At least one in two SA patients presents with a medical history of recent abdominal surgery. Onset of SA-associated symptoms typically occurs one or two months after such an intervention.

Both non-specific symptoms like fever, chills and anorexia as well as signs that indicate an abdominal lesion with respiratory compromise may be presented. The latter manifests in form of abdominal pain, tenderness over the inferior ribs, hiccup, dyspnea and tachycardia and non-productive cough. Pneumonia may develop. Additionally, gastrointestinal disorders like ileus may be reported. In some cases, pathological reduction of bowel movements may be the only symptom of an SA.

Abdominal wall tension increases if focal or generalized peritonitis develops; accordingly, an enhanced tension may be noted in the upper abdominal region, preferentially on the side of the abscess, or the whole abdomen may be affected. Patients with peritonitis have a high risk of developing sepsis, and sepsis is related to symptoms like high fever, hypotension, tachycardia, tachypnea, impairment of renal function and eventually shock and multiple organ failure.

Of note, persistence of post-operative symptoms and application of analgesics, anti-inflammatory drugs and possibly even antibiotics may mask this disease. This has been reported, for instance, in patients treated with microwave or radiofrequency ablation because of liver cancer [8].

Laboratory analyses of blood samples are usually carried out but reveal only unspecific leukocytosis, anemia and possibly enhanced concentrations of alanine transaminase and aspartate transaminase. Blood cultures may confirm bacteremia and if Bacteroides spp. or Clostridium spp. can be identified, the patient is highly suspicious for an intra-abdominal abscess. However, in order to diagnose a SA, imaging techniques have to be applied. Whereas plain radiography and sonography are valuable options, computed tomography scans constitute the most sensitive and specific approach [2].

SA corresponds to sub-diaphragmatic local masses with soft-tissue density, but are usually not the only pathological findings. The hemidiaphragm covering the abscess may bulge into the thoracic cavity and does not often contribute to respiration. Pleural effusion is common and anomalies may also be noted in the lungs: Signs of pneumonia or a lung abscess may be observed. With regards to the abdominal cavity, gas may become visible within the abscess and thus outside of the gastrointestinal tract. The use of contrast agents may be indicated to detect a possible site of leakage or perforation.

SA has to be drained, and patients need to be treated with antibiotics prior to and after drainage. Percutaneous drainage is the method of choice if the abscess is easily accessible. However, other routes of access may be chosen, e.g. an endoscopic, transgastric approach has been described. Utmost care has to be taken not to contaminate the tract of the catheter. This may lead to complications like recurrent SA or abscess formation in adjacent tissues [9]. In fact, open surgery may be the better option if there is a high risk of such complications, or if the properties of pus don't allow its passage through a catheter. In general though, the risk of post-laparotomy complications is significantly higher than that of contamination during catheter drainage. Patients may benefit from regular instillation of fibrinolytics into catheters [10].

With respect to drug therapy, the selection of an adequate antimicrobial is often based on empiric evidence. Although bacterial culture may be ordered after SA drainage and obtainment of a usable specimen, it can't usually be afforded to delay medical treatment until results are available. According to epidemiological studies, the most common bacteria encountered in SA belong to the family of Enterobacteriaceae (e.g., Escherichia coli, Klebsiella spp., Proteus spp.), the genera of Bacteroides and Clostridium. The latter are obligate anaerobic bacteria. There is barely a single antibiotic effective against all these pathogens and in many cases, more than one compound is prescribed. Anti-anaerobic cephalosporins or combinations of aminoglycosides and metronidazole have been proven effective in preventing bacterial spread before and after surgery.

SA is a potentially life-threatening disease and the prognosis may be worsened by existing comorbidities. With regards to SA and its complications, a poor outcome is often related to multiple abscesses and/or abscess formation after emergency interventions, even though the latter have apparently been carried out successfully. Also, intractable and recurrent abscesses are considered unfavorable prognostic factors. In sum, even recent publications still report mortality rates from 11 to 31% [7].

The vast majority of SA develops after perforation of the stomach or intestines and/or secondary to abdominal surgery carried out to treat gastrointestinal disorders. Gastric or duodenal ulcer, acute appendicitis as well as diverticulitis predispose for spontaneous perforation and are common causes of SA [2] [3]. Furthermore, a common medical history of a SA patient consists of ulcer, appendicitis, or diverticulitis, apparently successful treatment of this condition, and onset of SA-associated symptoms months later [4]. Consistently, most abscesses contain a plethora of aerobic and anaerobic bacterial species that form part of the gastrointestinal flora. Of note, translocation of intestinal bacteria does not require perforation of the respective hollow organ. Disorders like mesenteric artery thrombosis and subsequent mesenteric ischemia may imply serious damage of the bowel wall and increase permeability without producing intestinal perforation.

Moreover, a variety of non-gastrointestinal primary diseases may also lead to the formation of a SA. For instance, thoracic foci of infection, namely pneumonia, lung abscess and pleural empyema, may spread to the abdominal cavity and trigger a purulent inflammation here. Besides, tuberculosis has been related to SA only in isolated cases [5]. With regards to abdominal organs, gall bladder, liver, spleen and pancreas may serve as sources of pathogens if they present an infection, presumably induced during surgery. The possibility of an osteomyelitis leading to secondary SA has been described, but has rarely been reported.

Bacteria may also be inoculated upon perforating trauma, either directly into the abdominal cavity or into adjacent tissues.

Available epidemiological data date from several decades ago. Then, retrospective studies revealed changing patterns in causative events and etiologic agents of SA. Although gastrointestinal and biliary diseases that required surgical intervention have long since been the main cause of SA, the precise entities that account for the majority have changed. For instance, appendicitis was the main disease underlying SA formation in the middle of the 20th century, while its relative importance decreased until the 1970s. In contrast, colon surgery gained importance and even surpassed that of appendicitis during that same period in time [6].

These epidemiological developments presumably continued into the present time. On the one hand, constant improvement of sanitary conditions in operating rooms reduces the incidence of post-operative infection. On the other hand, advances in diagnostics allow for an early recognition of gastrointestinal diseases and thus augment the rate of abdominal surgery. At this moment, it can only be speculated which effect determines the development of overall incidence rates

Abscess formation marks an advanced stage of bacterial infection and inflammation. Thus, SA cannot form without pathogens reaching the upper abdominal cavity. According to the above described causes of SA, this may happen during a surgical intervention, when bacteria are involuntarily inoculated into the abdominal cavity; or if an infection spreads from adjacent tissues; or as a consequence of bacteremia. However, these are not necessarily unidirectional developments and pathogens contained in an SA may use these same routes for metastatic spread. Consequently, affected individuals are at risk of inflammation and/or abscess formation in peritoneum, liver, spleen and diaphragm. In fact, such disorders are possible comorbidities in SA patients. And because SA may serve as a source of bacteria that may eventually cause peritonitis, septicemia and multiple organ failure, it is a potentially life-threatening disease. This detrimental chain of pathophysiological events may be induced by abscess rupture, which initially causes an extensive inflammatory reaction in the abdominal cavity. Subsequent edema formation and extravasation of proteins are often severe and may cause shock. If pathogens gain access to circulation, they may spread to distant organs, trigger local inflammation and eventually organ failure.

No specific measures can be recommended to prevent SA.

Subphrenic abscess (SA) refers to the presence of a pus-filled, usually well-demarcated cavity in the upper abdomen and is caused by diverse bacterial species. Pathogens that reach this part of the abdominal cavity induce a local inflammatory reaction and adhesions between parietal and visceral peritoneum and omentum develop rapidly. To a certain degree, the focus of infection can be contained by these processes. While they helps to reduce the likelihood of generalized peritonitis - a secondary event that cannot be prevented in any case -, it does facilitate the formation of a SA.

As has been indicated above, SA contains distinct species of aerobic and anaerobic bacteria originating from the gastrointestinal tract. In fact, the majority of SA is diagnosed in people that either suffered a perforation of stomach or intestines, or that underwent abdominal surgery. In the latter scenario, pathogens may also originate from the digestive system (e.g., from an anastomotic leak), or they may have been involuntarily inoculated into the abdominal cavity. However, the possibility of lungs, pleura, gall bladder, liver, spleen and pancreas being the source of infection should also be considered in SA patients.

Symptoms arise from local infection and functional impairment of the diaphragm, potentially from secondary peritonitis and imminent shock. With regards to the former, dyspnea, upper abdominal pain that aggravates if pressure is exerted over ribs eight to eleven, and non-specific symptoms like malaise, fever, chills and loss of appetite usually manifest before detrimental consequences set in.

A single SA may be located on either side of the body, inferior of the diaphragm, but multiple SA or SA combined with distant foci of infection have also been described [1]. The precise location of a SA may guide the search for a possible source, if the latter cannot be deduced from anamnestic data and physical examination. It has to be noted though that overlooking either causative or consequential comorbidities may significantly worsen the outcome.

Diagnostic imaging, namely computed tomography, is a sensitive and specific technique to diagnose SA. Administration of antibiotics and abscess drainage are the mainstays of SA therapy. If treatment is initiated before the infection spreads any further, and if comorbidities don't imply a poor outcome, prognosis is generally good.

In general, the medical term abscess refers to the formation of a pus-filled cavity in a previously undefined space. This also applies to subphrenic abscess (SA), i.e., an abscess that forms below the diaphragm.

Under physiological conditions, the abdominal cavity is sterile. For a SA to develop, bacteria have to reach the upper abdomen, and this may happen if stomach or intestines perforate or if a patient has to undergo abdominal surgery. With regards to the former, gastric or duodenal ulcer, acute appendicitis as well as diverticulitis predispose for spontaneous perforation and are common causes of SA. Although any laparotomy bears the risk of involuntary inoculation of pathogens, surgical interventions to treat gastrointestinal disorders are most likely to lead to SA formation.

The incidence of SA is low, i.e., few patients who suffer from any of the above mentioned diseases or who undergo surgery will develop such an abscess. However, SA is potentially life-threatening. They interfere with respiration and bowel movements, but they also constitute a permanent source of bacteria that may spread to adjacent or distant tissues. Such complications may lead to peritonitis, sepsis and death.

Treatment mainly consists in drainage (possibly percutaneous) and antibiotic therapy. If the initiation of therapy is not unnecessarily delayed, the outcome is generally good. It is thus of utmost importance to report post-operative complications to the treating physician.

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