Intraabdominal Abscesses

Abstract

Intraabdominal abscesses continue pose challenge to surgeons due to their rather ominous presentation. Most often, high index of suspicion is required to initiate a diagnostic workup. The discovery of a wide variety of antibiotics, more aggressive surgical drainage techniques, intensive care management, and other factors have decreased mortality below 25% over the past century. Recently, more conservative, less invasive source control techniques have recently been developed. These include laparoscopic, needle, and percutaneous image-guided drainage techniques. This chapter will discuss the epidemiology of intraabdominal abscesses including frequency of occurrence of the various types and age and sex distribution. Relevant anatomy of the peritoneal cavity will be given. Risk factors will be discussed. Classification will include intraperitoneal, solid organ abscesses and retroperitoneal abscesses. Pathology and pathophysiology of the various types of abscesses will be discussed followed by clinical presentation, morbidity and complications. Aetiology and bacteriology of the abscess types will be elaborated. A discussion will be provided on resuscitation, patient evaluation and preoperative workup. Management will be discussed as follows: Overview, percutaneous image-guided drainage vs. open drainage, (including indications, anaesthesia, access and technique of drainage), pearls and postoperative/postprocedural care and complications. Prognosis of each abscess type will be given.

1. Introduction

Intra-abdominal abscesses can result from a number of conditions, including perforated hollow viscera, de novo intraabdominal infections, and following operative abdominal procedures [1]. Abscesses are well-defined collections of infected, purulent material which may be walled off from the remainder of the peritoneal cavity by inflammatory adhesions, loops of intestine and their mesentery, the omentum, or other abdominal viscera. Abscesses can develop within the peritoneal cavity as well as in the retroperitoneum. It may also occur within the tissues of intraabdominal solid organs [2].

The peritoneal cavity, tissues of intaraabdominal solid organs and the retroperitoneal space are normally sterile. A disruption of the gastrointestinal tract, external inoculation, such as through a penetrating abdominal injury, or seeding of blood-borne pathogens can cause intraabdominal infections and abscess formation. Less frequently, abscess may form from the urinary or gynaecological tract. The majority of abdominal infections are polymicrobial [3]. Prompt detection and treatment help to lower the high morbidity and mortality associated with this condition.

In the past, complicated intra-abdominal infections, such as peritonitis or intra-abdominal abscesses, were linked to high fatality rates of 90% or more. The discovery of a wide variety of antibiotics with various modes of action, more aggressive surgical drainage techniques, intensive care management, and other factors have decreased mortality below 25% over the past century [4]. More conservative, less invasive source control techniques have recently been developed. These comprise laparoscopic, needle, and percutaneous image-guided drainage methods.

2. Epidemiology

The incidence of intraabdominal absesses was reported to be 7% for of all patients managed for intraabdominal infections by an international study involving 309 hospitals across the world in 2016. The reported organ failure and septic shock as the commonest causes of death [5]. It is estimated that about 70% are postsurgical and that 6% of patients undergoing colorectal surgery may develop a postoperative abscess [3]. Barie et al. reported an incidence of intra-abdominal infection of 5.75% among 465 critically ill surgical patients managed for hollow viscus perforation and/or peritonitis from 1991 to 2002 with a mortality rate of 22.6% [6].

Hepatic abscesses constitute about 13% of all intra-abdominal abscesses. Due to its bigger size and better blood supply, the right lobe of the liver is where most of hepatic abscesses occur. According to a population-based research, hepatic abscesses have a yearly incidence of 3.6 cases per 100,000 people in North America with a male-to-female ratio of about 1.5 to 1. According to the study hepatic abscesses have no racial, or regional disparities in occurrence. Pyogenic liver abscess is commonly associated with cirrhosis, chronic renal failure, and a history of cancer [7]. Over the years, the average age of patients with pyogenic liver abscess has risen. With a reported mean age of 47 to 65 years, it is currently a condition that primarily affects middle-aged and older people. Risk factors for case fatality in older patients include age and an APACHE II (Acute Physiology and Chronic Health Evaluation II) score below 15 on admission. Pyogenic liver abscesses frequently develop in children who have impaired immune function, sickle cell anaemia, congenital hepatic fibrosis, polycystic liver disease. Hepatic abscesses may complicate liver transplantation [8].

Splenic abscess is an uncommon infection. The incidence of splenic abscess in autopsy series is reported to be 0.05–0.7%. Splenic abscess mostly follows haematogenous spread. It also results from endocarditis or seeding from some contiguous sites of infection. Other risk groups include immunosuppressed patients, hemoglobinopathies, and diabetes mellitus [9]. It is mostly solitary but can be multiple. Splenic abscess may coexist with extrasplenic abscesses including liver abscesses [10].

3. Surgical anatomy

The peritoneum, which is composed of a single sheet of simple squamous epithelium of mesodermal origin, is situated deep to the extraperitoneal fascia and fat. The peritoneal cavity is sealed in men, but it is exposed to the outside in females through the ostia of the fallopian tubes. The peritoneum has parietal and visceral components. The parietal peritoneum is the mesothelial layer that lines the inferior surface of the diaphragm, the anterior, lateral, and posterior abdominal wall surfaces, as well as the pelvis. The stomach, jejunum, ileum, transverse colon, liver, spleen, and the anterior portion of the retroperitoneal organs (duodenum, left and right colon, pancreas, kidneys, and adrenal glands) are mostly covered by the visceral peritoneum. Ligaments and mesentries partition the peritoneal cavity into nine potential spaces—right and left subphrenic, subhepatic, supramesenteric and inframesenteric, right and left paracolic gutters, pelvis, and lesser space (see Figure 1). These spaces are important sites of abscess collection following various disease processes [12, 13].

Figure 1.

Peritoneal cavity and its potential spaces [11].

The retroperitoneal space is located between the peritoneum and posterior parietal wall and runs from the diaphragm to the pelvic floor. Located in this region are the iliac and lumbar fossae which are continuous with one another. The diaphragm, spinal column, quadratus lumborum, and psoas major muscles respectively form the superior and posterior borders of the retroperitoneal region while levator ani muscles form the inferior border. The adrenal glands, kidneys, ascending and descending colons, duodenum, and lymph nodes are located in this region. The ureter, renal vessels, gonadal vessels, inferior vena cava, and aorta also pass through it. See Figure 2 [13, 15].

Figure 2.

Anatomy of the retroperitoneum [14].

4. Classification

Intra-abdominal abscesses are classified into (i) intraperitoneal, (ii) retroperitoneal, and (iii) visceral. Examples are listed in Table 1 [16]. Retroperitoneal abscesses are categorised as either primary or secondary depending on whether hematogenous dissemination caused the infection or if it was caused by an infection in a nearby contiguous structure [13].

Intraperitoneal	Retroperitoneal	Visceral
Subphrenic	Pancreatic	Hepatic
Subhepatic	Post-traumatic	Splenic
Right or left lower quadrant	Perinephric
Paracolic
Interloop
Lesser sac
Pelvic

Table 1.

Classification of intra-abdominal abscesses.

5. Intraperitoneal abscess

5.1 Aetiology and microbiology

Following perforation of a hollow viscus, as in ruptured appendix, gastric peptic perforation, typhoid ilial perforation, or perforated colonic or gastric cancer, peritonitis and/or intraaabdominal abscess may occur depending upon degree of contamination and containment ability of the peritoneum and other host factors. Other conditions that can cause intra-abdominal abscess formation include appendicitis, diverticulitis, Crohn disease, pancreatitis, and pelvic inflammatory disease. Post-operative complications such as anastomotic leak may also result in abcess formation. Subhepatic abscess may result from thoracic pathologies such empyema and lung abscess. Abscesses may form following penetrating abdominal injuries, notably those to the colon, liver, pancreas, and spleen [16]. The risk of developing intra-abdominal abscesses is increased by diabetes mellitus, malnutrition, HIV/AIDS, anaemia, and liver disease.

The primary source determines the microbiological spectrum of an intra-abdominal abscess. In intra-abdominal abscesses, various intestinal flora are typically prevalent, indicating the prevalence of concomitant illnesses originating from this anatomic location. Accordingly, coliform bacteria, particularly Escherichia coli and Bacteroides fragilis, are the main agents. Klebsiella spp., Proteus spp. and Enterobacter spp. are important coliforms in abscess formation. Others are streptococci, enterococci, and anaerobic bacteria. A particularly invasive anaerobic pathogen in abdominal infections and abscesses is B. fragilis which is an obligate anaerobic gram-negative bacillus. In the evolution of abdominal sepsis and an intra-abdominal abscess, coliform bacteria in a mixed form are mostly responsible for the early sepsis, whereas anaerobes are responsible for the late sequelae with abscess formation [6, 16].

Following penetrating abdominal injury, skin flora as well as bacteria on surfaces of sharp objects may be responsible for an intra-abdominal abscess. In females with pelvic inflammatory disease, Neisseria gonorrhoeae and Chlamydia spp. are the most often found pathogens [17]. Recent studies shows link between SARS-CoV-2 (Covid-19) infection and gastrointestinal complications such as bowel perforation and intraabdominal abscesses [18, 19].

5.2 Pathology and pathophysiology

Generally, local peritoneal infections usually resolve spontaneously or under appropriate antibiotic regime. However, once tissue destruction occurs, decomposition is inevitable because the micro-organisms in the dead tissue are no longer accessible to systemic antimicrobial agents.

Intra-abdominal abscesses are confined by an inflammatory barrier. The omentum, inflammatory adhesions, or neighbouring viscera may all be a part of this barrier. Bacteria from the GI tract, both aerobic and anaerobic, are typically present in the abscesses. Polymorphonuclear cells are induced by bacteria in the peritoneal cavity, particularly those coming from the large bowel. The viscera and omentum have a tendency to localise the infection location, resulting in a phlegmon. Anaerobe development is aided by the resultant hypoxia, which also reduces granulocyte bactericidal activity. Leucocyte phagocytic activity breaks down cellular and bacterial waste, generating a hypertonic environment that causes the abscess to expand in reaction to osmotic pressures. Abscess may spread to other actual or potential intraperitoneal spaces (see Figure 1). The thoracic cavity may become infected by subdiaphragmatic abscesses, leading to empyema, lung abscess, or pneumonia. A lower abdominal abscess may spread to the thigh or perirectal space. Most patients with intra-abdominal abscesses exhibit a moderate systemic reaction. Others experience a significant septic reaction, volume depletion, and a catabolic state. They may also have decreased urine output and tachycardia. Sequential organ failure strongly suggests intra-abdominal sepsis [2, 17, 20].

5.3 Clinical presentation and patient evaluation

One of the main challenges in the management of complicated intra-abdominal infections is early recognition. The associated high mortality can be reduced by early diagnosis, adequate source control and intervensions to restore anatomy and physiological function [5]. The presentation of intra-abdominal abscesses may be highly variable. Persistent abdominal pain, focal tenderness, spiking temperatures particularly the swinging variety, persistent tachycardia, prolonged ileus, leukocytosis, or intermittent polymicrobial bacteremia in patients with predisposing primary intra-abdominal disease or in those who have undergone abdominal surgery should raise the suspicion of an intrabadominal abscess.

In patients with deep seated abscess many of these features may not be present. Nonlocalizing debilitating disease, modest liver dysfunction, chronic gastrointestinal (GI) dysfunction, or persistent fever may be the only early warning signs. There are some indicators that could point to an intraabdominal abscess. Epigastric pain or discomfort and a painful, immovable epigastric enlargement may be felt in patients with abscesses in the smaller sac. Pain in the right upper abdomen, unexplained tarchypnoea and tarchycardia are common in subphrenic abscess. There may also be hiccups. Diaphragmatic irritation may cause referred in the right shoulder. Right lung examination may demonstrate pleural effusion or basal crepitations [17].

Pelvic abscess may develop after generalised peritonitis has been treated; it may also occur in conjunction with gangrenous appendicitis, ileal or duodenal rupture. In females, pelvic abscess can complicate septic abortion or pelvic inflammatory disease. Pelvic abscess localises in the Pouch of Douglas in females and in between the bladder and the rectum in males. Patients with pelvic abscesses may have lower abdominal pain, fluctuating temperatures, malaise, and anorexia. They may have diarrhoea, tenesmus from irritation of the rectum, or frequent and urgent urination from bladder irritation. Lower abdominal pain may be associated with a tender suprapubic mass, and a tender, boggy mass on the anterior wall of the rectum on digitalrectal examination. Pelvic abscess may about the iliopsoas muscle and present atypically with hip pains and limping due to referred pain [21].

Plain abdominal radiographs may show an air pocket under the diaphragm, a localised ileus, extraluminal gas, air-fluid levels, soft tissue masses that are mottled, the absence of psoas outlines, or visceral displacement. The chest radiograph may reveal pleural effusion, raised hemidiaphragm, basal infiltrates, or atelectasis in subphrenic or even subhepatic abscesses. An ultrasonography may identify the abscess location, size, and number. It is readily accessible and cheap with accuracy rate of more than 90%. It can be performed on patients in intensive care units who are immobile and critically sick.

The limitations of ultrasonography include of presence surgical dressings, open wounds, intestinal gas, intervening viscera, significant obesity, and stomas. It is also heavily operator-dependent. Computed tomography (CT) gives better details of abdominal abscesses than abdominal sonography. It has greater than 95% diagnostic accuracy and is not limited by the presence of ileus, stomas drains or dressings. The appearance of an air bubble within a fluid collection or a low-attenuation extraluminal mass is diagnostic of an intra-abdominal collection. CT scan can document inflammatory edema in the adjacent fat (obliteration of fat plane) and hyperemia in the abscess wall (enhancement). Until about postoperative day 7, when absorption of non-suppurative fluids (such as hematoma, seroma, or intraoperative irrigation fluid) should have been complete, CT is not advised for use in the immediate post-operative period for the purpose of identifying abscesses. Water-based oral contrast and intravenous (IV) contrast are used for good anatomic resolution. Extravasation of oral contrast indicates a fistula or an anastomotic leak. IV contrast may enhance the abscess by concentrating within the abscess wall. The use of oral and IV contrast may be limited by ileus, allergy to contrast material, and renal insufficiency. The limitations of CT include nonportability, a potential lack of patient participation, and a relative difficulty in accurately detecting intraloop abscesses. In the majority of hospitals in developing nations, it is also not easily accessible. Gallium-67 or indium-111-tagged leukocytes may be used to pinpoint the location of the inflammation. Such radio-isope scans take a lot of time, and they frequently provide false-positive results due to nonpyogenic inflammation, intestinal leukocyte buildup, surgical drains, and incisions. CT and MRI has largely replaced the use of radio-isope scan in the diagnosis of intarabdominal abscess except for viscereal abscesses such as liver abscesses [17].

5.4 Management

The following principles guide the management of intra-abdominal abscesses.

1. Resuscitation

2. Anti-microbial therapy

3. Source control

5.4.1 Resuscitation and supportive measures

While confirmation of diagnosis is pursued using appropriate imaging and laboratory tools, patient assessment and optimization is also carried out. The first step of resuscitation and optimization is determined by the patient’s specific problems. It is appropriate to focus on the ABCs (airway, breathing, and circulation) while tailoring the intervention to each patient’s divergence from normal physiology. Anaemia, dehydration, dyselectrolytemia, malnutrition and sepsis are all recognised and treated. Systemic diseases including diabetes mellitus, chronic kidney, and liver disease, are all assessed and optimised. When considering the patient’s presentation, the differential diagnosis of an intraabdominal abscess are sought after. Inflammatory bowel disease, prolonged ileus, and unexplained postoperative fever are among the differentials [2, 17, 18, 20].

5.4.2 Antimicrobial therapy

Appropriate bactericidal wide spectrum antibiotic are commenced while the causative bacterial agent(s) and their sensitivity pattern are identified. Antimicrobial management is typically standardised, and numerous regimens—either as monotherapy or combination therapy—have demonstrated varying effecacies. In the context of each intraabdominal abscess clinical scenario, empiric antimicrobial therapy should be comprehensive and should address all possible infectious agents. When there is evidence of candida involvement or when the patient has risk factors for invasive candidiasis such as immunodeficiency state or prolonged antibacterial therapy, antimicrobial coverage of Candida spp. is advised. Antimicrobial treatment should typically last 5–7 days. After a week, if sepsis still exists, a diagnostic workup and, if necessary, a surgical re-intervention should be considered [2, 5].

5.4.3 Source control/abscess drainage

The term source control refers to any physical actions performed to control an infection focus, such as the removal of necrotic tissue, surgical repair, resection, and/or exteriorization of the anatomical defect that is the source of peritoneal contamination [2]. Source control for intra-abdominal abscesses can be accomplished by either image-guided or open surgical drainage.

5.4.4 Abscess drainage (indications, methods/imaging, preparation and procedure)

Percutaneous image-guided drainage is a minimally invasive method of abscess source control which has been proven to be an effective alternative to surgery with comparable success rates and lower morbidity rates. It is cheaper with fewer complications, and avoids general anaesthesia.

It is performed for abscesses that are in readily accessible locations, unifocal and unilocular and without having to pass through hollow organs. Some multifocal and multiloculated abscesses can also be drained by this method but this may be more technically challenging. There is also the risk of incomplete drainage.

Drainage is accomplished by the use of image guidance such as computed tomography or ultrasonography. Where necessary, a local anaesthetic agent is injected into the skin. Sedation may be necessary for some uncooprative patients and in children. Skin preparation is done with clorhexidine, iodine solution or other suitable antiseptic agents. Trocar as well as Seldinger techniques are frequently employed for catheter placement. The choice of method is based on the surgeon’s preferences, experience, and clinical situation [22]. After the abscess has been located, the initial diagnostic aspiration is submitted for Gram stain and microbiological culture. The drainage catheter should be as small as possible to ensure safety while still being large enough to prevent the tube from being easily blocked (usually 8–12 Fr). Following entry into the abscess cavity, the catheter is connected to a closed drainage system. Suction or irrigation of these catheters does not seem to be beneficial, whilst flushing with saline once a day is suggested to maintain patency (Figure 3) [2, 5].

Figure 3.

CT-guided drainage of a subhepatic abscess [23].

5.4.5 Pearls and pitfalls

Heart rate, respiratory rate, blood pressure, and oxygen saturation should be actively monitored during percutaneous drainage of intraabdominal abscess because of the possibility of haemorrhage, and oversedation [22]. An abscess cavity normally decompresses following proper catheter insertion. To ensure tube patency, the catheter should be irrigated once daily. Within 48 hours of catheter placement, patients are expected to have an improvement in symptoms. With cessation of drainage, repeat imaging is done to check for any residual contents before extubation.

If abscess drainage increases or continues over time, an anatomic defect, a need for change in antibiotic therapy or background impaired immunity should be suspected. Bacteremia, sepsis, enterocutaneous fistula, vascular injury, and intrapleural catheterization are uncommon but possible complications of image-guided catheter insertion into the abdomen.

Smaller appendiceal abscesses in less ill patients may be successfully treated with antibiotics alone. If the abscess is of large volume, drainage can be achieved by percutaneous image-guided approach; interval appendectomy is performed after 6 weeks. If fever and leukocytosis persist after an initial drainage, an urgent appendectomy is performed during same hospital admission. Pelvic abscesses less than 2 cm in diameter can be treated conservatively; transvaginal or transrectal drainage with endoscopic ultrasonographic guidance is used to treat larger abscesses. A lower abdominal percutaneous approach is occasionally employed [13].

5.4.6 Surgical drainage

Surgical drainage of an intraabdominal abscess may be achieved by either a minimally invasive method (laparoscopic) or by an open technique (laparotomy). Indications for surgical drainage include (1) abscesses located deep to hollow organs not amenable to image-guided drainage, (2) multiple large volume abscesses, (3) a known intra-abdominal source requiring surgical intervention or (4) an abscess of unidentified aetiology.

Subhepatic abcess not completely drained by a percutaneous method, or if deep-seated with intervening gallbladder, bowel loops, or adhesions may require an open drainage. This may be performed extraperitoneally through the bed of the 12th rib for posterior abscess (Morrison’s pouch) or through a right subcostal incision if it is located anteriorly. If abdominal exploration is also required, transperitoneal drainage may be performed [20].

Laparoscopy is a minimally invasive method that allows for exploration of the abdominal cavity without the need for a large incision. Abscesses can be drained safely while also examining the whole peritoneal cavity. Anatomic defects can also be addressed by this method. Both laparotomy and laparoscopy have carry the risk of visceral injuries especially in the presence of bowel obstruction, adhesions, and loss of anatomic integrity from bowel edema. Careful examination is therefore necessary. Laparotomy also causes more metabolic response and prolonged hospital stay.

The prognosis of patients with an abdominal abscess before the era of advanced imaging was very high. Today, with the availability of ultrasonography and CT, the diagnosis is made much earlier, and, in many cases, drainage with the aid of these imaging modalities has helped lower morbidity and mortality. Generally, risk factors that increase mortality and morbidity in patients with intraabdominal abscess include advanced age, multi-organ failure, multiple recent surgeries, complex abscess and delay in diagnosis [3].

6. Retroperitoneal abscesses

6.1 Aetiology and microbiology

The origin of retroperitoneal infections and abscesses is commonly the organs and tissues present within or abutting the retroperitoneal space. Retroperitoneal abscesses are caused by a variety of conditions including complicated pancreatitis, retrocecal appendicitis, contained duodenal ulcer perforation, iatrogenic perforation during esophagogastroduodenoscopy (EGD) or endoscopic retrograde cholangiopancreatography (ERCP), and renal infections [12]. The bacteriological profile of retroperitoneal abscesses is related to the cause. Gram-negative rods like Proteus mirabilis and Escheritia coli are frequently involved in kidney infections and are frequently monomicrobial in nature. E. coli, Enterobacter spp., enterococci, and anaerobic species like Bacteroides are commonly involved if the source is GI tract. Retroperitoneal abscess may follow penetrating trauma to the central areas of the back. It may also be caused by spinal tuberculosis (TB) in immunocompromised patients and in patients in TB endemic areas of developing countries [12, 13]. Lumbar acupuncture was reported to cause retroperitoneal abscess [24].

6.2 Pathology and pathophysiology

Retroperitoneal abscess may be single or multiple, of small volume or of large quantity. Due to the substantial space and non-discrete boundaries of the retroperitoneum, abscessess can accumulate in large quantity prior to diagnosis. It may expand toward the peritoneal cavity or may track through areas of weakness on the posterior abdominal wall and appear on the subcutaneous space, eventually rupturing and draining through the skin. Patients usually have comorbidities such as diabetes mellitus, renal failure and malignancy. These contribute to increased morbidity of the disease [12, 13].

6.3 Clinical presentation and evaluation

Retroperitoneal abscesses are characterised by an insidious, poorly localised illness marked by diagnostic delay, inadequate drainage, and significant morbidity [25]. Lower abdominal or flank pain, which affects 60–75% of patients, fever and chills, which affect 30–90% of patients, malaise, and weight loss are the most typical symptoms of retroperitoneal abscess. Psoas abscess may cause referred pain in the hip, groin, or knee. Features of the primary infectious focus may be elicited in the history. Symptoms typically last for more than 1 week. In severe cases there may be features of sepsis. Chronic conditions like renal calculi, diabetes mellitus, HIV infection, or cancer are frequently identified in patients with retroperitoneal abscesses. CT confirms the diagnosis, identifies the location of the abscess, its size and relationship to neighbouring structures. The lesion appears as a hypodense retroperitoneal mass with surrounding inflammation. As many as one-third of these lesions contain gas. CT helps identify possible source of the infection offers details on the potential best drainage route [13].

6.4 Treatment

The principles of treatment of retroperitoneal abscesess include (i) patient optimization, (ii) use of broad spectrum antibiotics, (iii) drainage of the collection, and (iv) identification and treatment of the underlying retroperitoneal infectious source. All contributing co-morbid conditions are also addressed (see Section 5.5.1 above). Image-guided percutaneous drainage (Figure 4) is strongly preferred although operative drainage may occasionally be required for adequate drainage of complex or multiple collections. The prognosis in retroperitoneal abscess is commonly affected by delay in presentation and diagnosis. In rare instances of retroperitoneal necrotizing fasciitis, the mortality rate can be as high as 25% [2, 13].

Figure 4.

Drainage of a retroperitoneal fluid after pancreatic surgery (a). Percutaneous puncture with a Chiba needle (b), a 12Fr pigtail catheter placed (c) MIP reconstruction using the Seldinger technique. Repeat CT after 2 weeks with complete resolution (d) [26].

7. Visceral abscesses

7.1 Aetiology and microbiology

Pyogenic liver abscesses are the most common types of liver abscesses. They are caused by intestinal infections like acute appendicitis and diverticulitis, which spread to the liver through the portal circulation. Pyogenic liver abscesses can also develop as a direct result of infections like diverticulitis or Crohn’s disease spreading into the liver, impaired biliary drainage, subacute bacterial endocarditis, infected indwelling catheters, dental procedures, or other conditions. About 40% of these abscesses are monomicrobial, 40% are polymicrobial, while 20% culture-negative. Escherichia coli, (present in two-thirds of cases), Streptococcus faecalis, Klebsiella, and Proteus vulgaris are the most common bacterial agents. Bacteroides fragilis and other anaerobic organisms are cultured as well. Risk factors for pyogenic liver abscesses include diabetes mellitus, cirrhosis, pancreatitis, inflammatory bowel disease, pyelonephritis. Pyogenic liver abscess is seen in 17–36% of patients with lymphoma, leukaemia, and solid organ cancers [27]. Intestinal and extraintestinal amebiasis such as amoebic liver abscess are caused by the ubiquitous protozoan Entamoeba histolytica. Entamoeba dispar occassionally causes amoebic liver abscess. Splenic abscesses may result from extension from infections of a contiguous structure such as the colon, kidney, or pancreas. Most common organisms are Gram-positive cocci (Staphylococcus, Streptococcus, or Enterococcus spp.) and Gram-negative enteric bacteria. In immunocompromised individuals, splenic abscess may be caused by Mycobacterium tuberculosis, Mycobacterium avium, Actinomyces spp. and Candida spp [9, 28].

7.2 Pathology and pathophysiology

The liver is frequently exposed to loads of bacterial from the GI tract via the portal venous system. The liver’s reticuloendothelial cells clear this bacterial load without sequelae. However, when an inoculum of bacteria exceeds the ability of the liver to clear it, bacterial tissue invasion, neutrophil infiltration, and abscess formation occurs. Pyogenic liver abscesses are more frequently found in the right lobe of the liver due to its higher vascularity and oxygenation. Left lobe involvement occurs in only 20%. Bilobar involvement is uncommon. Approximately half of hepatic abscesses are solitary. The sizes of hepatic abscesses vary from less than 1 mm to 3 or 4 cm in diameter. If multiple, they may coalesce to give a honeycomb appearance. Amebic Abscesses are caused by Entamoeba histolytica. The parasite exists as cysts in a vegetative state which are acquired faeco-orally, passes through the stomach and small bowel and transform into trophozoites in the colon where it invades the colonic mucosa, forming typical flask-shaped ulcers. They enter the portal venous system and are carried to the liver. The superior-anterior aspect of the right lobe of the liver, close to the diaphragm, is where amebic abscesses are most frequently found. They have a necrotic central area that contains a thick, reddish-brown pus-like substance [27, 29].

Splenic abscesses are more common in tropical regions and are frequently seen in sickle cell patients in whom thrombosis and infarction of splenic vessels commonly occurs. Splenic abscess is seen in the following conditions: (a) hematogenous spread; (b) contiguous infection; (c) hemoglobinopathy; (d) immunosuppression and (e) trauma. Streptococci Spp. and Escherichia coli are the most prevalent organisms in most series. Mycobacterium tuberculosis and Salmonella typhii are occasionally isolated [29].

7.3 Clinical presentation and evaluation

Patients with pyogenic liver abscess presents with right upper quadrant pain and fever. Fever, jaundice, and right upper quadrant pain with tender hepatomegaly are the typical description of a hepatic abscess; however, only 10% of cases have this classic presentation. A thorough history and physical examination are therefore necessary in assessing these patients. Endogenous endophthalmitis, a rare complication unique to Klebsiella hepatic abscesses, affects about 3% of patients. Diabetics are more susceptible to this ocular complication. The best means of preserving visual function is early diagnosis and treatment [29].

Hepatic amoebiasis should be considered if right upper quadrant pain, fever, hepatomegaly, and a hepatic cystic lesion are present in a patient who resides in an endemic area or patient who migrated from amoebiasis endemic area. Diaphragmatic involvement may cause cough or dyspnea. Occasionally, rupture of the abscess into the peritoneal cavity may cause peritonitis. Rupture into the pleural space or pericardium has been reported but this represents an uncommon occurrence. Although the hepatic lesions follow an initial bowel infection, the presence of diarrhoea at the time of diagnosis of amoebic liver abscess is unusual Amoebic liver abscess can manifest with fever and pain in the right upper quadrant, weight loss. Shoulder pain or right-sided pleural pain are symptoms of diaphragmatic involvement. Between 10% and 35% of patients will experience gastrointestinal symptoms like nausea, vomiting, abdominal pain, abdominal swelling, diarrhoea, and constipation. Tender hepatomegaly or localised subcostal tenderness is typical. Elevated transaminase levels and jaundice are unusual, whereas leukocytosis is common. A slightly elevated alkaline phosphase level is the most typical biochemical abnormality. Fluorescent antibody tests for E. histolytica are typically positive and about 90% of patients continue to test positive for some time even after a clinical cure. Due to the high sensitivity of this serologic test, amebiasis is unlikely if the test is negative. However patients with Entmoeba dispar infection will have negative serologies. Periodic acid-Schiff stain of biopsies of the edge of the ulcers or the wall of an abscess may reveal the typical trophozoites. Amebic abscesses are usually seen on CT as well-defined hypodense round lesions with enhancement of the wall, somewhat ragged in appearance with a peripheral zone of edoema, the central cavity with septations as well as fluid levels [8, 27, 29].

The majority of patients with splenic abscess experience symptoms for 2–3 weeks before presentation. In about 33% of patients, symptoms include fever, left upper quadrant pain, leukocytosis, and splenomegaly. Both an ultrasound and a CT scan a have about 95% sensitivity and specificity in confirming the diagnosis [27, 30].

7.4 Treatment

Various treatment modalities have been developed for the management of pyogenic liver abscesses. The clinical situation determines which modality is most appropriate. They include the following.

• Unimodal treatment with broad-spectrum antibiotics alone

• Single or repeated needle aspiration and antibiotic therapy

• Image-guided percutaneous catheter drainage and antibiotic therapy

• Laparoscopic drainage and antibiotic therapy

• Laparotomy (open drainage) and antibiotic therapy

Fluoroquinolones (or aminoglycosides) and clindamycin (or metronidazole) are among first line agents used in empiric treatment of pyogenic liver abscess. Single-agent therapy with ticarcillin-clavulanate, imipenem-cilastatin, or piperacillin-tazobactam is also acceptable. Carbapenems are recommended when extended spectrum β-lactamase–producing strains are isolated or strongly suspected. Traditionally, 4 to 6 weeks antibiotic therapy is recommended however, a 2-week antibiotic regimen may suffice [8, 30].

Most patients with small pyogenic liver abscesses respond well to antibiotic therapy alone. Percutaneous image-guided drainage may be required if abscess volume is large or in patients with small abscesses who do not respond to initial antibiotic therapy. It should be noted however that pyogenic abscesses can be very viscous and catheter drainage may be ineffective. Needle aspiration (which is less invasive, less expensive, and avoids the complications associated with catheter placement and care) if frequently ineffective and carries greater recurrence rates with patients requiring additional intervention. Surgical drainage either via the laparoscopic or open approach may be necessary if initial treatment fails. Occasionally, an anatomic surgical resection can be performed in patients with recalcitrant or deep abscesses. Laparoscopic or open drainage is considered in patients with (1) multiple large volume abscesses, (2) a known intra-abdominal source requiring surgery, (3) an abscess of unidentified aetiology, (4) ascites, and (5) abscesses requiring transpleural passage. In the past, management of right-sided abscess is achieved by removing the 12th rib followed by extraperitoneal drainage. This avoids contaminating the peritoneal cavity.

Transperitoneal laparoscopic or open drainage has the following advantages: (1) treating the inciting pathology in the remainder of the abdomen/pelvis; (2) gaining access and exposing the entire liver for evaluation and treatment; and (3) access to the biliary tree for cholangiography and bile duct exploration if indicated [27, 30].

Pearl: It is important to keep in mind that in patients with presumed pyogenic abscess, a necrotic hepatic malignancy may be mistaken for a hepatic abscess. Therefore, early diagnosis and progression to surgical resection should be considered for patients who do not respond to initial broad spectrum antibiotic therapy.

Amebic liver abscess. Amebic liver abscess is primarily treated non-operatively. Metronidazole has excellent efficacy, low cost, and ability to treat both extraintestinal and intestinal amebiasis. The recommended dosage is 750 mg three times a day for 10 days. If defervescence does not occur after 72 hours or if the patient is critically sick, chloroquine may be added. Usually, amebic liver abscess responds within 48 to 72 hours of amebicidal therapy.

Image-guided drainage of amoebic liver is abscess indicated if there is bacterial suprainfection, a probable pyogenic liver abscess, and a large, left-sided abscess (segments 2 and 3) which poses danger of rupture into the pericardium. In addition to amebicides, pleuracentesis or pericardiocentesis, as appropriate, may be used to treat abscess rupture into the pleura or pericardium. Laparotomy is indicated for burst amebic abscesses into the peritoneum [27, 30].

Splenic abscess. Broad-spectrum antibiotics are started as soon as a splenic abscess is suspected, and depending on the results of the culture, the antibiotic regimen should be modified and continued for a further 14 days. The preferred treatment is splenectomy, although individuals who cannot tolerate the procedure can be offered percutaneous image-guided drainage as alternative. Patients with unilocular abscess can successfully be treated with percutaneous drainage [30, 31]. Lee et al. reported gender, age, number of abscess cavities, immunodeficiency state, underlying co-morbid diseases and type of microorganism as important prognostic factors in splenic abscess [9]. Chang et al. found high APACHE II scores and Gram negative bacillus abscess as additional prognostic factors. Mortality rate for splenic abscess range from 15 to 20% in previously healthy patients who have single unilocular lesions; it may as high as 80% for multiple abscesses in immunocompromised patients [10, 28].