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 Table of Contents  
Year : 2016  |  Volume : 11  |  Issue : 4  |  Page : 234-235

Epiploic appendagitis: An addition to the differential of acute abdomen in systemic sclerosis

1 Department of Internal Medicine and Rheumatology, Asian Institute of Medical Sciences, Faridabad, Haryana, India
2 Department of Radiodiagnosis, Asian Institute of Medical Sciences, Faridabad, Haryana, India
3 Department of Gastroenterology, Asian Institute of Medical Sciences, Faridabad, Haryana, India
4 Department of Surgery, Asian Institute of Medical Sciences, Faridabad, Haryana, India

Date of Web Publication8-Nov-2016

Correspondence Address:
Dr. Punit Pruthi
Department of Internal Medicine and Rheumatology, Asian Institute of Medical Sciences, Sector - 21/A Faridabad, Haryana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-3698.193590

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Keywords: Abdominal pain, acute abdomen, epiploic appendagitis, systemic sclerosis

How to cite this article:
Pruthi P, Singh AP, Kumar R, Prakash V, Munganda H. Epiploic appendagitis: An addition to the differential of acute abdomen in systemic sclerosis. Indian J Rheumatol 2016;11:234-5

How to cite this URL:
Pruthi P, Singh AP, Kumar R, Prakash V, Munganda H. Epiploic appendagitis: An addition to the differential of acute abdomen in systemic sclerosis. Indian J Rheumatol [serial online] 2016 [cited 2021 Apr 14];11:234-5. Available from:

A 53-year-old female who was known to have limited cutaneous systemic sclerosis (SSc) for around 15 years with organ involvement in the form of chronic skin tightening, Raynaud's phenomenon, mild inflammatory joint symptoms, gastroesophageal reflux disease, and Barrett's esophagus, presented with complaints of sudden onset severe right sided abdominal pain, nausea, fever, and reduced oral intake for the last 6 days. She was on low dose corticosteroids, proton pump inhibitors, prokinetics, and sustained release nifedipine before the presentation. On per abdomen examination, she was found to have tenderness (without rebound) over the right lumbar region, guarding, and normal bowel sounds.

She was investigated on the lines of acute abdomen. Her plain radiograph of abdomen neither show air-fluid levels nor evidence of perforation and chest X-ray was also normal. Ultrasound abdomen showed probe tenderness over the right lumbar region, fatty infiltration of liver and no significant pathology of appendix, pancreas, or kidneys. Her hematological parameters were: Hemoglobin 10.6 g/dl, total leukocyte count 4300/mm 3, platelet count 430,000/mm 3, and erythrocyte sedimentation rate of 73 mm/h (normal <20). Coagulation profile liver and kidney function tests were all normal. Her serum amylase was raised (602 U/ml, normal 25–125) but lipase was normal (66 U/ml, normal <65). Her blood culture was sterile, and urine examination was normal. Based on the clinical, laboratory, and radiological findings a provisional diagnosis of acute diverticulitis was kept, and she was started on intravenous fluid, ceftriaxone, metronidazole along with antiemetics and pantoprazole. Contrast-enhanced computed tomography (CT) scan of abdomen was done to confirm the diagnosis which revealed findings suggestive of epiploic appendagitis emailArticle.asp?issn=0973-3698;year=2016;volume=11;issue=4;spage=234;epage=235;aulast=Pruthi [Figure 1]. She was treated conservatively and became completely asymptomatic on day 6 of the illness. In view of spontaneous venous thrombosis thought to be one of the causes of EA her complete antiphospholipid antibody screen was done which was negative. She continues to be asymptomatic for more than 9 months after this event.
Figure 1: Contrast enhanced axial computed tomography image of abdomen. A 19 mm × 9 mm fat containing oval mass with thin hyperattenuating ring and increased surrounding fat density anterior to proximal ascending colon suggestive of epiploic appendagitis

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SSc may affect the gastrointestinal (GI) tract in around 90% of patients of whom almost 50% are symptomatic.[1],[2],[3] The most commonly involved GI structure is esophagus, and most common manifestation is gastroesophageal reflux.[1],[2] Stomach, small intestine, colon, and anorectal region may also be involved resulting in stomach dilatation, malabsorption, megacolon, chronic constipation, and fecal incontinence.[1],[2]

Acute abdominal crisis in an SSc patient is usually a result of acute diverticulitis, pseudo-obstruction of intestine and rarely due to small bowel perforation, pneumatosis cystoides intestinalis, small bowel volvulus, and acute pancreatitis.[1],[2],[3]

EA as a cause of acute abdominal pain in patients suffering from SSc or other connective tissue diseases has not yet been described in medical literature. The exact incidence of EA in the general population is not known, and it has been reported in 2–7 percent of patients who were suspected of having acute diverticulitis and in 0.3–1% of suspected acute appendicitis cases.[4] Epiploic appendages are small 1–2 cm thick and 0.5–5 cm long outpouchings of fat filled serosa covered structures present on the external surface of the colon projecting into the peritoneal cavity, each supplied by small branches of colonic end arteries and a small draining vein.[5] EA is an ischemic infarction of an epiploic appendage, which is caused either by torsion of an abnormally long appendage or due to spontaneous thrombosis of the central vein as the primary event.[5]

Clinical presentation is usually acute localized lower abdominal pain more commonly on the left side corresponding to the most commonly involved portion of the colon, i.e., rectosigmoid, along with other symptoms such as vomiting, bloating, diarrhea, and fever.[5],[6] The clinical picture may mimic acute diverticulitis, acute appendicitis, omental infarction, and mesenteric panniculitis.[4],[5],[6] Diagnosis is usually made by CT scan [5] which shows findings similar to those seen in this particular case [Figure 1]. A high attenuated central dot within the inflamed appendage that corresponds to a thrombosed appendageal draining vein is occasionally evident.[5] EA is usually a benign and self-limiting condition with majority of cases responding to analgesics and supportive treatment.[4],[6] The surgical option is considered in complicated cases such as the development of an abscess, bowel obstruction, intussusception or in cases whose symptoms do not improve with conservative management.[4],[6]

It is possible that vasculopathy of SSc may have contributed to the development of venous thrombosis or altered vascular dynamics thereby causing EA. In SSc patients presenting with acute abdomen, EA should also be considered as a differential so as to avoid unnecessary surgical exploration of the abdomen, as it is usually a self-limiting condition.

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  References Top

Boin F, Wigley FM. Clinical features and treatment of scleroderma. In: Firestein GS, Budd RC, Gabriel SE, McInnes IB, O'Dell JR, editors. Kelley's Textbook of Rheumatology. 9th ed. Philadelphia: Saunders; 2013. p. 1380-3.  Back to cited text no. 1
Domsic R, Fasanella K, Bielefeldt K. Gastrointestinal manifestations of systemic sclerosis. Dig Dis Sci 2008;53:1163-74.  Back to cited text no. 2
Hansi N, Thoua N, Carulli M, Chakravarty K, Lal S, Smyth A, et al. Consensus best practice pathway of the UK scleroderma study group: Gastrointestinal manifestations of systemic sclerosis. Clin Exp Rheumatol 2014;32 6 Suppl 86:S-214-21.  Back to cited text no. 3
Schnedl WJ, Krause R, Tafeit E, Tillich M, Lipp RW, Wallner-Liebmann SJ. Insights into epiploic appendagitis. Nat Rev Gastroenterol Hepatol 2011;8:45-9.  Back to cited text no. 4
Almeida AT, Melão L, Viamonte B, Cunha R, Pereira JM. Epiploic appendagitis: An entity frequently unknown to clinicians – Diagnostic imaging, pitfalls, and look-alikes. AJR Am J Roentgenol 2009;193:1243-51.  Back to cited text no. 5
Vázquez GM, Manzotti ME, Alessandrini G, Lemos S, Perret MC, Catalano HN. Primary epiploic appendagitis: Clinical features in 73 cases. Medicina (B Aires) 2014;74:448-50.  Back to cited text no. 6


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