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|Year : 2012 | Volume
| Issue : 1 | Page : 54-56
Mesenteric fat necrosis after recent surgery causing bowel obstruction: A case report and review of the literature
BR Green, A Reddy, M Jha
Department of Surgery, James Cook University Hospital, Marton Road, Middlesbrough, TS4 3BW, United Kingdom
|Date of Submission||30-May-2011|
|Date of Decision||15-Jul-2011|
|Date of Acceptance||30-Oct-2011|
|Date of Web Publication||25-Feb-2012|
B R Green
Department of Surgery, James Cook University Hospital, Marton Road, Middlesbrough, TS4 3BW
Mesenteric fat necrosis causing bowel obstruction is a rare occurrence with only one case reported in humans. It is due to accidental or surgical trauma to the adipose tissue with extracellular liberation of fat or enzymatic lysis of fat due to the release of lipases resulting in fibrosis. Preoperative imaging may often be misleading and fail to identify fat necrosis as the cause of bowel obstruction. As surgical intervention is the only suitable treatment option in cases of failed conservative treatment, the diagnosis is made postoperatively. There is no published advice on the management of mesenteric fat necrosis. We recommend safe operating techniques to minimize the risk of developing fat necrosis and its potential harmful consequences.
Keywords: Bowel obstruction, fat necrosis, post-surgical trauma
|How to cite this article:|
Green B R, Reddy A, Jha M. Mesenteric fat necrosis after recent surgery causing bowel obstruction: A case report and review of the literature. J Postgrad Med 2012;58:54-6
|How to cite this URL:|
Green B R, Reddy A, Jha M. Mesenteric fat necrosis after recent surgery causing bowel obstruction: A case report and review of the literature. J Postgrad Med [serial online] 2012 [cited 2014 Oct 1];58:54-6. Available from: http://www.jpgmonline.com/text.asp?2012/58/1/54/93253
Fat necrosis after recent surgery can cause bowel obstruction. Its incidence is rare but its effect potentially harmful. Safe operating technique to minimize risk of developing fat necrosis is paramount.
| :: Introduction|| |
Mesenteric fat necrosis causing bowel obstruction is a rare occurrence with only one case reported in humans. Preoperative imaging may often be misleading or fail to identify fat necrosis as the cause of bowel obstruction. As surgical intervention is the only suitable treatment option in cases of failed conservative treatment, the diagnosis is made retrospectively. We present a case report and review of the literature.
| :: Case Report|| |
A 75-year-old woman presented to her general practitioner with a three-month history of altered bowel habit. This was initially thought to be due to a recent increase in her thyroxine treatment, however, in view of her symptoms and age, she was referred for a routine outpatient colonoscopy. A polypoidal lesion was discovered in the distal sigmoid, biopsies from which confirmed mucinous adenocarcinoma. No other abnormality was demonstrated on this complete investigation. After staging computed tomography (CT) (T 3 N 0 M 0 , Stage 2) and multidisciplinary discussion she underwent a straightforward laparoscopic high anterior resection. She was discharged from hospital on Day 6 after an uneventful recovery.
Ten weeks later she was readmitted as an emergency with a short history of colicky abdominal pain, distension, and increasing constipation. On examination she had a distended, tympanic and tender abdomen with tinkling bowel sounds. Her observations and biochemical markers were otherwise normal. An urgent CT scan demonstrated large-bowel obstruction, thought to be due to a tight anastomotic stricture, with extensive intramural gas in the right colon and impending perforation [Figure 1].
|Figure 1: Large-bowel obstruction with impending cecal perforation (arrow)|
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She was taken to emergency theatre and had an on-table colonoscopy. The colorectal anastomosis looked healthy and passed the scope easily, however, there was a complete obstruction in the region of the splenic flexure. At laparotomy she was found to have an obstruction just proximal to the splenic flexure. There was also a large mass in the mesentery of the transverse colon with no evidence of any hematoma or infarction. There was massive distension of the proximal colon with serosal tears. The small bowel was normal. She underwent total colectomy with end ileostomy and was discharged 11 days later.
Histological evaluation of the specimen revealed an area of serosal puckering 22 cm from the distal resection margin. Proximal to this the colon was dilated to a diameter of 14 cm. Related to this area was a 3 cm firm mass in the mesocolon that was composed of an area of extensive fat necrosis. Several smaller nodules in the mesocolon and a 6 cm mass in the transverse mesocolon also exhibited the same findings. There was no evidence of residual malignancy. Sections through the anastomosis demonstrated some mucosal glandular distortion and submucosal fibrosis consistent with previous surgery. The pathologist's conclusion was that the bowel obstruction was a consequence of the nodules of fat necrosis [Figure 2]. Retrospective review of the CT scan images confirmed these subtle findings [Figure 3].
| :: Discussion|| |
Fat necrosis is a benign non-suppurative inflammatory process of adipose tissue. It is commonly due to accidental or surgical trauma to the adipose tissue with extracellular liberation of fat or enzymatic lysis of fat due to the release of lipases.  The brisk inflammatory response that follows the release of intracellular fat into the surrounding tissue results in polymorphs and macrophages phagocytosing the fat resulting in an inflammatory mass. Over time this scleroses resulting in a fibrotic mass that may be palpable if it is in superficial tissues. Common sites of fat necrosis are the breast and within the abdomen following acute pancreatitis.
Although fat necrosis as a cause of bowel obstruction is a well-documented entity in veterinary circles,  it is rare in humans with only one reported case in the literature.  The literature does identify causes of bowel obstruction where one of the pathological findings is indeed fat necrosis, however, this is only seen as a part of an overall process, for example mesenteric panniculitis,  heterotopic mesenteric ossification,  and sclerosing mesenteritis,  rather than a specific clinical entity. Distinguishing our case of fat necrosis from entities such as mesenteric panniculitis may be difficult as we may be dealing with a histological variant of one clinical entity, however, cases of mesenteric panniculitis and sclerosing mesenteritis tend to exhibit features of a chronic process rather than an acute sequalae of recent surgery. Furthermore, mesenteric panniculitis predominantly affects the mesentery of the small bowel  with only a handful of cases affecting the large-bowel mesentery.
As there appears to be little data on mesenteric fat necrosis, making the diagnosis preoperatively can be challenging, more so as it mimics other conditions such as chronic pancreatitis or intra-abdominal malignancy. Furthermore, the patient did not have any predisposing conditions that may lead to fat necrosis, for example autoimmune disorders or morbid obesity that may have raised clinical suspicion. Conventional imaging techniques include ultrasound, CT, and magnetic resonance imaging (MRI), although even then the conclusion may be misleading. Radionucleotide imaging has been used in the postoperative setting.  Often the diagnosis becomes apparent retrospectively due to the urgent mode of presentation and the often-subtle changes seen on emergency preoperative CT scanning being overlooked. A retrospective study of 563 consecutive patients with acute abdominal pain in whom diagnostic laparoscopy was indicated revealed an incidence of fat necrosis of 1.1%.  In our case the features of impending colonic perforation resulted in a postoperative diagnosis.
There is no published advice on the management of mesenteric fat necrosis presumably as most diagnoses are made postoperatively. There are reports of treatment options for mesenteric panniculitis, including steroids, immunosuppression therapy, antibiotics and tamoxifen,  however, surgery is usually the treatment of choice to remove the affected part of the bowel in symptomatic patients. In our case, due to its advanced clinical manifestation, surgery was the only option available.
The etiology and pathogenesis of fat necrosis causing bowel obstruction may be obscure but in this case it was most likely due to surgical trauma; either excessive use of the harmonic scalpel in order to achieve hemostasis or a retained piece of devascularised omentum. Why this patient developed acute bowel obstruction when others undergoing the same procedure with the same technique do not remains uncertain. Although this was an isolated event in our practice and it has not influenced our choice of surgical instruments, it serves as a constant reminder to ensure gentle tissue handling and to keep dissection to the minimum required to safely complete the procedure.
This case serves to encourage safe operating technique at all times. The instruments used in laparoscopic dissection cause little collateral damage if used in the recommended manner  thus limiting damage to the mesenteric or omental adipose tissue, and the propensity to cause fat necrosis. In addition it may raise awareness of alternative causes of bowel obstruction in the postoperative setting and aid in radiological diagnosis.
Fat necrosis after recent surgery causing bowel obstruction is a rare occurrence. Our case illustrates the difficulty in diagnosis and serves to raise awareness of the condition as a cause of postoperative bowel obstruction. In advanced clinical presentations, surgery is the only safe treatment option. We encourage safe operating techniques to minimize the risk of developing fat necrosis and its potentially harmful consequences.
Dr. J Fletcher carried out the radiological investigations and provided the images used in the report. Dr. D Henderson performed the histopathological analysis of the specimen.
| :: References|| |
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[Figure 1], [Figure 2], [Figure 3]