Patients with ascites underwent routine paracentesis, the incidence of active SBP ranged from 10% to 27% at the time of hospital admission.

Infection of the peritoneal fluid (ascites) with gram-negative bacteria is the most common cause of SBP. The most frequently isolated gram negative bacterial species in ascitic fluid from those with SBP are "E. coli" and "Klebsiella". Gram-positive cocci species, such as "streptococci" and "staphylococci", have historically been responsible for less than 25% of SBP cases though the incidence of such cases has been increasing. Anaerobic and fungal infections of the ascitic fluid are rare but have been reported with organisms such as "Aeromonas", "Bordetella bronchiseptica", "Candida" species, "Salmonella paratyphi A", and "Pasteurella multocida".

Inflammation can spread to other parts of the gut in patients with typhlitis. The condition can also cause the cecum to become distended and can cut off its blood supply. This and other factors can result in necrosis and perforation of the bowel, which can cause peritonitis and sepsis.

Historically, the mortality rate for typhlitis was as high as 50%, mostly because it is frequently associated with bowel perforation. More recent studies have demonstrated better outcomes with prompt medical management, generally with resolution of symptoms with neutrophil recovery without death

If properly treated, typical cases of surgically correctable peritonitis (e.g., perforated peptic ulcer, appendicitis, and diverticulitis) have a mortality rate of about <10% in otherwise healthy patients. The mortality rate rises to about 40% in the elderly, or in those with significant underlying illness, as well as cases that present late (after 48 hours).

Without being treated, generalised peritonitis almost always causes death. The stage magician Harry Houdini died this way, having contracted streptococcus peritonitis after his appendix ruptured and was removed too late to prevent spread of the infection.

Depending on the severity of the patient's state, the management of peritonitis may include:

- General supportive measures such as vigorous intravenous rehydration and correction of electrolyte disturbances.

- Antibiotics are usually administered intravenously, but they may also be infused directly into the peritoneum. The empiric choice of broad-spectrum antibiotics often consist of multiple drugs, and should be targeted against the most likely agents, depending on the cause of peritonitis (see above); once one or more agents are actually isolated, therapy will of course be target on them.

- Gram positive and gram negative organisms must be covered. Out of the cephalosporins, cefoxitin and cefotetan can be used to cover gram positive bacteria, gram negative bacteria, and anaerobic bacteria. Beta-lactams with beta lactamase inhibitors can also be used, examples include ampicillin/sulbactam, piperacillin/tazobactam, and ticarcillin/clavulanate. Carbapenems are also an option when treating primary peritonitis as all of the carbapenems cover gram positives, gram negatives, and anaerobes except for ertapenem. The only fluoroquinolone that can be used is moxifloxacin because this is the only fluoroquinolone that covers anaerobes. Finally, tigecycline is a tetracycline that can be used due to its coverage of gram positives and gram negatives. Empiric therapy will often require multiple drugs from different classes.

- Surgery (laparotomy) is needed to perform a full exploration and lavage of the peritoneum, as well as to correct any gross anatomical damage that may have caused peritonitis. The exception is spontaneous bacterial peritonitis, which does not always benefit from surgery and may be treated with antibiotics in the first instance.

Typhlitis is a medical emergency and requires prompt management. Untreated typhlitis has a poor prognosis, particularly if associated with pneumatosis intestinalis (air in the bowel wall) and/or bowel perforation, and has significant morbidity unless promptly recognized and aggressively treated.

Successful treatment hinges on:

1. Early diagnosis provided by a high index of suspicion and the use of CT scanning

2. Nonoperative treatment for uncomplicated cases

3. Empiric antibiotics, particularly if the patient is neutropenic or at other risk of infection.

In rare cases of prolonged neutropenia and complications such as bowel perforation, neutrophil transfusions can be considered but have not been studied in a randomized control trial. Elective right hemicolectomy may be used to prevent recurrence but is generally not recommended

"...The authors have found nonoperative treatment highly effective in patients who do not manifest signs of peritonitis, perforation, gastrointestinal hemorrhage, or clinical deterioration. Recurrent typhlitis was frequent after conservative therapy (recurrence rate, 67 percent), however," as based on studies from the 1980s

The newborn`s exposure to the maternal vaginal bacterial flora which contains aerobic and anaerobic bacterial flora can lead to the development of anaerobic bacterial infection. These infections include cellulitis of the site of fetal monitoring (caused by "Bacterodes" spp.), bacteremia, aspiration pneumonia (caused by "Bacterodes" spp.), conjunctivitis (caused by clostridia,) omphalitis (caused by mixed flora), and infant botulism. Clostridial species may play a role in necrotizing enterocolitis. Management of these infection necessitates treating of the underlying condition(s) when present, and administration of proper antimicrobial therapy

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.

Pylephlebitis (also called pyelophlebitis and infective suppurative thrombosis of the portal vein) is an uncommon thrombophlebitis of the portal vein or any of its branches (i.e. a portal vein thrombosis) that is caused by infection. It is usually a complication of intraabdominal sepsis, most often following diverticulitis, perforated appendicitis, or peritonitis. Considered uniformly lethal in the pre-antibiotic era, it still carries a mortality of 10-30%.

It typically presents with fever, rigors, and right upper quadrant abdominal pain, but sometimes abdominal pain may be absent. Liver function test abnormalities are usually present but frank jaundice is uncommon. In the modern era, it is usually diagnosed by CT scans of the abdomen and pelvis. Bacteriology is often polymicrobial and blood cultures are positive in some cases. A significant fraction of people presenting with this condition have an underlying hypercoagulable state.

Treatment is with a prolonged course of broad-spectrum antibiotics, with the addition of anticoagulants if other clots are present outside the portal vein or if fever persists on antibiotic therapy.

It is a cause of portal hypertension and can cause bowel ischemia sometimes leading to bowel infarction.

Intraabdominal infection (IAI) is a group of infections that occur within the abdominal cavity. They vary from appendicitis to fecal peritonitis. Risk of death despite treatment is often high.

The epidemiology of TOA is closely related to that of pelvic inflammatory disease which is estimated to one million people yearly.

Subphrenic abscess is a disease characterized by an accumulation of infected fluid between the diaphragm, liver, and spleen. This abscess develops after surgical operations like splenectomy.

Presents with cough, increased respiratory rate with shallow respiration, diminished or absent breath sounds, hiccups, dullness in percussion, tenderness over the 8th–11th ribs, fever, chills, anorexia and shoulder tip pain on the affected side. Lack of treatment or misdiagnosis could quickly lead to sepsis, septic shock, and death. It is also associated with peritonitis.

Most people with appendicitis recover easily after surgical treatment, but complications can occur if treatment is delayed or if peritonitis occurs. Recovery time depends on age, condition, complications, and other circumstances, including the amount of alcohol consumption, but usually is between 10 and 28 days. For young children (around 10 years old), the recovery takes three weeks.

The possibility of peritonitis is the reason why acute appendicitis warrants speedy evaluation and treatment. People with suspected appendicitis may have to undergo a medical evacuation. Appendectomies have occasionally been performed in emergency conditions (i.e., not in a proper hospital), when a timely medical evacuation was impossible.

Typical acute appendicitis responds quickly to appendectomy and occasionally will resolve spontaneously. If appendicitis resolves spontaneously, it remains controversial whether an elective interval appendectomy should be performed to prevent a recurrent episode of appendicitis. Atypical appendicitis (associated with suppurative appendicitis) is more difficult to diagnose and is more apt to be complicated even when operated early. In either condition, prompt diagnosis and appendectomy yield the best results with full recovery in two to four weeks usually. Mortality and severe complications are unusual but do occur, especially if peritonitis persists and is untreated.

Another entity known as appendicular lump is talked about. It happens when the appendix is not removed early during infection and omentum and intestine adhere to it, forming a palpable lump. During this period, surgery is risky unless there is pus formation evident by fever and toxicity or by USG. Medical management treats the condition.

An unusual complication of an appendectomy is "stump appendicitis": inflammation occurs in the remnant appendiceal stump left after a prior incomplete appendectomy. Stump appendicitis can occur months to years after initial appendectomy and can be identified with imaging modalities like ultrasound.

Complications of TOA are related to the possible removal of one or both ovaries and fallopian tubes. Without these reproductive structures, fertility can be affected. Surgical complications can develop and include:

- Allergic shock due to anesthetics

- A paradoxical reaction to a drug

- Infection

Emergency action may be required if severe abdominal pain develops, particularly if it is accompanied by fever, rapid heart rate, tenderness when the abdomen is pressed, bloody diarrhea, frequent diarrhea, or painful bowel movements.

Colonoscopy is contraindicated, as it may rupture the dilated colon resulting in peritonitis and septic shock.

Causes of high serum-ascites albumin gradient (SAAG or transudate) are:

- Cirrhosis – 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)

- Heart failure – 3%

- Hepatic venous occlusion: Budd–Chiari syndrome or veno-occlusive disease

- Constrictive pericarditis

- Kwashiorkor (childhood protein-energy malnutrition)

Causes of low SAAG ("exudate") are:

- Cancer (metastasis and primary peritoneal carcinomatosis) – 10%

- Infection: Tuberculosis – 2% or spontaneous bacterial peritonitis

- Pancreatitis – 1%

- Serositis

- Nephrotic syndrome

- Hereditary angioedema

Other rare causes:

- Meigs syndrome

- Vasculitis

- Hypothyroidism

- Renal dialysis

- Peritoneum mesothelioma

- Abdominal tuberculosis

In the majority of cases, amoebas remain in the gastrointestinal tract of the hosts. Severe ulceration of the gastrointestinal mucosal surfaces occurs in less than 16% of cases. In fewer cases, the parasite invades the soft tissues, most commonly the liver. Only rarely are masses formed (amoebomas) that lead to intestinal obstruction.(Mistaken for Ca caecum and appendicular mass) Other local complications include bloody diarrhea, pericolic and pericaecal abscess.

Complications of hepatic amoebiasis includes subdiaphragmatic abscess, perforation of diaphragm to pericardium and pleural cavity, perforation to abdominal cavital "(amoebic peritonitis)" and perforation of skin "(amoebiasis cutis)".

Pulmonary amoebiasis can occur from hepatic lesion by haemotagenous spread and also by perforation of pleural cavity and lung. It can cause lung abscess, pulmono pleural fistula, empyema lung and broncho pleural fistula. It can also reach the brain through blood vessels and cause amoebic brain abscess and amoebic meningoencephalitis. Cutaneous amoebiasis can also occur in skin around sites of colostomy wound, perianal region, region overlying visceral lesion and at the site of drainage of liver abscess.

Urogenital tract amoebiasis derived from intestinal lesion can cause amoebic vulvovaginitis "(May's disease)", rectovesicle fistula and rectovaginal fistula.

"Entamoeba histolytica" infection is associated with malnutrition and stunting of growth.

Acute appendicitis seems to be the end result of a primary obstruction of the appendix. Once this obstruction occurs, the appendix becomes filled with mucus and swells. This continued production of mucus leads to increased pressures within the lumen and the walls of the appendix. The increased pressure results in thrombosis and occlusion of the small vessels, and stasis of lymphatic flow. At this point spontaneous recovery rarely occurs. As the occlusion of blood vessels progresses, the appendix becomes ischemic and then necrotic. As bacteria begin to leak out through the dying walls, pus forms within and around the appendix (suppuration). The end result is appendiceal rupture (a 'burst appendix') causing peritonitis, which may lead to sepsis and eventually death. These events are responsible for the slowly evolving abdominal pain and other commonly associated symptoms.

The causative agents include bezoars, foreign bodies, trauma, intestinal worms, lymphadenitis and, most commonly, calcified fecal deposits that are known as appendicoliths or fecoliths. The occurrence of obstructing fecaliths has attracted attention since their presence in people with appendicitis is higher in developed than in developing countries. In addition an appendiceal fecalith is commonly associated with complicated appendicitis. Fecal stasis and arrest may play a role, as demonstrated by people with acute appendicitis having fewer bowel movements per week compared with healthy controls.

The occurrence of a fecalith in the appendix was thought to be attributed to a right-sided fecal retention reservoir in the colon and a prolonged transit time. However, a prolonged transit time was not observed in subsequent studies. From epidemiological data, it has been stated that diverticular disease and adenomatous polyps were unknown and colon cancer exceedingly rare in communities exempt from appendicitis. And acute appendicitis has been shown to occur antecedent to cancer in the colon and rectum. Several studies offer evidence that a low fiber intake is involved in the pathogenesis of appendicitis. This low intake of dietary fiber is in accordance with the occurrence of a right-sided fecal reservoir and the fact that dietary fiber reduces transit time.

If the condition does not improve, the risk of death is significant. In case of poor response to conservative therapy, a colectomy is usually required.

In Germany, 90% of cases of infectious enteritis are caused by four pathogens, Norovirus, Rotavirus, "Campylobacter" and "Salmonella". Other common causes of infectious enteritis include bacteria such as "Shigella" and "E. coli," as well as viruses such as adenovirus, astrovirus and calicivirus. Other less common pathogens include "Bacillus cereus, Clostridium perfringens, Clostridium difficile" and "Staphylococcus aureus".

"Campylobacter jejuni" is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in 2 year old and smaller children with diarrhoea. It has been linked to consumption of contaminated water and food, most commonly poultry and milk. The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.

Rotavirus is responsible for infecting 140 million people and causing 1 million deaths each year, mostly in children younger than 5 years. This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world. It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility. The net result of these changes is induced diarrhoea.

Enteritis necroticans is an often fatal illness, caused by β-toxin of "Clostridium perfringens". This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in developing countries, however has also been documented in post-World War II Germany. Risk factors for enteritis necroticans include decreased trypsin activity, which prevent intestinal degradation of the toxin, and reduced intestinal motility, which increases likelihood of toxin accumulation.

The differential diagnoses of acute abdomen include but are not limited to:

1. Acute appendicitis

2. Acute peptic ulcer and its complications

3. Acute cholecystitis

4. Acute pancreatitis

5. Acute intestinal ischemia (see section below)

6. Acute diverticulitis

7. Ectopic pregnancy with tubal rupture

8. Ovarian torsion

9. Acute peritonitis (including hollow viscus perforation)

10. Acute ureteric colic

11. Bowel volvulus

12. Bowel obstruction

13. Acute pyelonephritis

14. Adrenal crisis

15. Biliary colic

16. Abdominal aortic aneurysm

17. Familial Mediterranean fever

18. Hemoperitoneum

19. Ruptured spleen

20. Kidney stone

21. Sickle cell anaemia

Complications involve portal vein thrombosis and splenic vein thrombosis: clotting of blood affects the hepatic portal vein or varices associated with splenic vein. This can lead to portal hypertension and reduction in blood flow. When a liver cirrhosis patient is suffering from thrombosis, it is not possible to perform a liver transplant, unless the thrombosis is very minor. In case of minor thrombosis, there are some chances of survival using cadaveric liver transplant.

Causes (listed in order of decreasing frequency) include endometritis, urinary tract infection, pneumonia/atelectasis, wound infection, and septic pelvic thrombophlebitis. Septic risk factors for each condition are listed in order of the postpartum day (PPD) on which the condition generally occurs.

- PPD 0: atelectasis risk factors include general anesthesia, cigarette smoking, and obstructive lung disease.

- PPD 1–2: urinary tract infections risk factors include multiple catheterization during labor, multiple vaginal examinations during labor, and untreated bacteriuria.

- PPD 2–3: endometritis ( the most common cause ) risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and multiple vaginal examinations during labor.

- PPD 4–5: wound infection risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and multiple vaginal examination during labor.

- PPD 5–6: septic pelvic thrombophlebitis risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and diffuse difficult vaginal childbirth.

- PPD 7–21: mastitis risk factors include nipple trauma from breastfeeding.

Ischemic enteritis is uncommon compared to ischemic colitis due to the highly vascularised nature of the small intestine, allowing for sufficient blood flow in most situations. It develops due to circulatory shock of mesenteric vessels in the absence of major vessel occlusion, often associated with an underlying condition such as hypertension, arrhythmia or diabetes. Thus it has been considered to be associated with atherosclerosis. Surgical treatment is usually required due to the likelihood of stenosis or complete occlusion of the small intestine. Ischemic damage can range from mucosal infarction, which is limited only to the mucosa; mural infarction of the mucosa and underlying submucosa; to transmural infarction of the full thickness of the gastrointestinal wall. Mucosal and mural infarcts in and of themselves may not be fatal, however may progress further to a transmural infarct. This has the potential for perforation of the wall, leading to peritonitis.

In 2010 it caused about 55,000 deaths worldwide down from 68,000 in 1990.

In older textbooks it is often stated that 10% of the world's population is infected with "Entamoeba histolytica". It is now known that at least 90% of these infections are due to "E. dispar". Nevertheless, this means that there are up to 50 million true "E. histolytica" infections and approximately seventy thousand die each year, mostly from liver abscesses or other complications. Although usually considered a tropical parasite, the first case reported (in 1875) was actually in St Petersburg in Russia, near the Arctic Circle. Infection is more common in warmer areas, but this is both because of poorer hygiene and the parasitic cysts surviving longer in warm moist conditions.