abdominal abscess

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INTRODUCTION Infection is defined by identification of microorganisms in host tissue or the bloodstream, plus an inflammatory response to their presence. Abscess is a confined surgical infection surrounded by a pyogenic membrane. Intra-abdominal abscess continues to be an important and serious problem in surgical practice. Appropriate treatment is often delayed because of the obscure nature of many conditions resulting in abscess formation, which can make diagnosis and localization difficult. The associated pathophysiologic effects may become life threatening or lead to extended periods of morbidity with prolonged hospitalization. Delayed diagnosis and treatment of this condition can also lead to increased mortality rates; therefore, the economic impact of delaying treatment is significant. HISTORY The first intra-abdominal operation to treat infection via "source control" (i.e., surgical intervention to eliminate the source of infection) was appendectomy. This operation was pioneered by Charles McBurney at the New York College of Physicians and Surgeons, among others. McBurney's classic report on early operative intervention for appendicitis was presented before the New York Surgical Society in 1889. Appendectomy for the treatment of appendicitis, previously an often fatal disease, was popularized after the 1902 coronation of King Edward VII of England was delayed due to his need for an appendectomy, which was performed by Sir Frederick Treves. The king desperately needed an appendectomy but strongly opposed going into the hospital, protesting, "I have a coronation on hand." However, Treves was adamant, stating, "It will be a funeral, if you don't have the operation." Treves carried the debate, and the king lived. Concurrent with the development of numerous antimicrobial agents were advances in the field of clinical microbiology. Sir Alexander Fleming, after serving in the British Army Medical Corps during World War I, continued work on the natural antibacterial action of the blood and antiseptics. In 1928, while studying influenza virus, he noted a zone of inhibition around a mold colony (Penicillium notatum) that serendipitously grew on a plate of Staphylococcus, and he named the

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Page 1: abdominal abscess

INTRODUCTION

Infection is defined by identification of microorganisms in host tissue or the bloodstream, plus an inflammatory response to their presence. Abscess is a confined surgical infection surrounded by a pyogenic membrane. Intra-abdominal abscess continues to be an important and serious problem in surgical practice. Appropriate treatment is often delayed because of the obscure nature of many conditions resulting in abscess formation, which can make diagnosis and localization difficult. The associated pathophysiologic effects may become life threatening or lead to extended periods of morbidity with prolonged hospitalization. Delayed diagnosis and treatment of this condition can also lead to increased mortality rates; therefore, the economic impact of delaying treatment is significant.

HISTORY

The first intra-abdominal operation to treat infection via "source control" (i.e., surgical intervention to eliminate the source of infection) was appendectomy. This operation was pioneered by Charles McBurney at the New York College of Physicians and Surgeons, among others. McBurney's classic report on early operative intervention for appendicitis was presented before the New York Surgical Society in 1889. Appendectomy for the treatment of appendicitis, previously an often fatal disease, was popularized after the 1902 coronation of King Edward VII of England was delayed due to his need for an appendectomy, which was performed by Sir Frederick Treves. The king desperately needed an appendectomy but strongly opposed going into the hospital, protesting, "I have a coronation on hand." However, Treves was adamant, stating, "It will be a funeral, if you don't have the operation." Treves carried the debate, and the king lived.

Concurrent with the development of numerous antimicrobial agents were advances in the field of clinical microbiology. Sir Alexander Fleming, after serving in the British Army Medical Corps during World War I, continued work on the natural antibacterial action of the blood and antiseptics. In 1928, while studying influenza virus, he noted a zone of inhibition around a mold colony (Penicillium notatum) that serendipitously grew on a plate of Staphylococcus, and he named the active substance penicillin. This first effective antibacterial agent subsequently led to the development of hundreds of potent antimicrobials, set the stage for their use as prophylaxis against postoperative infection, and became a critical component of the armamentarium to treat aggressive, lethal surgical infections.

The concepts that resident microbes were nonpathogenic until they entered a sterile body cavity at the time of surgery, and that many, if not most, surgical infections were polymicrobial in nature, became critical ideas and were promulgated by a number of clinician-scientists over the last several decades.6,7 These tenets became firmly established after microbiology laboratories demonstrated the invariable presence of aerobes and anaerobes in peritoneal cultures obtained at the time of surgery for intra-abdominal infection due to a perforated viscus or gangrenous appendicitis.

William Osler, a prolific writer and one of the fathers of American medicine, made an observation in 1904 in his treatise The Evolution of Modern Medicine that was to have profound implications for the future of treatment of infection: "Except on few occasions, the patient appears to die from the body's response to infection rather than from it.” Expanding knowledge of the multiple pathways activated

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during the response to invasion by infectious organisms has permitted the design of new therapies targeted at modifying the inflammatory response to infection, which seems to cause much of the end-organ dysfunction and failure. Preventing and treating this process of multiple organ failure during infection is one of the major challenges of modern critical care and surgical infectious disease.

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ANATOMY

A thorough understanding of peritoneal anatomy is required to understand the typical areas of abscess formation. The peritoneum is the largest serous membrane in the body, and its arrangements are complex. In males it forms a closed sac, but in females it is open at the lateral ends of the uterine tubes. It consists of a single layer of flat mesothelial cells lying on a layer of loose connective tissue. The mesothelium usually forms a continuous surface, but in some areas may be fenestrated. The submesothelial connective tissue may also contain macrophages, lymphocytes and adipocytes (in some regions). Lymphocytes provide both cellular and humoral immunological defence mechanisms within the peritoneal cavity.

The intraperitoneal fluid is directed by gravity to dependent sites within the peritoneal cavity, and also flows in a cephalad direction as a consequence of the negative upper intra-abdominal pressures which are generated by respiration.

In utero, the alimentary tract develops as a single tube suspended in the coelomic cavity by ventral and dorsal mesenteries. Ultimately, the ventral mesentery is largely resorbed, although some parts persist in the upper abdomen and form structures such as the falciform ligament. The mesenteries of the intestines in the adult are the remnants of the dorsal mesentery.

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For clinical purposes the peritoneal cavity can be divided into several spaces because pathological processes are often contained within these spaces and their anatomy may influence diagnosis and treatment. It is useful to divide the peritoneal cavity into two main compartments, supramesocolic and inframesocolic .

Right subphrenic space - It lies between the diaphragm and the anterior, superior and right lateral surfaces of the right lobe of the liver. It is bounded on the left side by the falciform ligament and behind by the upper layer of the coronary ligament. It is a relatively common site for collections of fluid after right sided abdominal inflammation.

Right subhepatic space(hepatorenal recess) – It lies between the right lobe of the liver and the right kidney. It is bounded superiorly by the inferior layer of the coronary ligament, laterally by the right lateral abdominal wall, posteriorly by the anterior surface of the upper pole of the right kidney and medially by the second part of the duodenum, hepatic flexure, transverse mesocolon and part of the head of the pancreas. In the supine position the posterior right subhepatic space is more dependent than the right paracolic gutter: postoperative infected fluid collections are common in this location.

Lesser sac(Omental bursa) - The lesser sac is a space that lies posterior to the stomach and gastrohepatic ligament. Superiorly lies the caudate lobe of the liver, and inferiorly the transverse mesocolon. The lesser sac communicates with the greater sac through the foramen of Winslow.

Left subphrenic space - It lies between the diaphragm, the anterior and superior surfaces of the left lobe of the liver, the anterosuperior surface of the stomach and the diaphragmatic surface of the spleen. It is the commonest site of fluid collection after upper abdominal, particularly splenic, surgery.

Left perihepatic space - It is sometimes subdivided into anterior and posterior spaces. The posterior perihepatic space is also known as the left subhepatic space or gastrohepatic recess. The left anterior perihepatic space lies between the anterosuperior surface of the left lobe of the liver and diaphragm.

Inframesocolic compartment - It lies below the transverse mesocolon and transverse colon as far as the true pelvis. It is divided in two unequal spaces by the root of the mesentery of the small intestine. It contains the right and left paracolic gutters lateral to the ascending and descending colon. As a consequence of the mobility of the transverse mesocolon and mesentery of the small intestine, disease

Supramesocolic compt.

Rt. supramesocolic

Rt. Subphrenic Rt. Subhepatic Lesser sac

Lt. supramesocolic

Lt. Subphrenic Lt. perihepatic

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processes are rarely well contained within these spaces, and fluid within the infracolic space tends to descend into the pelvis or the paracolic gutters.

Extraperitoneal subphrenic spaces - There are two potential ‘spaces' which actually lie outside the peritoneal coverings of the abdomen, but are of clinical relevance because of the possibility that fluid collections will accumulate in them. The right extraperitoneal space is bounded by the two layers of the coronary ligament, the bare area of the liver and the inferior surface of the right dome of the diaphragm. The left extraperitoneal space lies anterior to the left suprarenal gland and upper pole of the left kidney. It contains extraperitoneal connective tissue.

Any of the spaces of the peritoneum may develop a collection, but the subphrenic, subhepatic and pelvic spaces are the commonest since they are most well defined by the fixed peritoneal folds and organs forming their boundaries. These spaces are also the most dependent spaces within the peritoneum in the supine position and consequently any initially free fluid tends to gravitate to them.

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ETIOLOGY

Intraperitoneal infections generally arise because a normal anatomic barrier is disrupted. This disruption may occur when the appendix, a diverticulum, or an ulcer ruptures; when the bowel wall is weakened by ischemia, tumor, or inflammation (e.g., in inflammatory bowel disease); or with adjacent inflammatory processes, such as pancreatitis or pelvic inflammatory disease, in which enzymes (in the former case) or organisms (in the latter) may leak into the peritoneal cavity.

Pathogens isolated from 900 patients with intra-abdominal infectionsAerobic bacteria % Obligate anaerobic bacteria %Escherichia coli 51 Bacteroides, unspecified 72Proteus spp. 16 Fusobacteria   7Klebsiella spp. 14 Veillonella   2Enterobacter spp.   6Pseudomonas spp.   7 Propionibacteria   5Streptococci 12 Clostridia 23Staphylococci   5 Peptostreptococci 21Enterococci 17Other   8 Other 21

Data from: Wittmann DH. Intra-abdominal infection: pathophysiology and treatment. Marcel Dekker, New York.

RISK FACTORS

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These risk factors may be related to the patient's capacity to defend against an infectious threat, the infectious challenge itself as represented by the number and pathogenicity of the bacteria, the extent of any associated injury, and environmental factors such as the hospital bacterial flora.

Patient factors

  ─Older age

  ─Immunosuppression

  ─Obesity

  ─Diabetes mellitus

  ─Chronic inflammatory process

  ─Malnutrition

 ─Peripheral vascular disease

  ─Anemia

  ─Radiation

  ─Chronic skin disease

  ─Carrier state (e.g., chronic Staphylococcus carriage) 

  ─Recent operation

Local factors

  ─Poor skin preparation

  ─Contamination of instruments

  ─Inadequate antibiotic prophylaxis

  ─Prolonged procedure

  ─Local tissue necrosis

  ─Hypoxia, hypothermia

Microbial factors

  ─Prolonged hospitalization (leading to nosocomial organisms)

  ─Toxin secretion

  ─Resistance to clearance (e.g., capsule formation)Improper preoperative management is an organizational problem including failure to give a preoperative bath with antiseptic soaps or solutions, and shaving of the operative site the night before operation.

PATHOPHYSIOLOGY

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Abdominal abscesses have been classically divided into three categories: intraperitoneal, retroperitoneal, and visceral. Intraperitoneal abscesses generally develop one of two ways. The first is a result of diffuse peritonitis in which loculations of purulent material form in the most dependent areas. The second mode of formation is due to a contiguous disease process or injury in which the host defenses adequately prevented diffuse peritonitis and walled off the process.

Retroperitoneal abscesses form in the potential space between the peritoneum and the transversalis fascia lining the posterior aspect of the abdominal cavity.

Visceral abscesses develop within the confines of one of the abdominal viscera such as the liver, pancreas, or gallbladder. These abscesses typically form as a result of hematogenous or lymphatic seeding from various sites, or in the case of the gallbladder, infectious cholecystitis.

The relatively low-oxygen, static environment of the colon is accompanied by the exponential growth of microbes that comprise the most extensive host endogenous microflora. Anaerobic microbes outnumber aerobic species approximately 100:1 in the distal colorectum, and approximately 1011 to 1012

CFU/g are present in feces. Large numbers of facultative and strict anaerobes (Bacteroides fragilis,distasonis, and thetaiotaomicron,Bifidobacterium, Clostridium,Eubacterium, Fusobacterium, Lactobacillus, and Peptostreptococcus species) as well as several orders of magnitude fewer aerobic microbes (Escherichia coli and other Enterobacteriaceae, Enterococcus faecalis and faecium, Candida albicans and other Candida spp.) are present. It is of great interest that only some of these microbial species predominate in established intra-abdominal infection.

Initially, several primitive and relatively nonspecific host defenses act to contain the nidus of infection, which may include microbes as well as debris, devitalized tissue, and foreign bodies, depending on the nature of the injury. These defenses include the physical barrier of the tissue itself, as well as the capacity of proteins such as lactoferrin and transferrin to sequester the critical microbial growth factor iron, thereby limiting microbial growth. In addition, fibrinogen within the inflammatory fluid has the ability to trap large numbers of microbes during the process in which it polymerizes into fibrin. Within the peritoneal cavity, unique host defenses exist, including a diaphragmatic pumping mechanism whereby particles including microbes within peritoneal fluid are expunged from the abdominal cavity via specialized structures on the undersurface of the diaphragm. Concurrently, containment by the omentum, the so-called "gatekeeper" of the abdomen and intestinal ileus, serves to wall off infection. However, the latter processes and fibrin trapping have a high likelihood of contributing to the formation of an intra-abdominal abscess.

Microbes also immediately encounter a series of host defense mechanisms that include resident macrophages and low levels of complement (C) proteins and immunoglobulins (Ig, antibodies).

Resident macrophages secrete a wide array of substances in response to the above-mentioned processes, some of which appear to regulate the cellular components of the host defense response. Macrophage cytokine synthesis is upregulated. Secretion of tumor necrosis factor-α (TNF-α), of interleukins (IL)-1β, 6, and 8; and of interferon-γ (INF-γ) occurs within the tissue milieu, and, depending on the magnitude of the host defense response, the systemic circulation. Concurrently, a

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counterregulatory response is initiated consisting of binding proteins (TNF-BP), cytokine receptor antagonists (IL-1ra), and anti-inflammatory cytokines (IL-4 and IL-10). The interaction of microbes with these first-line host defenses leads to microbial opsonization (C1q, C3bi, and IgFc), phagocytosis, and both extracellular (C5b6-9 membrane attack complex) and intracellular microbial destruction (phagocytic vacuoles). Concurrently, the classical and alternate complement pathways are activated both via direct contact with and via IgM>IgG binding to microbes, leading to the release of a number of different complement protein fragments (C3a, C4a, C5a) that are biologically active, acting to markedly enhance vascular permeability. Bacterial cell wall components and a variety of enzymes that are expelled from leukocyte phagocytic vacuoles during microbial phagocytosis and killing act in this capacity as well.

Simultaneously, the release of substances to which polymorphonuclear leukocytes (PMNs) in the bloodstream are attracted takes place. These consist of C5a, microbial cell wall peptides containing N-formyl-methionine, and macrophage secretion of cytokines such as IL-8. This process of host defense recruitment leads to further influx of inflammatory fluid into the area of incipient infection, and is accompanied by diapedesis of large numbers of PMNs, a process that begins within several minutes and may peak within hours or days.

The magnitude of the response and eventual outcome generally are related to several factors: (1) the initial number of microbes, (2) the rate of microbial proliferation in relation to containment and killing by host defenses, (3) microbial virulence, and (4) the potency of host defenses.

HISTORY & EXAMINATION

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In surgical practice, extravisceral abscesses form following failed anastomoses, infection of intraperitoneal fluid collections following abdominal surgery, contained leakage from a spontaneous visceral perforation, or residual loculations following diffuse peritonitis.

High spiking fevers, chills, abdominal pain, anorexia, and delay of return of bowel function in the postoperative patient are typical presenting signs and symptoms of intraperitoneal abscess.

Subphrenic abscesses can present with vague upper quadrant abdominal pain, referred shoulder pain, and occasionally hiccoughs. Typically, paracolic and interloop abscesses present with localized tenderness and may manifest as a palpable mass on abdominal examination. Abscesses may also cause local irritation of the urinary bladder causing frequency, or of the rectum resulting in diarrhea and tenesmus.

Criteria for Systemic Inflammatory Response Syndrome (SIRS)

General variables

Fever (core temp >38.3°C)

Hypothermia (core temp <36°C)

Heart rate >90 bpm

Tachypnea

Altered mental status

Significant edema or positive fluid balance (>20 mL/kg over 24 hours)

Hyperglycemia in the absence of diabetes

Inflammatory variables

Leukocytosis (WBC >12,000)

Leukopenia (WBC <4000)

Bandemia (>10% band forms)

Plasma C-reactive protein >2 s.d. above normal value

Plasma procalcitonin >2 s.d. above normal value

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Hemodynamic variables

Arterial hypotension (SBP <90 mm Hg, MAP <70, or SBP decrease >40 mm Hg)

SvO2 >70%

Cardiac index >3.5 L/min per square meter

Organ dysfunction variables

Arterial hypoxemia

Acute oliguria

Creatinine increase

Coagulation abnormalities

Ileus

Thrombocytopenia

Hyperbilirubinemia

Tissue perfusion variables

Hyperlactatemia

Decreased capillary filling

bpm = beats per minute; MAP = mean arterial pressure; SBP = systolic blood pressure; s.d. = standard deviations; SvO2 = venous oxygen saturation; WBC = white blood cell count.

Systemic Inlammatory Response Syndrome (SIRS) - Two or more of the following conditions: (1) fever (oral temperature >38°C) or hypothermia (<36°C); (2) tachypnea (>24 breaths/min); (3) tachycardia (heart rate >90 beats/min); (4) leukocytosis (>12,000/µL), leukopenia (<4,000/µL), or >10% bands; may have a noninfectious etiology.

Sepsis - SIRS that has a proven or suspected microbial etiology.

Severe sepsis - Sepsis with one or more signs of organ dysfunction—for example:

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1. Cardiovascular: Arterial systolic blood pressure ≤90 mmHg or mean arterial pressure ≤70 mmHg that responds to administration of intravenous fluid

2. Renal: Urine output <0.5 mL/kg per hour for 1 h despite adequate fluid resuscitation

3. Respiratory: PaO2/FIO2 ≤250 or, if the lung is the only dysfunctional organ, ≤200

4. Hematologic: Platelet count <80,000/µL or 50% decrease in platelet count from highest value recorded over previous 3 days

5. Unexplained metabolic acidosis: A pH ≤7.30 or a base deficit ≥5.0 mEq/L and a plasma lactate level >1.5 times upper limit of normal for reporting lab

6. Adequate fluid resuscitation: Pulmonary artery wedge pressure ≥12 mmHg or central venous pressure ≥8 mmHg.

The PIRO Staging System stratifies patients based on their predisposing conditions (P), the nature and extent of the infection (I), the nature and magnitude of the host response (R), and the degree of concomitant organ dysfunction (O). Two patients, both in the intensive care unit (ICU), who develop criteria consistent with septic shock. While both have infection and sepsis-associated hypotension, one might expect a different outcome in a young, healthy patient who develops urosepsis than in an elderly, immunosuppressed lung transplant recipient who develops invasive fungal infection.

Clinical trials evaluating the utility of this scoring system for prognostication and for examination of the impact of adjuvant therapies are underway.

INVESTIGATIONS

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Abdominal plain films can be helpful in identifying air-fluid levels in the upright or decubitus positions, extraluminal gas, or a soft tissue mass displacing the bowel. Chest radiographs may help to differentiate subphrenic from pleural fluid collections.

The initial use of ultrasound in the diagnosis of intra-abdominal fluid collections was found to have several advantages and disadvantages. The accuracy of ultrasound in the diagnosis of intra-abdominal abscesses was found to be 97% with a sensitivity of 93% and a specificity of 99%. Ultrasonography allows for a rapid and complete examination of the abdomen, even in extremely ill patients. When one considers the cost of ultrasound, it remains an important tool. In addition, it usually does not require transportation of a critically ill patient, as it can be performed at the bedside, an important consideration.

The utility of ultrasound, however, is dependent on the skills and experience of the operator. These are several limitations to the utility of ultrasound. First, in regions other than the pelvis, the right upper quadrant, and the left upper quadrant when the spleen is present, optimal imaging is difficult to achieve

Second, in patients with an ileus, a situation that is not uncommon with an intra-abdominal abscess, imaging is distorted by bowel gas. Other common issues in surgical patients that can impede ultrasound include staples, wound dressings, and stomas. Next, it was found that the ultrasonic characteristics of abscesses and hematomas overlapped. Furthermore, the nature of the fluid as determined by ultrasound could only occasionally help determine the composition of the fluid collection.

Computed tomography (CT) scanning has rapidly emerged as an accurate and frequently used modality in this disease process. Detection of 97% of abdominal abscesses has been reported. Criteria for identification of an abscess have been well described and include identification of an area of low CT attenuation in an extraluminal location or within the parenchyma of solid abdominal organs. The density of abscesses usually falls between that of water and solid tissue. Other radiological signs of an abscess are mass effect that replaces or displaces normal anatomic structures, a lucent center that is not enhanced after the intravenous administration of a contrast medium, enhancing rim around the lucent center after contrast administration, and gas in the fluid collection. One of the major advantages of CT over ultrasound is the ability to detect abscesses in the retroperitoneum and pancreatic area.

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There are some disadvantages to CT scanning. Occasionally, there may be a solid-appearing collection that is really an abscess with a high leukocyte and protein content. Also, necrotic tumor and tissue can occasionally demonstrate intracavitary gas and not be infected. Next, septations and other signs of loculated abscesses can be seen much better with ultrasound than CT. Finally, CT scanning is sometimes unable to differentiate between subphrenic and pulmonic fluid, a relatively common situation in abdominal surgery.

TREATMENT

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The initial management of a patient with an intra-abdominal abscess includes preparation for potential operative or percutaneous management as well as initiating antibiotic therapy. Initially, antibiotic coverage should be broad with coverage for enteric aerobes and anaerobes. Following successful drainage of the abscess, however, one should quickly tailor the antibiotics to culture results. Depending on the clinical status of the patient, early discontinuation of antibiotic therapy should be considered if adequate drainage is achieved. Aggressive fluid resuscitation is appropriate for most patients, and correction of acid-base and electrolyte abnormalities should be undertaken. If the leukocyte count is elevated, standard evaluation should also include blood culture, urinalysis and urine culture, assessment of central venous catheter status, and routine chest imaging. The physician should also anticipate an ileus and the need for an alternative source of nutrition such as parenteral nutrition. Nasogastric tube placement is warranted if nausea and vomiting are present.

Percutaneous drainage - Percutaneous drainage of abscesses has become an established technique and a safe alternative to surgery. Advantages of percutaneous techniques include avoidance of general anesthesia, lower costs, and the potential for fewer complications. Prerequisites for catheter drainage include an anatomically safe route to the abscess, a well-defined unilocular abscess cavity, concurring surgical and radiologic evaluation, and senior surgical back-up for technical failure. Contraindications to catheter drainage include absence of appropriate access routes, internal septations and loculations, and presence of a coagulopathy.8 Multiple abscesses, abscesses with enteric connections as seen with enterocutaneous fistulas, and the need to traverse solid viscera are not contraindications.It is unclear whether percutaneous drainage is best done with ultrasound or CT guidance. CT provides for more precise identification of organs and bowel loops and is more accurate for planning of drainage route.8 Once the abscess is identified, initial diagnostic aspiration should be sent for Gram's stain and microbiological culture. Most commonly used catheters range in size from 8.0–12.0F. With appropriate catheter placement, the abscess cavity typically decompresses and collapses. Irrigation of the catheter should be done once daily to ensure tube patency. As catheter drainage decreases, repeat CT scanning can be performed to evaluate for residual contents. If drainage increases over time or continues at a steady rate, the development of an enteric fistula must be suspected. Potential complications of catheter placement include bacteremia, sepsis, vascular injury, enteric puncture, cutaneous fistula, or transpleural catheter placement.Studies comparing outcomes of surgical and percutaneous drainage of intra-abdominal abscesses demonstrate that both methods have similar results. There were no differences between percutaneous and surgical drainage in patient morbidity, mortality, or duration of hospital stay1.

Surgical drainage - Surgical drainage is the preferred method of management of ill-defined abscesses, fungal abscesses, infected hematomas, necrotic tumor masses, and interloop abscesses. Open surgical drainage can be used for situations in which percutaneous techniques are unlikely to be successful or following failed attempts at minimally-invasive drainage.The transperitoneal approach allows for examination of the entire abdominal cavity and allows for the drainage of multiple abscesses. Subphrenic abscesses and right subhepatic abscesses

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may be approached by lateral abdominal incisions. After the patient has been adequately hydrated and appropriate antibiotics have been given, an incision is made and meticulous attention is paid to protecting the wound with antibiotic-soaked sponges (or if large enough, antibiotic-soaked wound towels which are sewn in) to help prevent postoperative wound issues. Once abscess cavities are identified, they are entered and drained quickly to minimize spillage and contamination of the rest of the peritoneal cavity. The abscess cavity then should be widely opened. Specimens should be sent for Gram's stain and culture. In the case of resistant abscesses, a biopsy of the abscess cavity can be sent to pathology for further evaluation. Copious warm antibiotic irrigation must be used at the end of the operation to properly cleanse the abdominal cavity. Closed suction drains should be placed in dependent positions to reduce the risk of reaccumulation. In extremely contaminated cases, the incision may be left open and packed to prevent wound infection. However, there is little to be lost by a subcuticular closure after antibiotic irrigation of the abscess cavity and the wound, with a closed suction drain placed subcutaneously. Drains should be kept in for at least 10 days, as suppuration occurs late.

Laparoscopic drainage – laparoscopic drainage of certain abscesses may be an alternative to open surgical drainage. Advantages include decreased morbidity compared with large laparotomy wounds, as well as faster postoperative recovery and shorter hospital stay. Studies have shown this method of abscess drainage to be effective in the treatment of liver, appendiceal, tubo-ovarian and pelvic abscesses.2

Postoperatively, antibiotics should be tailored to culture results and parenteral nutrition should be started if required. Since ileus is not uncommon in these patients, caloric requirements via the enteric route can be difficult to achieve. However, if possible, trophic tube feeds should be initiated to prevent atrophy of intestinal villi. It is extremely important to prevent the drains from becoming obstructed. Routine flushing with normal saline or antibiotic solution may be required.

Formerly, the presence of an intra-abdominal abscess mandated surgical reexploration and drainage. Today, the vast majority of such abscesses can be effectively diagnosed via abdominal computed tomographic (CT) imaging techniques and drained percutaneously. Surgical intervention is reserved for those with abscesses in proximity to vital structures such that percutaneous drainage would be hazardous, and those in whom an ongoing source of contamination (e.g., enteric leak) is identified. The necessity of antimicrobial agent therapy and precise guidelines that dictate duration of catheter drainage have not been established. A short course (3 to 7 days) of antibiotics that possess aerobic and anaerobic activity seems reasonable, and most practitioners leave the drainage catheter in situ until it is clear that cavity collapse has occurred, output is less than 10 to 20 mL/d, no evidence of an ongoing source of contamination is present, and the patient's clinical condition has improved.

PREVENTION

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Infections can be minimized if wound management follows these principles.

1. Tissue should be handled gently, and operative trauma kept at a minimum.

2. Further contamination should be minimized by use of aseptic techniques.

3. Devitalized tissue, debris, and traumatic foreign bodies should be removed.

4. Complete hemostasis should be achieved.

5. Blood supply is essential for healing and should not be impaired.

6. Formation of dead space should be avoided during closure.

7. The wound should be closed by layer-to-layer approximation without tension.

8. Operative time should be kept to a minimum to reduce the numbers of bacteria entering the wound.

9. The wound may be irrigated with liberal amounts of sterile saline/Ringer's lactate solution prior to closure.

Resistance of the host to infection is intimately involved with the magnitude of trauma and the early inflammatory response. Three primary factors interact in infection:

1. the extent of tissue injury;

2. the inoculum (quantity) and toxic products (quality) of infecting micro-organisms;

3. the host's defense capacity.

When therapy must be started empirically it should be calculated and targeted at the most likely pathogens and the following points should be considered:

1. the spectrum of pathogens known to be typical;

2. the pathogenicity, synergism, and antagonism exhibited by bacteria in various mixed infections;

3. the concentration of antibiotic that can be achieved at the site of infection;

4. the side-effects of antimicrobials;

5. the negative interaction of antibiotics with host defense mechanisms;

6. the results of well-controlled clinical studies of unselected patients.

Antibiotics that reliably kill bacteria should be given preference, such as penicillin for infections by group A streptococci or clostridia and no penicillins, or extended-spectrum penicillins with and without b-lactamase inhibitors, against E. coli and Klebsiella.

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RECENT ADVANCES

Local administration of a high dose of APC by peritoneal lavage is an effective therapeutic strategy in polymicrobial peritonitis, to rebalance coagulation and fibrinolysis without raising the risk of severe bleeding.3

BIBLIOGRAPHY

1. Hemming A, Davis NL, Robins RE. Surgical versus percutaneous drainage of intra-abdominal abscesses. Am J Surg 1991;161:593 [PubMed: 2031543]

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2.3. Suzanne Q. van veen, Marcel Levi, Arlene K. van Vliet. Peritoneal lavage with activated protein C

alters compartmentalized coagulation and fibrinolysis and improves survival in polymicrobial peritonitis. Crit Care Med 2006 Vol. 34, No. 11, 2799-2805.