Stable patients presenting to A&E (accident and emergency department) or ER (emergency room) with severe abdominal pain will almost always have an abdominal x-ray and/or a CT scan. These tests can provide a differential diagnosis between simple and complex pathologies. However, in the unstable patient, fluid resuscitation and a FAST-ultrasound are done first, and if the latter is positive for free fluid, straight to surgery. They may also provide evidence to the doctor whether surgical intervention is necessary.

Patients will also most likely receive a complete blood count (or full blood count in the U.K.), looking for characteristic findings such as neutrophilia in appendicitis.

Traditionally, the use of opiates or other painkillers in patients with an acute abdomen has been discouraged before the clinical examination, because these would alter the examination. However, the scientific literature does not reveal any negative results from these alterations.

A diagnosis of peritonitis is based primarily on the clinical manifestations described above. Rigidity (involuntary contraction of the abdominal muscles) is the most specific exam finding for diagnosing peritonitis (+ likelihood ratio: 3.9). If peritonitis is strongly suspected, then surgery is performed without further delay for other investigations. Leukocytosis, hypokalemia, hypernatremia, and acidosis may be present, but they are not specific findings. Abdominal X-rays may reveal dilated, edematous intestines, although such X-rays are mainly useful to look for pneumoperitoneum, an indicator of gastrointestinal perforation. The role of whole-abdomen ultrasound examination is under study and is likely to expand in the future. Computed tomography (CT or CAT scanning) may be useful in differentiating causes of abdominal pain. If reasonable doubt still persists, an exploratory peritoneal lavage or laparoscopy may be performed. In patients with ascites, a diagnosis of peritonitis is made via paracentesis (abdominal tap): More than 250 polymorphonucleate cells per μL is considered diagnostic. In addition, Gram stain is almost always negative, whereas culture of the peritoneal fluid can determine the microorganism responsible and determine their sensitivity to antimicrobial agents.

In normal conditions, the peritoneum appears greyish and glistening; it becomes dull 2–4 hours after the onset of peritonitis, initially with scarce serous or slightly turbid fluid. Later on, the exudate becomes creamy and evidently suppurative; in dehydrated patients, it also becomes very inspissated. The quantity of accumulated exudate varies widely. It may be spread to the whole peritoneum, or be walled off by the omentum and viscera. Inflammation features infiltration by neutrophils with fibrino-purulent exudation.

On x-rays, gas may be visible in the abdominal cavity. Gas is easily visualized on x-ray while the patient is in an upright position. The perforation can often be visualised using computed tomography. White blood cells are often elevated.

Diagnosis is made by paracentesis (needle aspiration of the ascitic fluid). SBP is diagnosed if the fluid contains neutrophils (a type of white blood cell) at greater than 250 cells per mm (equals a cell count of 250 x10/L) fluid in the absence of another reason for this (such as inflammation of one of the internal organs or a perforation). The fluid is also cultured to identify bacteria. If the sample is sent in a plain sterile container 40% of samples will identify an organism, while if the sample is sent in a bottle with culture medium the sensitivity increases to 72–90%.

There may be signs of septic shock. A physical examination reveals abdominal tenderness and possible loss of bowel sounds. An abdominal radiography shows colonic dilation. White blood cell count is usually elevated. Severe sepsis may present with hypothermia or leukopenia.

All people with cirrhosis might benefit from antibiotics (oral fluoroquinolone norfloxacin) if:

- Ascitic fluid protein <1.0 g/dL. Patients with fluid protein <15 g/L and either Child-Pugh score of at least 9 or impaired renal function may also benefit.

- Previous SBP

People with cirrhosis admitted to the hospital should receive prophylactic antibiotics if:

- They have bleeding esophageal varices

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 differential diagnosis includes colon cancer, inflammatory bowel disease, ischemic colitis, and irritable bowel syndrome, as well as a number of urological and gynecological processes.

People with the above symptoms are commonly studied with computed tomography, or CT scan. The CT scan is very accurate (98%) in diagnosing diverticulitis. In order to extract the most information possible about the patient's condition, thin section (5 mm) transverse images are obtained through the entire abdomen and pelvis after the patient has been administered oral and intravascular contrast. Images reveal localized colon wall thickening, with inflammation extending into the fat surrounding the colon. The diagnosis of acute diverticulitis is made confidently when the involved segment contains diverticula. CT may also identify patients with more complicated diverticulitis, such as those with an associated abscess. It may even allow for radiologically guided drainage of an associated abscess, sparing a patient from immediate surgical intervention.

Other studies, such as barium enema and colonoscopy, are contraindicated in the acute phase of diverticulitis because of the risk of perforation.

The severity of diverticulitis can be radiographically graded by the Hinchey Classification.

Surgical intervention is nearly always required in form of exploratory laparotomy and closure of perforation with peritoneal wash. Occasionally they may be managed laparoscopically.

Conservative treatment including intravenous fluids, antibiotics, nasogastric aspiration and bowel rest is indicated only if the person is nontoxic and clinically stable.

Typhlitis is diagnosed with a radiograph CT scan showing thickening of the cecum and "fat stranding".

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.

The main diagnostic tools are blood tests, X-rays of the abdomen, CT scanning, and/or ultrasound. If a mass is identified, biopsy may determine the nature of the mass.

Radiological signs of bowel obstruction include bowel distension and the presence of multiple (more than six) gas-fluid levels on supine and erect abdominal radiographs.

Contrast enema or small bowel series or CT scan can be used to define the level of obstruction, whether the obstruction is partial or complete, and to help define the cause of the obstruction.

According to a meta-analysis of prospective studies by the Cochrane Collaboration, the appearance of water-soluble contrast in the cecum on an abdominal radiograph within 24 hours of oral administration predicts resolution of an adhesive small bowel obstruction with a pooled sensitivity of 97% and specificity of 96%.

Colonoscopy, small bowel investigation with ingested camera or push endoscopy, and laparoscopy are other diagnostic options.

Routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation should be performed. Most experts recommend a diagnostic paracentesis be performed if the ascites is new or if the patient with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as microbiological culture, Gram stain and cytopathology.

The "serum-ascites albumin gradient" (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites. A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive as a cause.

Ultrasound investigation is often performed prior to attempts to remove fluid from the abdomen. This may reveal the size and shape of the abdominal organs, and Doppler studies may show the direction of flow in the portal vein, as well as detecting Budd-Chiari syndrome (thrombosis of the hepatic vein) and portal vein thrombosis. Additionally, the sonographer can make an estimation of the amount of ascitic fluid, and difficult-to-drain ascites may be drained under ultrasound guidance. An abdominal CT scan is a more accurate alternate to reveal abdominal organ structure and morphology.

The diagnosis is usually suspected clinically but often requires the aid of diagnostic imaging modalities, most commonly radiography. Specific radiographic signs of NEC are associated with specific Bell's stages of the disease:

Bell's stage 1/Suspected disease:

- Mild systemic disease (apnea, lethargy, bradycardia, temperature instability)

- Mild intestinal signs (abdominal distention, increased gastric residuals, bloody stools)

- Non-specific or normal radiological signs

Bell's stage 2/Definite disease:

- Mild to moderate systemic signs

- Additional intestinal signs (absent bowel sounds, abdominal tenderness)

- Specific radiologic signs (pneumatosis intestinalis or portal venous air)

- Laboratory changes (metabolic acidosis, thrombocytopaenia)

Bell's stage 3/Advanced disease:

- Severe systemic illness (hypotension)

- Additional intestinal signs (striking abdominal distention, peritonitis)

- Severe radiologic signs (pneumoperitoneum)

- Additional laboratory changes (metabolic and respiratory acidosis, disseminated intravascular coagulation)

More recently ultrasonography has proven to be useful as it may detect signs and complications of NEC before they are evident on radiographs, specifically in cases that involve a paucity of bowel gas, a gasless abdomen, or a sentinel loop. Diagnosis is ultimately made in 5–10% of very low-birth-weight infants (<1,500g).

Once a child is born prematurely, thought must be given to decreasing the risk for developing NEC. Toward that aim, the methods of providing hyperalimentation and oral feeds are both important. In a 2012 policy statement, the American Academy of Pediatrics recommended feeding preterm infants human milk, finding "significant short- and long-term beneficial effects," including reducing the rate of NEC by a factor of two or more.

A study by researchers in Peoria, IL, published in "Pediatrics" in 2008, demonstrated that using a higher rate of lipid (fats and/or oils) infusion for very low birth weight infants in the first week of life resulted in zero infants developing NEC in the experimental group, compared with 14% with NEC in the control group. (They started the experimental group at 2 g/kg/d of 20% IVFE and increased within two days to 3 g/kg/d; amino acids were started at 3 g/kg/d and increased to 3.5.)

Neonatologists at the University of Iowa reported on the importance of providing small amounts of trophic oral feeds of human milk starting as soon as possible, while the infant is being primarily fed intravenously, in order to prime the immature gut to mature and become ready to receive greater oral intake. Human milk from a milk bank or donor can be used if mother's milk is unavailable. The gut mucosal cells do not get enough nourishment from arterial blood supply to stay healthy, especially in very premature infants, where the blood supply is limited due to immature development of the capillaries, so nutrients from the lumen of the gut are needed.

A Cochrane review published in April 2014 has established that supplementation of probiotics enterally "prevents severe NEC as well as all-cause mortality in preterm infants."

Increasing amounts of milk by 30 to 40 ml/kg is safe in infant who are born weighing very little. Not beginning feeding an infant by mouth for more than 4 days does not appear to have protective benefits.

Data from the NICHD Neonatal Research Network's Glutamine Trial showed that the incidence of NEC among extremely low birthweight (ELBW, <1000 g) infants fed with more than 98% human milk from their mothers was 1.3%, compared with 11.1% among infants fed only preterm formula, and 8.2% among infants fed a mixed diet, suggesting that infant deaths could be reduced by efforts to support production of milk by mothers of ELBW newborns.

Research from the University of California, San Diego found that higher levels of one specific human milk oligosaccharide, disialyllacto-N-tetraose, may be protective against the development of NEC.

Fetal and neonatal bowel obstructions are often caused by an intestinal atresia, where there is a narrowing or absence of a part of the intestine. These atresias are often discovered before birth via an ultrasound, and treated with using laparotomy after birth. If the area affected is small, then the surgeon may be able to remove the damaged portion and join the intestine back together. In instances where the narrowing is longer, or the area is damaged and cannot be used for a period of time, a temporary stoma may be placed.

Vascular disorders are more likely to affect the small bowel than the large bowel. Arterial supply to the intestines is provided by the superior and inferior mesenteric arteries (SMA and IMA respectively), both of which are direct branches of the aorta.

The superior mesenteric artery supplies:

1. Small bowel

2. Ascending and proximal two-thirds of the transverse colon

The inferior mesenteric artery supplies:

1. Distal one-third of the transverse colon

2. Descending colon

3. Sigmoid colon

Of note, the splenic flexure, or the junction between the transverse and descending colon, is supplied by the most distal portions of both the inferior mesenteric artery and superior mesenteric artery, and is thus referred to medically as a watershed area, or an area especially vulnerable to ischemia during periods of systemic hypoperfusion, such as in shock.

Acute abdomen of the ischemic variety is usually due to:

1. A thromboembolism from the left side of the heart, such as may be generated during atrial fibrillation, occluding the SMA.

2. Nonocclusive ischemia, such as that seen in hypotension secondary to heart failure, may also contribute, but usually results in a mucosal or mural infarct, as contrasted with the typically transmural infarct seen in thromboembolus of the SMA.

3. Primary mesenteric vein thromboses may also cause ischemic acute abdomen, usually precipitated by hypercoagulable states such as polycythemia vera.

Clinically, patients present with diffuse abdominal pain, bowel distention, and bloody diarrhea. On physical exam, bowel sounds will be absent. Laboratory tests reveal a neutrophilic leukocytosis, sometimes with a left shift, and increased serum amylase. Abdominal radiography will show many air-fluid levels, as well as widespread edema.

Acute ischemic abdomen is a surgical emergency. Typically, treatment involves removal of the region of the bowel that has undergone infarction, and subsequent anastomosis of the remaining healthy tissue.

In regards to the diagnosis of idiopathic sclerosing mesenteritis, a CT scan which creates cross-section pictures of the affected individuals body, can help in the assessment of the condition.

Twenty percent of infants born with meconium peritonitis will have vomiting and dilated bowels on x-rays which necessitates surgery.

Meconium peritonitis is sometimes diagnosed on prenatal ultrasound where it appears as calcifications within the peritoneum.

Ascites exists in three grades:

- Grade 1: mild, only visible on ultrasound and CT

- Grade 2: detectable with flank bulging and shifting dullness

- Grade 3: directly visible, confirmed with the fluid wave/thrill test

The Mayo Clinic in Rochester reported a large study of 92 patients, with widely ranging severity of their symptoms. The majority were male, with an average age of 65 years. They commonly had abdominal pain (70%), diarrhea (25%) and weight loss (23%). Depending on the stage of the scarring and fibrosis, several different treatments, including surgery for bowel obstruction, or drugs were used to halt the progression of the disease.

In that case series, 56% of patients received only pharmacological therapy, most often receiving tamoxifen with a reducing dose of reducing prednisone, or also had colchicine, azathioprine or thalidomide.

Their findings suggest that sclerosing mesenteritis can be debilitating although relatively benign. Symptomatic patients benefited from medical therapy, usually tamoxifen and prednisone, but further follow-up information would strengthen these results.

Meconium peritonitis refers to rupture of the bowel prior to birth, resulting in fetal stool (meconium) escaping into the surrounding space (peritoneum) leading to inflammation (peritonitis). Despite the bowel rupture, many infants born after meconium peritonitis "in utero" have normal bowels and have no further issues.

Infants with cystic fibrosis are at increased risk for meconium peritonitis.

Stercoral perforation is the perforation or rupture of the intestine's walls by its internal contents, such as foreign objects, or, more commonly, by hardened feces (fecalomas) which may form in long constipations or other diseases which cause obstruction of transit, such as Chagas disease, Hirschprung's disease, toxic colitis and megacolon.

Stercoral perforation is a very dangerous, life-threatening situation, as well as a surgical emergency, because the spillage of contaminated intestinal contents into the abdominal cavity leads to peritonitis, a rapid bacteremia (bacterial infection of the blood), with many complications.