World J. Surg. 14, 191-195, 1990

World Journal of Surgery 9 1990 by the Soci6t6

Internationale de Chirurgie

Intraabdominal Infections and Gut Origin Sepsis K a r s t e n Offenbartl, M . D . , and Stig B e n g m a r k , M.D. Intraabdominal postoperative or posttraumatic infections remain a major threat to life in spite of generation after generation of increasingly effective antimicrobial drugs indicating the importance of immunological host defense failure following major trauma or surgical complications. The spectrum of infectious postoperative or posttraumatic complications can, in part, be explained by pathogenic factors inherent to the methodology of modern surgical intensive care and techniques. This report presents a survey of the historical background as well as current concepts of the multiple systems organ failure syndrome as related to postoperative or posttraumatic intraabdominal infectious complications. The pathophysiology of nosocomial infectious complications in the intensive care unit setting is analyzed. The concept of "gut origin sepsis" is presented and possible preventive and therapeutic actions discussed. A judicious use of antimicrobial drugs on strict indications is emphasized as is the importance of increased knowledge of the interactions between the gut flora, antibiotics, and absence of enteral nutrition.

The association between acute renal failure, adult respiratory distress syndrome (ARDS), and multiple systems organ failure (MSOF) with septic surgical complications in the late 1960's and in the 1970's [1-7] has prompted many basic research studies. These studies have increased our understanding of the metabolic and inflammatory response to trauma and infection. Furthermore, we now know that viable abscess appears to be a consequence rather than a cause of uncontrolled systemic inflammatory response and multiple systems organ failure. The uncontrolled systemic inflammatory response appears to be the initiating event eventually leading to a "leaky gut," that hypothetically acts as a focus of infections. The initiating event may often be a severe blunt trauma, a technical complication of abdominal surgery, a severe intraabdominal infection, or a ruptured aortic aneurysm often associated with an initial period of unstable systemic circulation. It usually occurs 2-3 weeks following injury or the beginning of the sickness, and is sometimes referred to as the 2-3 weeks crisis. The following presentation will focus on what is currently recognized as the pathophysiology of severe septic complications following initial improvement from severe intraabdominal infections.

little or no evidence that antibiotic therapy has decreased the overall incidence of intraabdominal abscesses." The authors emphasized the importance of the surgical drainage of pus in the resolution of the disease. Earlier, Kornhall [1] presented an analysis of 298 cases of acute renal failure associated with surgical disease. He demonstrated that, in acute renal failure, the highest mortality is usually reported among the surgical cases. Furthermore, in surgical patients who present with acute renal failure, one should view this as a complication of intraabdominal abscess disease. Today, 20 years later, advances in life and organ support, diagnostic imaging, and the percutaneous drainage of abscesses has helped us to diminish the morbidity associated with intraabdominal disease; however, failure to control the focus of the sepsis still results in significant morbidity and mortality. Our own observations in major liver resections and subtotal pancreatectomies for malignancies suggest that infectious complications in spite of the uniform use of prophylactic and therapeutic antibiotics are still a major problem [9]. In 6% of presumably clean major liver resections, intraabdominal abscesses developed postoperatively while postoperative infection complicates one-third of subtotal pancreatectomies despite antibiotic prophylaxis. Once again, such data indicate the importance of host resistance factors and the impact of traumatic injury to host immune barriers as important determinants of postoperative infection. These clinical observations have been readily substantiated by experimental evidence from our laboratory demonstrating decreased host resistance factors against Escherichia coli infection in chronic biliary obstruction [10]. With time after the induction of biliary obstruction, host resistant determinants such as reticuloendothelial function (e.g., bacterial clearance from the bile and bacterial uptake per unit liver weight) have been shown to decrease significantly. The historical development of the understanding of surgeryrelated organ failure is presented in Table 1.

Historical and Current Aspects

Gut Origin Sepsis: Basic Considerations

In 1973, Altemeier and associates [8], following review of 501 cases of intraabdominal abscesses, concluded that "there is

The single most important determinant of infection is the host. Surgery and trauma break the host barriers that protect the integrity of the host tissues against potentially pathogenic microorganisms (PPM). Further changes induced by measures inherent to optimal postoperative or posttraumatic care then

Reprint requests: Stig Bengmark, M.D., Department of Surgery, Lund University, S-221 85 Lund, Sweden.


World J. Surg. Vol. 14, No. 2, Mar./Apr. 1990

Table 1. The historical development of the understanding of surgery-

related organ failure. Time period


Clinical picture

1940's-1950's 1960's

Hemorrhagic shock Trauma-hemorrhage


Sepsis, hidden infection


Systemic inflammatory response

Renal failure Pulmonary failure, ARDS (adult respiratory distress syndrome) Multiple organ failure syndrome Gut origin sepsis

Table 2. The flow scheme of a nosocomial infection.

Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7 Step 8

Damage to the host barriers, decreased colonization resistance Acquisition of a nosocomial bacterial strain Colonization of a wound or mucosal surface Invasion of deep tissues Host response to invasion = infection Systemic inflammatory response to a localized or blood-borne infection = sepsis Antibiotic treatment Superinfection with a new nosocomial microorganism resistant against the antibiotic agent of step 7

establish the foundation for colonization with nosocomial microflora and subsequent invasive infection. Man lives in a complex ecosystem largely in a symbiotic relationship with his microflora, which, under normal circumstances, work in concert with host factors in establishing a protective barrier against infection by PPM [11, 12]. A thorough presentation of this topic has been published by van Saene and coworkers [13]. These authors stressed that practically all infections arising in the intensive care setting are of a primary nosocomial and secondary endogenous origin. The microbial ecology of the intestinal tract is well-documented to be of importance for the gut barrier function. A review of the various terminology associated with nosocomial microbial invasion is outlined in Table 2. The fate of the PPM relative to the microbial ecology of the host can be described in certain well-defined steps: First, acquisition of a nosocomial PPM, e.g., in the SICU, (surgical intensive care unit) means the contamination of skin, mucosal membranes, or a wound with the organism. The next step is " p a s s a g e , " which m e a n s that the organism " t a k e s r o o t " and multiples to high concentrations. "Colonization resistance" can be defined as t h e host capacity to prevent colonization/infection with aerobic bacteria. This function is characteristic of the host and not of the microorganism. Infection is the host response to the invasion of microorganisms through skin, wound, or mucosal membranes. A "superinfection'" is an infection occurring after antibiotic treatment, usually with a multiresistant Gram-negative nosocomial bacterial strain. " S e p s i s " as a clinical term is the systemic inflammatory response of the host to an invading microorganism. This response is, thus, another entirely hostdependent function and, consequently, not dependent on the type of invading organism. The septic response is further nonspecific for microorganism invasion but should rather be

apprehended as an integral part of the metabolic response of the host to an injury. Other agents that can activate this systemic inflammatory response are, e.g., dead or injured tissue, large hematoma, and severe microcirculatory flow injury after perfusion derangements [5]. The validity of this concept is further demonstrated by the low percentage of positive blood cultures in "clinically septic" patients with multiple systems organ failure. A review of our own intensive care patients with organ failure reveals that only 15% of blood cultures are positive despite "clinical sepsis." This finding corresponds well with the syndrome of "nonbacteriemic clinical sepsis" of Meakins and the low percentage of positive blood cultures in severely traumatized patients in Border's presentation on gut origin sepsis [4, 6]. Factors Damaging the Host Barriers

In a typical surgical critical care unit, the patient is connected to numerous lines and catheters, any of which may be colonized by nosocomial or endogenous flora. Furthermore, the upper respiratory airways and the nasogastric tubes establish a communication between the upper airways and the stomach, which may allow the direct aspiration of bacteria into the lung. Wounds and drains further constitute contact between deep tissue and the microbial environments, thus favoring colonization. The diminished gastric acid production by H2-receptor antagonists or antacids prevents gastroduodenal hemorrhage. This decrease in function of the important acid " b a r r i e r " allows enhanced growth and colonization of the upper gut with microbes. Furthermore, gastric and colonic stasis resulting from intraabdominal disease or injury disrupts the normal microbial ecology of the intestinal tract. The microflora of the upper airways and intestinal tract can be altered in composition or numbers by a variety of broad spectrum antibiotics which results in a decrease in the colonization resistance of the gut [11, 13, 14]. Under these circumstances, nosocomial flora may contaminate the skin, the wounds' mucosal membranes, and the mucosal surfaces of the patient, thereby setting the stage for colonization of the intestinal tract by Gram-negative, multiresistant flora [11], Multifactorial abdominal distension together with supine position results in basal pulmonary atelectasis and the gastroesophageal reflux of the stomach contents with high concentrations of bacteria. Aspiration then results in contamination of the deep airways with troublesome Gram-negative bacteria which often leads to pneumonia. Beside changes in composition of the microflora, the intestinal tract is a target organ for a variety of other changes induced by a severe injury. An initial phase of circulatory instability and hypoperfusion is known to severely effect the integrity of the intestines, resulting in ulcerated lesion and edema [15]. Bacterial translocation over the intestinal wall can be induced experimentally by hemorrhagic shock, the combination of the burn wound and endotoxemia, malnutrition and antibiotic-induced microflora changes, and by experimentallyinduced intraabdominal abscesses [16-19]. Hepatic failure and cholestasis can reduce the excretion of bile salt immune globulin into the gut, reducing the intraluminal capacity to detoxify endotoxin and microorganisms. The systemic inflammatory response of a severe disease seriously alters the growth and

K. Offenbartl and S. Bengmark: Gut Origin Sepsis

Table 3. Gut origin sepsis: Etiological moments. Cause


Major trauma, severe illness Splanchnic ischemia Malnutrition and gut disuse Exposition to intensive care environment and systemic antibiotics Acquisition of a nosocomial microflora

Immunocompromised host

Gut mucosal damage Absorption and translocation of toxins and microorganisms

Gut mucosal ulcerations Qualitatively defective gut mucosa Decrease in colonization resistance, acquisition of a nosocomial microflora Altered gut microflora, dominance of Gram-negative aerobic rods (potentially pathogenic organisms) Absorption of microorganisms and toxins, translocation of microorganisms and toxins Hepatic injury, systemic inflammatory response, vicious circle of further gut mucosal damage

integrity of tissue such as the gut mucosa, which is dependent on rapidly dividing cells [5, 17, 20-24]. The net result of the above factors is a gastrointestinal tract which acts as a continuous source for pathogenic bacteria and toxins. These then enter the portal circulation, lymphatics, and, possibly, the peritoneal cavity and continue to fuel the systemic conditions leading to organ failure [4--6, 17]. This "gut origin sepsis" is accordingly the combined results of a wide variety of pathophysiological changes induced by disease or injury, the host response to injury, and environmental/iatrogenic factors (Table 3). Successful treatment in this late stage of disease is extremely difficult. Prevention, based on intervention of the various unknown pathogenic cofactors, must be the prime goal for the future. Prevention of Gut Origin Sepsis

The essential preventive measures against mucosal barrier deficiency of gut origin sepsis can be divided into 4 main categories: 1. Optimal resuscitation of shock and trauma victims as estimated by flow-dependent oxygen consumption. 2. Continuous and balanced metabolic support. 3. Protection of the gut mucosa against atrophy. 4. Protection of the microbial ecology of the host against colonization with a pathogenic nosocomial flora. Prolonged shock and the incomplete resuscitation of shock are frequently associated with the development of MSOF [5]. Shock, in surgical practice, is a diverse collection of lifethreatening circulatory disease conditions which can occur following many different etiological events: most commonly after hemorrhage, trauma, sepsis, and in myocardial dysfunction [25]. The central issue in the pathophysiology of shock is the altered capacity of the organisms to sustain an adequate oxygen uptake, delivery, and consumption. Tissue hypoperfusion in shock is characterized by a generalized microcirculatory blood flow maldistribution that prohibits an effective oxygen delivery to large fractions of the peripheral circulation. The ultimate goal of our resuscitative measures in shock must be to increase the oxygen delivery, by an increase in peripheral blood flow, until no further increase in oxygen consumption can be


achieved (the so-called flow dependency of oxygen consumption). There exist, today, practical devices for measuring oxygen consumption as related to cardiac output in SICU patients. Monitoring with such equipment has proven to be superior to the regularly used clinical criteria for determining optimal perfusion [26--28]. The wide adaption of such methodology may provide promising progress in future critical care delivery. Until then, surgeons, anesthesiologists, and intensive care physicians must be aware of the relationship between subclinical hypoperfusion and subsequent development of sepsis/organ failure. A large amount of our current knowledge concerning the relationships between malnutrition, metabolic support, and organ failure/sepsis complex emanates from the impressive clinical and laboratory research efforts conducted by Border, Cerra, and Siegel. Current concepts on this subject have recently been reviewed by Cerra [5] and further clinical support for the relationship between blunt trauma, protein malnutrition, and gut origin sepsis was presented by Border and coworkers [6]. A more detailed review of this subject is beyond the scope of the present discussion. The current concepts may, however, be summarized as follows: 1. Enteral nutrition should be the preferred route of administration. Whole proteins should be preferred over amino acids. 2. The primary goal of the surgical care delivered must be aimed at facilitation of enteral nutrition as early as possible. 3. Emphasis must be put on protein synthesis in order to preserve organ structures and functions. Protein support should preferably reach levels of 3 g/kg body weight per day. 4. The metabolic support should be balanced, with mixed fuel, (i.e., 30-40% of nonprotein calories as fat). 5. The results of the metabolic support should be individualized, preferably by measuring resting energy expenditure and the respiratory quotient at bedside. The gut is, together with skeletal muscle and the connective tissues, a pool of mobile amino acids that can be mobilized after injury. Nutritional depletion and the absence of enteral nutrition is further associated with morphological and microbiological changes in the gut. In order to protect the gut mucosa against atrophy, the injured patient must receive an optimal metabolic support, preferably enterally, according to the above presented guidelines. The last preventive measure to be discussed is how to prevent the pathogenic nosocomial flora from colonizing and subsequently infecting the susceptible surgical patient. The ultimate goal of this prevention is to strengthen the colonization resistance of the gut microflora. Such prevention can be achieved by early mobilization of the postoperative or trauma patient, enteral nutrition instead of or adjunct to parenteral nutritional support, and the judicious use of antibiotics. In multitrauma patients, there exist considerable data which suggest that early surgery for stabilization of fractures is preferred over delayed operation in terms of reduced posttraumatic infectious complications [6, 29, 30]. The early surgery approach reduces the number of ventilator days and also the time period of exposure to the nosocomial microbial environment. The van Saene group from Groningen has proposed that patients exposed to the SICU undergo a selective decontami-


nation of the intestine. This technique, which eradicates the potentially pathogenic facultative Gram-negative bacteria and fungi, requires continuous use of nonabsorbable antibiotics for local decontamination of oropharynx, intestines, and wounds starting on the arrival of the patient in the SICU. In addition, the patients receive a short course of systemic cephotaxim treatment in order to eradicate community-acquired pathogenic microorganisms. Through this technique, the authors succeeded in reducing the nosocomial infection rates from 80% to 15% [11, 13, 31]. The success of selective decontamination indicates the importance of a normal gut flora as a resistance factor in the severely sick patient. The use of antibiotic combinations to control nosocomial flora did not induce any problems with acquired resistant pathogens in the hands of the Groningen group. From a historic point of view, however, the widespread use of potent antimicrobials always led to the emergence of nosocomial infectious problems. F o r the future, we would like to propose a more "biological" approach toward maintaining the colonization resistance of the gut flora. One mainstay for such an approach is enteral nutrition. Another possible way would be to administer " p r o t e c t i v e " anaerobic bacteria to patients during and after antibiotic therapy. In December, 1987, Gorbach and associates [32] presented observations on successful treatment of relapsing Clostridium difficile colitis with lactobacilli. We have employed a similar approach in 3 patients in the SICU with presumed severe gut origin sepsis. The patients, all of whom had severe complications following abdominal surgery and persistent sepsis in spite of long-term systemic antibiotic treatment, received large doses of lactobacilli enterally 1-2 days after antibiotics were discontinued. All 3 patients recovered from their complications eventually and were discharged from the hospital. These findings require further investigation; however, the results appear encouraging. Furthermore, laboratory investigations are necessary to evaluate the role of " p r o t e c t i v e " gut microflora in experimental sepsis. Finally, it is important to study the impact of antimicrobials on the microbial ecology of one patient and to learn how to administer antibiotics in such a way that colonization resistance of the normal microflora is maintained [12, 33]. This may be of minor importance in the majority of regular, noncomplicated surgical patients, but a major factor for decreased morbidity in a substantial proportion of those patients in our intensive care facilities. R6sum6

Les infections intra-abdominales postoprratoires ou post-traumatiques continuent de menacer le pronostic vital malgr6 une am61ioration constante des antibiotiques ce qui met l'accent sur l'6chec des moyens de d6fense immunologiques a p r r s les traumatismes majeurs ou les complications chirurgicales. Le spectre des complications infectieuses postop6ratoires ou posttraumatiques peut, en partie, 6tre expliqu6 par des facteurs pathogrniques inh6rents h la mrthode des soins intensifs et techniques modernes. Ce travail pr6sente l'historique et les concepts actuels de d6faillance polyviscrrale en rapport avec des complications infectieuses intra-abdominales postoprratoires ou post-traumatiques. La pathophysiologie des complications infectieuses nosocomiales dans l'unit6 des soins inten-

World J. Surg. Vol. 14, No. 2, Mar./Apr. 1990

sifs est analys6e. L a conception de sepsis "d'origine intestinale" est pr6sent6e et les actions prrventive et thrrapeutique sont discutres. L'utilisation judicieuse des antibiotiques est soulign6e, ainsi que les interactions entre la flore intestinale, les antibiotiques et l'absence de nutrition ent6rale. Resumen

Las infecciones intraabdominales postoperatorias o postraum~iticas siguen representando una amenaza grave para la vida a pesar de generaci6n tras generaci6n de drogas antimicrobianas de creciente efectividad, lo cual sefiala la importancia de la falla de los mecanismos inmunes de defensa del hursped que se presenta despu6s de trauma mayor o acompafiando las complicaciones quirtirgicas. E1 espectro de las complicaciones infecciosas postoperatorias o postraumfiticas puede ser explicado en parte por factores patog6nicos inherentes a la tecnologia y metodologia del moderno cuidado intensivo del paciente en estado crftico. E1 presente informe reporta una revisi6n de los antecedentes hist6ricos y de los conceptos actuales sobre el sindrome de falla org~inica multisist6mica relacionado con complicaciones infecciosas intraabdominales postoperatorias o postraumfiticas. Se analiza la patofisiologfa de las complicaciones infecciosas nosocomiales en el marco de la unidad de cuidado intensivo. Se hace 6nfasis sobre el uso juicioso de drogas antimicrobianas segt~n indicaciones estrictas, asi como sobre la importancia de un mayor conocimiento sobre las interacciones entre la flora intestinal, los antibi6ticos, y la ausencia de nutrici6n enteral. References

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Intraabdominal infections and gut origin sepsis.

Intraabdominal postoperative or posttraumatic infections remain a major threat to life in spite of generation after generation of increasingly effecti...
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