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LETTER TO THE EDITOR
Year : 2019  |  Volume : 8  |  Issue : 1  |  Page : 80-81

An unusual case of colonic perforation


1 Department of Pathology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India
2 Department of Surgical Gastroenterology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India
3 Department of Surgical Oncology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India

Date of Submission02-Feb-2018
Date of Acceptance14-Sep-2018
Date of Web Publication26-Apr-2019

Correspondence Address:
Dr. Rashmi Patnayak
Department of Pathology, Sri Venkateswara Institute of Medical Sciences, Tirupati - 517507, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JDRNTRUHS.JDRNTRUHS_12_18

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How to cite this article:
Patnayak R, Vuvula S, Reddy VR, Jena A. An unusual case of colonic perforation. J NTR Univ Health Sci 2019;8:80-1

How to cite this URL:
Patnayak R, Vuvula S, Reddy VR, Jena A. An unusual case of colonic perforation. J NTR Univ Health Sci [serial online] 2019 [cited 2019 Sep 16];8:80-1. Available from: http://www.jdrntruhs.org/text.asp?2019/8/1/80/257157



Sir,

Patients with Crohn's disease (CD) have many intestinal complications. Colonic perforation is unusual in patients with CD. During the course of illness, 1%–2% of patients may present with colonic perforation.[1] This rarity may be explained by chronic inflammatory nature of the condition with accompanying fibrosing strictures.[2] We describe a case of colonic perforation in a young male as an initial manifestation of CD.

A 24-year-old male came to the emergency department with complaint of pain abdomen which started on the same afternoon. Initially, the pain was localized in the left lumbar region and later on progressed to a diffuse type of pain. The pain was burning and nonradiating in nature. He had multiple episodes of nonbilious vomitting. There was no history of consumption of spicy food or alcohol intake before the onset of pain. He gave a history of epigastric pain on taking food and loss of appetite. There was no history of loss of weight, abdominal distension, gastrointestinal bleed, and jaundice. His diet was mixed and sleep pattern was normal. He was not a known smoker or alcoholic. There was no irregularity in his bowels and bladder habits. There was no history of diabetes mellitus, hypertension, tuberculosis, asthma, epilepsy, or coronary artery disease. There were no similar complaints in the family. He was moderately built, afebrile, conscious, and coherent. The ultrasonographic findings were suggestive of appendicular perforation. His routine laboratory investigations were within normal limit. After this, the patient was admitted to surgical gastroenterology department. His contrast-enhanced computed tomography (CECT) showed moderate free fluid in the abdomen with air foci within pelvis. Enhanced thickening of peritoneum was noted in pelvis and hypochondrium. Thickening of bowel loops and enlarged lymph nodes in bilateral inguinal regions, extrailiac regions, aortocaval region, and paraaortic region were noted. CECT impression was peritonitis due to sealed-off perforation. He underwent diagnostic laparoscopy with right hemicolectomy and end ileostomy under general anesthesia.

The right hemicolectomy specimen exhibited creeping fat on the external surface. The cut section showed perforations at a distance of 9 and 11 cm from distal resected margin; mucosa showed cobble stone appearance [Figure 1]. The histopathological examination showed presence of ulceration and transmural inflammation. There were presence of noncaesating granulomas in all the layers and also in the lymph nodes. The histopathology was reported as CD. Ziehl–Neelson stain for acid-fast bacilli was negative [Figure 2].
Figure 1: (a) Right hemicolectomy specimen – external surface showing the presence of creeping fat; (b) cut surface of colon with cobblestone appearance

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Figure 2: (a) Mucosal epithelium showing lymphoid aggregate (hematoxylin and eosin ×100); (b) presence of granuloma in the muscle layer (hematoxylin and eosin ×100); (c) serosal aspect showing presence of granulomas and chronic inflammatory cells (hematoxylin and eosin ×100); (d) granulomas comprising multinucleated giant cells and lymphoid cells (hematoxylin and eosin ×200)

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Postoperative stay was uneventful. The patient was discharged with healthy wound and in situ functioning colostomy. Larsson G et al. in a study found that intestinal tuberculosis (ITB) and CD were equally common in Southern India.[3] Differentiating ITB from CD remains an important clinical challenge as it has therapeutic significance. In India, both diseases are prevalent. The final diagnosis is based on a combination of clinical history with endoscopic studies, culture, and polymerase chain reaction for Mycobacterium tuberculosis, biopsy, radiological investigations, and response to therapy.[4] The histological differentiation of ITB and CD is most commonly made on mucosal biopsies. The features suggestive of ITB include caesation necrosis, acid-fast bacilli, confluent granulomas, a lymphoid cuff around granulomas, granulomas larger than 400 μm in diameter, five or more granulomas in biopsies from one segment, granulomas located in the submucosa or in granulation tissue, often as palisaded epithelioid histiocytes, and disproportionate submucosal inflammation. Features that favor a diagnosis of CD on mucosal biopsies include infrequent (<5 μm), small (<200 μm in size) granulomas that are poorly organized and discrete or isolated.[4] In the present case, there was transmural inflammation and presence of granulomas. These granulomas were not confluent and there was no caesation necrosis. Considering the gross and microscopic features, the diagnosis of CD was favored.

The free perforation as a complication of CD is rare because of the accompanying fibrous reaction and adhesion to adjacent viscera. Approximately 1%–2% of patients with CD present as free perforation. Most of the reported cases in world literature include intestinal perforation. Free colonic perforation is considered to be a rare entity.[1] In acute CD, free perforation is facilitated by the lack of fibrosis and adhesions. The other mechanisms proposed for precipitating bowel perforation are distal obstruction by increasing the intraluminal pressure and steroid therapy by diminishing the immune response.[1]

This case was not a known case of CD. Few such cases where a CD presented for the first time with free colonic perforation were reported previously.[1]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Roy MK, Delicata RJ, Carey PD. Crohn's disease presenting with acute colonic perforation. Postgrad Med J1997;73:645-6.  Back to cited text no. 1
    
2.
Bunni J, Monkhouse SJW, Armstrong CP. Colonic perforation following mild abdominal trauma in a patient with Crohn's disease: A case report. World J Emerg Surg 2008;3:13.  Back to cited text no. 2
    
3.
Larsson G, Shenoy T, Ramasubramanian R, Balakumaran LK, Småstuen MC, Bjune GA, et al. Routine diagnosis of intestinal tuberculosis and Crohn's disease in Southern India. World J Gastroenterol 2014;20:5017-24.  Back to cited text no. 3
    
4.
Pulimood AB, Amarapurkar DN, Ghoshal U, Phillip M, Pai CG, Reddy DN, et al. Differentiation of Crohn's disease from intestinal tuberculosis in India in 2010. World J Gastroenterol 2011;17:433-43.  Back to cited text no. 4
    


    Figures

  [Figure 1], [Figure 2]



 

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