cultures has become questionable. Think, how many times did you act, changing antibiotics, based on peritoneal culture results? Probably never! As you saw above, the micro- biology of IAI is predictable, the pathogens being “covered” by the broad-spectrum empiric agents started by you prior to the operation (> Chap. 7). Furthermore, usually after a few days, when culture and sensitivity results are available, the antibiotics are no longer necessary. Being a modern surgeon you stopped them at the appropriate time (> Chap. 42). Recently we conducted an audit among infection disease (ID) specialists and a group of surgeons interested in surgical infections.
We asked them the following question: a patient undergoes a laparotomy 3 hours after receiving a gunshot injury to his abdomen. At operation you find a hole in the left colon and fecal peritoneal contamination. Would you send the peritoneal fluid for culture and sensitivity?
Guess what was the response? Almost all (95%) of ID specialists would send the pure s**t for culture – as if they do not know what kind bacteria it contains!
But now you know better than they: you know that this patient had peritoneal contamination – necessitating source control, peritoneal toilet and prophylactic peri-operative antibiotics. Nothing more!
[If you want to read much more about this topic, then find a copy of the recently published book Source Control (edited by M. Schein and J. Marshall), Springer, Berlin Heidelberg New York, 2002]
“Shakiness of the hand may be some bar to the successful performance of an operation, but he of a shaky mind is hopeless.” (Sir William MacEwen, 1848–1924)
