Peritonitis

Peritonitis
Classification and external resources
Pronunciation	/pɛrᵻtəˈnaɪtᵻs/
Specialty	General surgery
ICD-10	K65
ICD-9-CM	567
DiseasesDB	9860
MedlinePlus	001335
eMedicine	med/2737
Patient UK	Peritonitis
MeSH	D010538

Peritonitis is an inflammation of the peritoneum, the thin tissue that lines the inner wall of the abdomen and covers most of the abdominal organs. Peritonitis may be localized or generalized, and may result from infection (often due to rupture of a hollow abdominal organ as may occur in abdominal trauma or inflamed appendix) or from a non-infectious process.

Signs and symptoms

Abdominal pain and tenderness

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.^[1] 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.

Collateral manifestations

• Diffuse abdominal rigidity ("washboard stomach") is often present, especially in generalized peritonitis
• Fever
• Sinus tachycardia
• Development of ileus paralyticus (i.e., intestinal paralysis), which also causes nausea, vomiting and bloating.

Complications

• Sequestration of fluid and electrolytes, as revealed by decreased central venous pressure, may cause electrolyte disturbances, as well as significant hypovolemia, possibly leading to shock and acute renal failure.
• A peritoneal abscess may form (e.g., above or below the liver, or in the lesser omentum
• Sepsis may develop, so blood cultures should be obtained.
• Complicated peritonitis typically involves multiple organs.

Causes

Infected peritonitis

• Perforation of part of the gastrointestinal tract is the most common cause of peritonitis. Examples include perforation of the distal esophagus (Boerhaave syndrome), of the stomach (peptic ulcer, gastric carcinoma), of the duodenum (peptic ulcer), of the remaining intestine (e.g., appendicitis, diverticulitis, Meckel diverticulum, inflammatory bowel disease (IBD), intestinal infarction, intestinal strangulation, colorectal carcinoma, meconium peritonitis), or of the gallbladder (cholecystitis). Other possible reasons for perforation include abdominal trauma, ingestion of a sharp foreign body (such as a fish bone, toothpick or glass shard), perforation by an endoscope or catheter, and anastomotic leakage. The latter occurrence is particularly difficult to diagnose early, as abdominal pain and ileus paralyticus are considered normal in patients who have just undergone abdominal surgery. In most cases of perforation of a hollow viscus, mixed bacteria are isolated; the most common agents include Gram-negative bacilli (e.g., Escherichia coli) and anaerobic bacteria (e.g., Bacteroides fragilis). Fecal peritonitis results from the presence of faeces in the peritoneal cavity. It can result from abdominal trauma and occurs if the large bowel is perforated during surgery.
• Disruption of the peritoneum, even in the absence of perforation of a hollow viscus, may also cause infection simply by letting micro-organisms into the peritoneal cavity. Examples include trauma, surgical wound, continuous ambulatory peritoneal dialysis, and intra-peritoneal chemotherapy. Again, in most cases, mixed bacteria are isolated; the most common agents include cutaneous species such as Staphylococcus aureus, and coagulase-negative staphylococci, but many others are possible, including fungi such as Candida.
• Spontaneous bacterial peritonitis (SBP) is a peculiar form of peritonitis occurring in the absence of an obvious source of contamination. It occurs in patients with ascites, in particular, in children.
• Intra-peritoneal dialysis predisposes to peritoneal infection (sometimes named "primary peritonitis" in this context).
• Systemic infections (such as tuberculosis) may rarely have a peritoneal localisation.
• Pelvic inflammatory disease^[2]

Non-infected peritonitis

• Leakage of sterile body fluids into the peritoneum, such as blood (e.g., endometriosis, blunt abdominal trauma), gastric juice (e.g., peptic ulcer, gastric carcinoma), bile (e.g., liver biopsy), urine (pelvic trauma), menstruum (e.g., salpingitis), pancreatic juice (pancreatitis), or even the contents of a ruptured dermoid cyst. It is important to note that, while these body fluids are sterile at first, they frequently become infected once they leak out of their organ, leading to infectious peritonitis within 24 to 48 hours.
• Sterile abdominal surgery, under normal circumstances, causes localised or minimal generalised peritonitis, which may leave behind a foreign body reaction and/or fibrotic adhesions. However, peritonitis may also be caused by the rare case of a sterile foreign body inadvertently left in the abdomen after surgery (e.g., gauze, sponge).
• Much rarer non-infectious causes may include familial Mediterranean fever, TNF receptor associated periodic syndrome, porphyria, and systemic lupus erythematosus.

Risk factors

• Previous history of peritonitis
• History of alcoholism
• Liver disease
• Fluid accumulation in the abdomen
• Weakened immune system
• Pelvic inflammatory disease

Diagnosis

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.

Pathology

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.

Treatment

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 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.^[3] 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.^[4] The exception is spontaneous bacterial peritonitis, which does not always benefit from surgery and may be treated with antibiotics in the first instance.

Prognosis

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 patient. The mortality rate rises to about 40% in the elderly, and/or in those with significant underlying illness, as well as in cases that present late (after 48 hours).

If untreated, generalised peritonitis is almost always fatal.

Notable cases

• On May 13, 1864, 21-year-old Private William Christman of Pennsylvania, who had died of peritonitis, became the first military man buried at Arlington.
• American poet Henry Wadsworth Longfellow also died due to peritonitis on Friday March 24, 1882.
• 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.^[5][6]
• On October 31, 1926, 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.^[7][8]
• In 1947, drummer Ringo Starr of the Beatles contracted peritonitis, falling into a coma for three days as a result.^[9] He contracted it again on April 28, 1979.^[10]
• Rhythm and blues singer Chuck Willis died from peritonitis in 1958 at the peak of his popularity.
• 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.
• 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.^[11]
• 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.^[12]

References

1. "Biology Online's definition of peritonism". Retrieved 2008-08-14.
2. Ljubin-Sternak, Suncanica; Mestrovic, Tomislav (2014). "Review: Clamydia trachonmatis and Genital Mycoplasmias: Pathogens with an Impact on Human Reproductive Health". Journal of Pathogens 2014 (183167): 1. doi:10.1155/2014/183167. PMC 4295611. PMID 25614838.
3. Appropriate Prescribing of Oral Beta-Lactam Antibiotics
4. "Peritonitis: Emergencies: Merck Manual Home Edition". Retrieved 2007-11-25.
5. "Valentino Loses Battle With Death: Greatest of Screen Lovers Fought Valiantly For Life" (PDF). The Plattsburgh Sentinel. Associated Press. August 24, 1926. p. 1. Retrieved 2010-05-15.
6. Gilbert King (13 June 2012). "The "Latin Lover" and His Enemies". Smithsonian.com. Smithsonian Institution. Retrieved 30 May 2014.
7. Kalush, William; Sloman, Larry (October 2006). The Secret Life of Houdini: The Making of America's First Superhero. Simon & Schuster. ISBN 978-0-7432-7207-0.
8. SmarterEveryDay (26 December 2013). "How Houdini DIED (in Slow Motion) - Smarter Every Day 108" (Video upload). SmarterEveryDay on YouTube. Google, Inc. Retrieved 30 May 2014.
9. Womack, Kenneth. Beatles Encyclopedia, The: Everything Fab Four: Everything Fab Four.
10. Harry, Bill. The Ringo Starr Encyclopedia.
11. Lentz, Robert J. (2011). Gloria Grahame, Bad Girl of Film Noir: The Complete Career. Mcfarland. ISBN 0-786-43483-X.
12. Worsley, Henry. BBC News: Explorer Henry Worsley dies in Antarctic crossing.

External links

• Peritonitis disease causes, treatment treatment basis
• Article on peritonitis at AllRefer.com
• Genuit T and Napolitano L. 2004. Peritonitis and Abdominal Sepsis at Emedicine.com
• Peritonitis at HealthCentral.com
• openabdomen.org - Peritonitis, Medical and Surgical Therapy Reviewed
• Microbiology for Surgical Infections. Diagnosis, Prognosis and Treatment (Eds Kateryna Kon and Mahendra Rai). Elsevier, 2014. http://www.sciencedirect.com/science/book/9780124116290