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==Diagnosis== 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.<ref>Nishijima, D. K., Simel, D. L., Wisner, D. H., & Holmes, J. F. (2012). Does this adult patient have a blunt intra-abdominal injury?. JAMA, 307(14), 1517β1527. https://doi.org/10.1001/jama.2012.422</ref> If focal peritonitis is detected, further work-up should be done. If diffuse peritonitis is detected, then urgent surgical consultation should be obtained, and may warrant surgery without further 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 people with [[ascites]], a diagnosis of peritonitis is made via [[paracentesis]] (abdominal tap): More than 250 [[polymorphonuclear cells]] per ΞΌL 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.<ref>{{Cite journal |last1=Spalding |first1=Drc |last2=Williamson |first2=Rcn |date=January 2008 |title=Peritonitis |url=http://www.magonlinelibrary.com/doi/10.12968/hmed.2008.69.Sup1.28050 |journal=British Journal of Hospital Medicine |language=en |volume=69 |issue=Sup1 |pages=M12βM15 |doi=10.12968/hmed.2008.69.Sup1.28050 |pmid=18293728 |issn=1750-8460}}</ref><ref>{{Cite journal |last1=Ludlam |first1=H A |last2=Price |first2=T N |last3=Berry |first3=A J |last4=Phillips |first4=I |date=September 1988 |title=Laboratory diagnosis of peritonitis in patients on continuous ambulatory peritoneal dialysis |journal=Journal of Clinical Microbiology |volume=26 |issue=9 |pages=1757β1762 |doi=10.1128/jcm.26.9.1757-1762.1988 |pmid=3183023 |pmc=266711 |issn=0095-1137}}</ref> ===Pathology=== In normal conditions, the peritoneum appears greyish and glistening; it becomes dull 2β4 hours after the onset of peritonitis, initially with scarce [[serous]] or slightly [[turbid]] fluid. Later on, the [[exudate]] becomes creamy and evidently [[suppurative]]; in people who are dehydrated, 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 [[Greater omentum|omentum]] and [[viscera]]. [[Inflammation]] features infiltration by [[neutrophils]] with fibrino-purulent exudation.<ref>{{Cite journal |last1=Arvind |first1=Sharda |last2=Raje |first2=Shweta |last3=Rao |first3=Gayatri |last4=Chawla |first4=Latika |date=February 2019 |title=Laparoscopic Diagnosis of Peritoneal Tuberculosis |journal=[[Journal of Minimally Invasive Gynecology]] |language=en |volume=26 |issue=2 |pages=346β347 |doi=10.1016/j.jmig.2018.04.006|pmid=29680232 |s2cid=5041460 |doi-access=free }}</ref>
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