The main manifestations of peritonitis are acute abdominal pain, abdominal tenderness and abdominal guarding, which are exacerbated by moving the peritoneum, e.g., coughing (forced cough may be used as a test), flexing one's hips, or eliciting the Blumberg sign (a.k.a. rebound tenderness, meaning that pressing a hand on the abdomen elicits less pain than releasing the hand abruptly, which will aggravate the pain, as the peritoneum snaps back into place). The presence of these signs in a patient is sometimes referred to as peritonism. The localization of these manifestations depends on whether peritonitis is localized (e.g., appendicitis or diverticulitis before perforation), or generalized to the whole abdomen. In either case, pain typically starts as a generalized abdominal pain (with involvement of poorly localizing innervation of the visceral peritoneal layer), and may become localized later (with the involvement of the somatically innervated parietal peritoneal layer). Peritonitis is an example of an acute abdomen.
A diagnosis of peritonitis is based primarily on the clinical manifestations described above. 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.
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 targeted 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.
The Swiss Freudian psychiatrist and psychoanalyst Hermann Rorschach, best known for developing a projective test known as the Rorschach inkblot test, died of peritonitis in 1922 at the age of 37.
Artist George Bellows died of peritonitis on January 8, 1925 after failing to tend to a ruptured appendix.
Actor Rudolph Valentino died of peritonitis on August 23, 1926, after suffering a ruptured appendix. He also developed pleuritis in his left lung and died several hours after entering into a comatose state.
On October 31, 1926, famous magician and escape artist Harry Houdini died of peritonitis due to a surprise stomach punch. Many believe that it was a fan who Houdini willingly asked to punch him (as this was indeed part of his act), but in reality, it was a surprise by a man named Jocelyn Gordon Whitehead. It is possible, however, that the punch was only the tipping point, and the stomach punches over the years weakened his stomach muscles more and more.
Japanese professional wrestling legend Rikidōzan died of peritonitis on 15 December 1963 after being stabbed in the abdomen by a urine soaked knife by a member of the Yakuza a week prior.
Kenneth Pinyan, age 45, died in 2005 in what became known as the Enumclaw horse sex case. Pinyan had engaged in receptive anal sex with a horse, leading to his death due to acute peritonitis.
Henry Worsley died on 24 January 2016 while attempting to be the first person to cross the Antarctic unaided due to bacterial peritonitis, and died of "complete organ failure" after he had covered 913 miles and only had 30 miles to go. He had spent 71 days travelling out of an expected 75.
Actress Gloria Grahame contracted peritonitis and died in 1981 after a doctor accidentally punctured her bowel during a procedure to drain excess fluid from her abdomen.