Surgical Infections and Antibiotic Use

Surgical infections encompass a wide-ranging group of diseases, which account for a large burden of mortality and morbidity worldwide. Surgical infections include de novo infectious diseases that require surgery or procedural interventions for cure; common examples include abscesses, intraabdominal infections such as cholangitis and appendicitis, and necrotizing soft tissue infections (NSTIs), all of which are dealt with in detail in this chapter. Another major type of surgical infection is surgical site infections (SSIs)—infections occurring at the site within 30 days of a surgical procedure. SSIs account for 20% of health care–acquired infections and result in significant morbidity and hospital costs.

Surgical infections may lead to sepsis, a life-threatening organ dysfunction due to a dysregulated host response to infection. Sepsis is the leading cause of in-hospital mortality in the United States. Sepsis is estimated to affect 30 million people worldwide each year, although this is likely an underestimate given the paucity of data from low- and middle-income countries. Early and effective source control is important for the successful treatment of sepsis. This requires that the physician recognize when the source of infection is amenable to a surgical cure and effects this without delay in conjunction with other treatments such as fluid resuscitation and antibiotics. The Surviving Sepsis Campaign (SSC) provides expert consensus on guidelines for the treatment of sepsis, which should be familiar to all surgeons treating patients with infection.

Surgical Site Infections

SSIs are the most common and costly of all hospital-acquired infections, accounting for 20% of all hospital infections. It is associated with increased length of stay and a twofold to eleven fold increase in the risk of mortality. In the United States, there are more than 40 million surgical operations performed and 2% to 5% are complicated by SSIs. There is an estimated annual incidence ranging from 160,000 to 300,000, with an annual cost of SSIs in the United States estimated at $3.5 billion to $10 billion. The increased cost is due to prolonged hospitalization, increase in emergency room visits, readmission, antibiotic costs, and additional procedural costs. About 60% of SSIs are preventable with evidence-based guidelines ; as a result, SSI is one of the quality metrics frequently used to assess quality of surgical care, which is then linked to performance ranking, reimbursement, and patient satisfaction.

Classification of Surgical Site Infection

The most commonly used definition of SSI is that of the Centers for Disease Control and Prevention (CDC). The SSI must occur within 30 days after the operative procedure if no implant is left in place, or within 1 year if implant is in place, and the infection appears to be related to the operative procedure. SSIs are classified based on the depth and tissue layers involved as superficial incisional, deep incisional, and organ/space ( Table 11.1 ). Standardization of reporting plays an important role in ensuring accurate data collection for research, quality improvement, and public reporting.

Table 11.1

CDC/NHSN classification of surgical site infection.

Classification	Definition
Superficial incisional SSI (SIS)	Infection occurs within 30 days after the operative procedure and involves only skin and subcutaneous tissue of the incision and had at least one of the following: a. Purulent drainage from the superficial incision. b. Organisms isolated from an aseptically obtained culture of fluid or tissue from the superficial incision. c. At least one of the following signs or symptoms of infection: pain or tenderness, localized swelling, redness, or heat, and superficial incision is deliberately opened by surgeon and is culture positive or not cultured. A culture-negative finding does not meet this criterion. d. Diagnosis of superficial incisional SSI by the surgeon or attending physician.
Deep incisional SSI (DIS)	Infection occurs within 30 days after the operative procedure if no implant is left in place or within 1 year if implant is in place and the infection appears to be related to the operative procedure and involves deep soft tissues (e.g., fascial and muscle layers) of the incision and patient has at least one of the following: a. Purulent drainage from the deep incision but not from organ/space component of the surgical site. b. Deep incision spontaneously dehisces or is deliberately opened by a surgeon and is culture-positive or not cultured when the patient has at least one of the following signs or symptoms: fever (>38°C) or localized pain or tenderness. A culture-negative finding does not meet this criterion. c. An abscess or other evidence of infection involving the deep incision is found on direct examination, during reoperation, or by histopathologic or radiologic examination. d. Diagnosis of a deep incisional SSI by a surgeon or attending physician. Wound that has both superficial and deep incisional infection is classified as DIS.
Organ/space SSI	Infection occurs within 30 days after the operative procedure if no implant is left in place or within 1 year if implant is in place and the infection appears to be related to the operative procedure and infection involves any part of the body, excluding the skin incision, fascia, or muscle layers, that is opened or manipulated during the operative procedure and patient has at least one of the following: a. Purulent drainage from a drain that is placed through a stab wound into the organ/space. b. Organisms isolated from an aseptically obtained culture of fluid or tissue in the organ/space. c. An abscess or other evidence of infection involving the organ/space that is found on direct examination, during reoperation, or by histopathologic or radiologic examination. d. Diagnosis of an organ/space SSI by a surgeon or attending physician.

Classification

Definition

Superficial incisional SSI (SIS)

Infection occurs within 30 days after the operative procedure and involves only skin and subcutaneous tissue of the incision and had at least one of the following:

a.
Purulent drainage from the superficial incision.
b.
Organisms isolated from an aseptically obtained culture of fluid or tissue from the superficial incision.
c.
At least one of the following signs or symptoms of infection: pain or tenderness, localized swelling, redness, or heat, and superficial incision is deliberately opened by surgeon and is culture positive or not cultured. A culture-negative finding does not meet this criterion.
d.
Diagnosis of superficial incisional SSI by the surgeon or attending physician.

Deep incisional SSI (DIS)

Infection occurs within 30 days after the operative procedure if no implant is left in place or within 1 year if implant is in place and the infection appears to be related to the operative procedure and involves deep soft tissues (e.g., fascial and muscle layers) of the incision and patient has at least one of the following:

a.
Purulent drainage from the deep incision but not from organ/space component of the surgical site.
b.
Deep incision spontaneously dehisces or is deliberately opened by a surgeon and is culture-positive or not cultured when the patient has at least one of the following signs or symptoms: fever (>38°C) or localized pain or tenderness. A culture-negative finding does not meet this criterion.
c.
An abscess or other evidence of infection involving the deep incision is found on direct examination, during reoperation, or by histopathologic or radiologic examination.
d.
Diagnosis of a deep incisional SSI by a surgeon or attending physician.

Wound that has both superficial and deep incisional infection is classified as DIS.

Organ/space SSI

Infection occurs within 30 days after the operative procedure if no implant is left in place or within 1 year if implant is in place and the infection appears to be related to the operative procedure and infection involves any part of the body, excluding the skin incision, fascia, or muscle layers, that is opened or manipulated during the operative procedure and patient has at least one of the following:

a.
Purulent drainage from a drain that is placed through a stab wound into the organ/space.
b.
Organisms isolated from an aseptically obtained culture of fluid or tissue in the organ/space.
c.
An abscess or other evidence of infection involving the organ/space that is found on direct examination, during reoperation, or by histopathologic or radiologic examination.
d.
Diagnosis of an organ/space SSI by a surgeon or attending physician.

CDC , Centers for Disease Control and Prevention; NHSN , National Healthcare Safety Network; SSI , surgical site infection.

Risk Factors for Surgical Site Infection

The CDC classifies wound into four groups: clean, clean-contaminated, contaminated, and dirty-infected ( Table 11.2 ), with progressively increasing risk of SSIs. In addition, patient, environmental, and treatment factors can increase the risk of subsequent development of SSIs ( Box 11.1 ). Of particular interest are risk factors amenable to preoperative optimization such as smoking cessation, protein-calorie malnutrition, and obesity. In general, laparoscopic surgical approaches carry a lower risk of SSIs compared with open techniques for the same procedure.

Table 11.2

CDC surgical wound classification.

Classification	Description
I—Clean	An uninfected operative wound in which no inflammation is encountered and the respiratory, alimentary, genital, or uninfected urinary tract is not entered. In addition, clean wounds are primarily closed and, if necessary, drained with closed drainage. Operative incisional wounds that follow no penetrating (blunt) trauma should be included in this category if they meet the criteria.
II—Clean-contaminated	An operative wound in which the respiratory, alimentary, genital, or urinary tracts are entered under controlled conditions and without unusual contamination. Specifically, operations involving the biliary tract, appendix, vagina, and oropharynx are included in this category, provided no evidence of infection or major break in technique is encountered.
III—Contaminated	Open, fresh, accidental wounds. In addition, operations with major breaks in sterile technique (e.g., open cardiac massage) or gross spillage from the gastrointestinal tract and incisions in which acute, no purulent inflammation is encountered are included in this category.
IV—Dirty-infected	Old traumatic wounds with retained devitalized tissue and those that involve existing clinical infection or perforated viscera. This definition suggests that the organisms causing postoperative infection were present in the operative field before the operation.

CDC , Centers for Disease Control and Prevention.

Box 11.1

Risk factors for the development of surgical site infection.

Patient Factors

Alcoholism
Ascites
Age
Chronic inflammation
Diabetes
History of skin or soft tissue infection
Hyperbilirubinemia >1 mg/dL
Hypercholesterolemia
Hypoalbuminemia
Hypoxemia
Immunosuppression
Malignancies
Malnutrition
Obesity
Peripheral vascular disease
Postoperative anemia
Preexisting infection
Recent radiotherapy
Smoking
Steroid therapy

Environmental Factors

Contamination
Inadequate antisepsis
Inadequate disinfection
Inadequate ventilation
Increased operating room traffic

Treatment Factors

Blood transfusion
Contamination: poor scrubbing technique, breach in asepsis, poor gloving, etc.
Drains
Emergency surgery
High wound classification
Hypothermia
Hypoxemia
Inadequate or inappropriate antibiotic prophylaxis
Poor glycemic control
Prolonged operation

Surgical Site Infection Prevention

Numerous interventions have been proposed to reduce the risk of SSI. In 2002, the CDC and Center for Medicare and Medicaid Services initiated the Surgical Infection Prevention Project to reduce SSIs, and in 2006, this became the expanded Surgical Care Improvement Program. The U.S. Congress authored the Deficit Reduction Act of 2005, which mandates hospital reporting process and outcome and quality improvement measures to be made available to the public and Center for Medicare and Medicaid Services. The act also allows payment adjustment downward for health care–associated infections that could have been prevented through application of evidence-based strategies. These interventions can be broadly divided into three stages: preoperative, intraoperative, and postoperative strategies.

The CDC provided a new and updated evidence-based recommendation for the prevention of SSIs. Preventive measures for SSI include a full-body bath or shower with soap (antimicrobial or nonantimicrobial) or an antiseptic agent the night before or the morning of the operation, appropriate antimicrobial prophylaxis before incision, and skin preparation with an alcohol-based agent unless contraindicated. In clean and clean-contaminated procedures, additional prophylactic antimicrobial agents should not be administered even in the presence of a drain nor should topical antimicrobials be applied to the surgical incision. Maintenance of normothermia, glycemic control with targets less than 200 mg/dL, and the provision of supplemental oxygen are other adjunct measures proposed to reduce SSI in the perioperative bundle.

In addition to the 2017 CDC guideline for the prevention of SSI, a randomized study showed that prophylactic use of negative pressure dressings for closed laparotomy wounds significantly reduces the incidence of SSI at 30 days postoperatively, concomitantly decreasing length of stay (6.1 vs. 14.7 days; P = 0.01).

Treatment of Surgical Site Infection

There are five steps in the treatment of SSI ( Box 11.2 ). Once SSI is diagnosed, it is paramount to obtain a high-quality specimen for Gram stain and culture to identify the causative pathogens. With the increasing prevalence of multidrug resistant organisms associated with wound infection, identification of the causative pathogen and its antimicrobial susceptibility helps guide appropriate antibiotic therapy as well as facilitate rapid de-escalation, which is important in preventing unnecessary antibiotic use that facilitates further development of resistant organisms.

Box 11.2

Treatment strategies for surgical site infection.

1.
Pathogen identification.
2.
Source control by opening the incision in superficial or deep surgical site infections (SSIs) or by image-guided percutaneous drainage, laparoscopic, or open drainage if indicated in organ space SSIs.
3.
Immediate empiric antibiotic coverage.
4.
Timely antibiotic de-escalation.
5.
Local wound care.

Source control in superficial and deep SSI usually requires opening of the incision site and irrigation, drainage, and debridement of devitalized or infected tissue as needed. Organ space infections often can be controlled by image-guided drainage using computed tomography (CT) scan or ultrasound (US) if localized and well contained. However, where there are multiple sites or widespread infection–interloop abscesses between loops of small intestine, for example, surgical drainage is necessary and can be performed either by laparoscopic or open approach.

Necrotizing Soft Tissue Infections

NSTIs are rapidly progressing skin and soft tissue infections associated with necrosis of the dermis, subcutaneous tissue, superficial fascia, deep fascia, or muscle. This definition includes a variety of conditions, such as Fournier gangrene affecting the perineum and genitalia, Meleney streptococcal gangrene, and clostridial myonecrosis. While a wide range of organisms might be responsible and different body regions and tissues are affected, these infections are grouped together due to the common characteristics of rapid progression, irreversible tissue necrosis, high rates of sepsis, and mortality rates between 10% and 25%. Patients with NSTIs are often referred to regional burn centers because of the need for intensive care, multiple operations, and resource-intensive complex reconstruction of large tissue and skin defects.

Although uncommon compared with other skin infections such as cellulitis or abscesses, the incidence of NSTI appears to be increasing in the United States. This is often attributed to the increased prevalence of obesity, type 2 diabetes mellitus, and people living with chronic immunosuppression, all of which may predispose an individual to NSTI. ^, While these conditions do increase risk, NSTIs may also be diagnosed in previously healthy young adults and even children, although this is rare. NSTIs are rarely “idiopathic”; a minor wound or injury almost always precedes the devastating infection, often by several weeks. NSTI caused by streptococci and clostridia often have a fulminant course with rapid onset of symptoms and worsening over days or even hours and may be rapidly progressing to death if untreated. In contrast, infections caused by mixed flora, staphylococcus, and gram-negative organisms often have an indolent course over days to weeks, which may mislead clinicians into not considering the diagnosis of NSTI.

Since the progression of NSTI is often fulminant, patient prognosis depends on early recognition and administration of appropriate treatment as soon as possible.

Diagnosis

A major obstacle to the effective treatment of NSTIs and one reason for the high mortality of these conditions is delay in diagnosis. Since these infections affect subcutaneous tissues, muscle, and fascia, visible skin changes on the surface are often underwhelming, misleading clinicians as to the true extent of ongoing necrosis below. The most common clinical features of NSTIs present in 90% of cases are erythema, warmth, and pain—unfortunately, common symptoms and signs that are also present in mild infections such as cellulitis and in almost every case of inflammation from any cause. Crepitus, skin necrosis, and bullae are much more specific to NSTI but unfortunately are present less than 40% of the time, rendering them markedly less useful in diagnosis. Signs of skin and tissue necrosis are pathognomonic and should provoke urgent resuscitation and surgery; however, the lack of obvious necrosis and a superficial appearance similar to cellulitis should not deter the surgeon from further investigation, including local wound exploration, if necessary, based on the patient’s systemic signs and symptoms.

Signs and symptoms of systemic illness (i.e., sepsis) are much more likely to be a feature of NSTI than simple skin infections and should prompt serious consideration of the diagnosis. While fever may be present in nearly every infection, hypotension should not be and should serve as a warning sign if present. Similarly, organ failure such as renal failure or hypoxia should not be present with cellulitis or an uncomplicated abscess; these findings on clinical and laboratory examination, in conjunction with pain in a focal body region, should be considered highly suspicious for NSTIs and treated accordingly. The laboratory risk indicator for necrotizing fasciitis scoring system was developed based on laboratory values commonly deranged in NSTIs ( Table 11.3 ); it has been shown to be useful in differentiating NSTI from other infections, although correlation of laboratory risk indicator for necrotizing fasciitis score with outcome in NSTI is less robust, and recent metaanalyses have disputed its value. Nonetheless, whether utilizing a formal scoring system or not, any sign of systemic derangement such as unexpected hyperglycemia, acute renal failure, or hyponatremia will place the burden firmly on the surgical team to disprove the diagnosis of NSTI, requiring further evaluation such as imaging studies or direct surgical exploration.

Table 11.3

Laboratory risk indicator for necrotizing fasciitis (LRINEC) scoring system.

Variable	Units	Score
C-reactive protein	≥150 mg/L	4 points
White blood cell count (per mm)	15–25 >25	1 point 2 points
Hemoglobin	11.0–13.5 g/dL <11 g/dL	1 point 2 points
Serum sodium	≥135 mmol/L <135 mmol/L	1 point 2 points
Serum creatinine	>1.6 mg/dL (or >141 pmol/L)	2 points
Serum glucose	>180 mg/dL (or >10 mmol/L)	1 point
Risk Category	Lrinec Score, points	Probability of Nstis, (%)
Low	≤5	<50
Intermediate	6–7	50–75
High	≥8	>75

LRINEC , Laboratory risk indicator for necrotizing fasciitis; NSTIs , necrotizing soft tissue infections.

Imaging

Given the difficulty of diagnosing NSTIs based on physical examination alone, there has been much interest in the use of imaging modalities to differentiate NSTI from other infections. US, magnetic resonance imaging, and CT scans have all been evaluated for their efficacy in NSTI diagnosis; based on ease of access and interpretability of results, CT is the most commonly favored modality for adjuvant imaging. Features suggestive of NSTI on CT include gas in the soft tissues (the easiest finding for nonradiologists to diagnose and the most specific), multiple fluid collections, absence or heterogeneity of tissue enhancement by intravenous (IV) contrast, and significant inflammatory changes under the fascia. Using these criteria, the sensitivity of CT in identifying NSTI was 100%, the specificity 98%, the positive predictive value 76%, and the negative predictive value 100% in one series of 184 patients.

Local Exploration

Given the difficulty in diagnosis and the increase in mortality associated with delays in definitive treatment, surgical exploration of the questionable area is a very reasonable next step when the diagnosis remains in doubt. This requires a full-thickness elliptical excision of all tissues down through fascia and including muscle to rule out necrotizing fasciitis or myositis in addition to subcutaneous infection.

A 2-cm elliptical excision on an extremity will usually suffice and can be performed under local anesthesia at the bedside. In areas of adiposity such as the pannus or groin, this will be easier performed in the operating room. The surgeon should visually inspect for tissue necrosis, dishwater fluid or purulence, greyish discoloration of tissues, or failure of the muscle to react to electrocautery. The tissue at the edges of the incision should be firm and resist pressure—the “push” test. If the surgeon is able to dissect more than a centimeter subcutaneously with blunt finger pressure alone, this is considered a positive finding and wide debridement in the operating room is indicated. Any fluid encountered should be collected and sent for immediate Gram stain and culture in addition to at least 1 cm ³ of skin and subcutaneous tissue and samples from fascia and muscle.

Treatment of Necrotizing Soft Tissue Infections

Surgery

Surgical debridement is the mainstay of NSTI treatment. All affected tissue should be sharply excised with at least 1 cm rim of normal tissue ( Fig. 11.1 ). The “push” test described previously will allow the surgeon to quickly delineate the extent of resection necessary. Bleeding is not an indication of tissue viability, since the presence of active infection will often cause these areas to be hyperemic; significant blood loss is often encountered so the surgical team should be prepared for this eventuality. The use of tourniquets in extremity dissection and attention to hemostasis are necessary to prevent sudden major blood loss from destabilizing an already unstable patient. All questionable tissue should be resected at the initial operation; the need for multiple operations and the spread of infection both increase the risk of mortality.

Fig. 11.1, Surgical debridement of necrotizing soft tissue infection.

While skin-sparing procedures have been shown in limited series to improve eventual reconstructive options for both cosmesis and function, it is essential that the skin not be directly involved in these cases and that wide undermining be able to be performed to remove all necrotic tissue, which remains the mainstay of NSTI treatment.

Antibiotics

Broad-spectrum antibiotics should be initiated as soon as the diagnosis is suspected; once the patient is clinically improving and culture results are available, these may be de-escalated to one or two agents. In general, it is advisable to give one broad-spectrum agent effective against most gram-positive and gram-negative organisms and ensure Methicillin-resistant S. aureus coverage and good anaerobic coverage, tailored to local antibiogram. The impact of anaerobes in NSTI outcomes has been underrecognized due to the difficulty of growing anaerobes in conventional culture media; however, recent studies using 16S ribonucleic acid (RNA) sequencing have demonstrated that anaerobes are likely a significant contributor to mortality in NSTIs. Finally, there is evidence that clindamycin has toxin-neutralization properties, especially in streptococcal and clostridial infections; for this reason, we routinely add clindamycin to the initial regimen.

Resuscitation

Patients demonstrating sepsis and septic shock should be managed in an intensive care unit (ICU), using the standard guidelines for sepsis. These include early, goal-directed resuscitation with isotonic fluids, vasopressor support as needed with norepinephrine and vasopressin, and control of hyperglycemia. The use of adjuncts such as IV immunoglobulin and hyperbaric oxygen has been described; however, there is insufficient evidence to recommend routine use. While there is no specific evidence for the use of antioxidants or steroids in NSTIs, recent studies suggest that IV thiamine, vitamin C, and hydrocortisone in combination might improve outcomes in sepsis. Further investigation is warranted as to the utility of this approach in NSTIs.

Wound Care and Reconstruction

The large soft tissue defects that result from appropriate debridement of NSTI will require extensive reconstructive procedures once the patient has recovered from the acute episode. We routinely leave the debrided area completely open to air, sometimes under heat lamps, for the first 48 hours after surgery; a spritz of antibiotic irrigation is used to keep the muscle from drying out excessively, and lubricant is used to cover tendons and other vulnerable areas. This approach allows for continuous evaluation of the wound in the ICU, facilitating the earlier recognition of spreading infection and removing the need for scheduled second-look operations. Removing the need for dressing changes also reduces the pain experienced by the patient, and this approach is surprisingly well tolerated by patients and families alike, after the indications are explained. In body areas such as the groin or under intertriginous folds where it is not possible to leave the tissue exposed to air, we use conventional wet-to-dry gauze dressings changed once or twice a day.

Once the infection is resolved, the wound is placed in a negative pressure vacuum dressing and reconstructive procedures, usually a skin graft, is planned in 2 to 4 weeks. This allows time for the patient to engage in rehabilitation with physical therapy and optimal nutrition in order to optimize the chances of a good long-term outcome. The inclusion of tissue substitutes such as acellular dermal matrix and regeneration templates in reconstruction may improve cosmetic and functional outcomes, although this increases cost significantly.

Specific Infections

Intraabdominal Abscess

Intraabdominal infections encompass a wide range of infections that have been classified previously in a variety of ways, including classification based on the nature of the infection (uncomplicated and complicated), the setting of infection (community acquired vs. hospital acquired), and severity of the infection as well as risk of significant morbidity, mortality, and failure of treatment (low, moderate, and high risk).

This chapter focuses on one of these infections (i.e., intra-abdominal abscess) in the surgical patient.

Definition, Etiology, and Classification of Intraabdominal Abscess

Intraabdominal abscess refers to a localized walled-off collection of infected fluid within the confines of the abdomen (peritoneal cavity, retroperitoneum, and pelvic cavity) that occurs as a result of the protective containment of the host’s intraabdominal defense mechanisms. Failure of the host intraabdominal defense mechanisms to wall off and localize the infection leads to an uncontained infection with acute diffuse peritonitis and systemic infection associated with a high morbidity and mortality.

An abscess can develop at a later stage of what was previously uncontained intraabdominal “free-floating infection.” With the intraabdominal host defense mechanisms against infection in effect, there is, then, the development of a capsular wall around the inflammatory fluid or infected fluid for containment, resulting in a walled-off abscess. A previously uninfected fluid collection that becomes walled off may later become secondarily infected from systemic bacteremia or from external translocation via a drain or instrumentation, for example, secondary infection of a post pancreatitis pseudocyst ( Fig. 11.2 ).

Fig. 11.2, (A) Retroperitoneal abscess that developed in a previously walled-off infected pancreatic necrosis cavity that had been operatively debrided by robotic pancreatic necrosectomy. (B) Percutaneous large bore drainage of the retroperitoneal abscess. (C) Complete resolution of the retroperitoneal abscess 6 weeks after percutaneous drainage.

On the other hand, intra-abdominal fluid may already be infected at the onset and then become walled off (e.g. purulent fluid from ruptured acute appendicitis or leaked hollow viscus contaminated fluid like in a colonic anastomotic leak) ( Table 11.4 ).

Table 11.4

Types of intraabdominal abscess.

Type of INTRAABDOMINAL Abscess	Etiology/examples
Primary intraabdominal abscess (established infections that rupture into peritoneal cavity and become walled-off into abscesses)	Ruptured acute appendicitis abscess, acute diverticulitis with abscess
Delayed primary intraabdominal abscess (microbial-laden hollow viscus fluid leaking into abdomen and transforming into walled-off abscess with time)	Gastrointestinal perforation or postoperative anastomotic leak leading to abscess formation later, subhepatic abscess developing later from infected fluid around after cholecystectomy for acute cholecystitis
Secondary intraabdominal abscess (previously sterile walled-off intra-abdominal fluid collection becomes secondarily infected, transforming into abscess)	Postpancreatitis sterile pseudocyst with secondarily infection from systemic bacteremia or microbial translocation into it via external drain; loculated sterile ascitic/intra-abdominal fluid secondarily infection for external instrumentation or systemic infection.

Intraabdominal abscesses can, therefore, be classified into the following categories based on location, etiology, and severity ( Box 11.3 ).

Box 11.3

Intraabdominal abscesses classifications.

Etiology

Primary intraabdominal abscess
Delayed primary intraabdominal abscess
Secondary intraabdominal abscess

Intraabdominal Location

Intraperitoneal abscess
Retroperitoneal abscess
Pelvic abscess
Solid organ intraparenchymal abscess

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here