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CASE SERIES  
Year : 2011  |  Volume : 4  |  Issue : 3  |  Page : 430-432
Adult necrotizing enterocolitis and non occlusive mesenteric ischemia


Department of Surgical Disciplines, M.O.S.C Medical College, Kolenchery, Cochin, Kerala, India

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Date of Submission23-Jul-2010
Date of Acceptance02-May-2011
Date of Web Publication16-Aug-2011
 

   Abstract 

Adult necrotizing enterocolitis and non occlusive mesenteric ischemia are rare causes of acute abdomen in adults. Accurate preoperative diagnosis is often difficult in these cases. Here, four cases of massive bowel necrosis with varying segments of small and large bowel involvement are described, all of whom underwent surgery. These cases give an opportunity to review the literature on such lethal diseases including non occlusive intestinal necrosis, neonatal necrotizing enterocolitis and adult necrotizing enterocolitis. The similarities and differences in etiology, pathophysiology, clinical and radiological findings are discussed.

Keywords: Adult, intestinal ischemia, necrotizing enterocolitis, non occlusive mesenteric ischemia

How to cite this article:
Zachariah SK. Adult necrotizing enterocolitis and non occlusive mesenteric ischemia. J Emerg Trauma Shock 2011;4:430-2

How to cite this URL:
Zachariah SK. Adult necrotizing enterocolitis and non occlusive mesenteric ischemia. J Emerg Trauma Shock [serial online] 2011 [cited 2017 May 27];4:430-2. Available from: http://www.onlinejets.org/text.asp?2011/4/3/430/83881



   Introduction Top


Necrotizing enterocolitis (NEC) is an acquired, sometimes fatal, multifactorial syndrome characterized by segmental, inflammatory, or ischemic necrosis of the small and large intestine. [1] It primarily affects premature neonates of low birth weight. The incidence varies from 1 to 3/1000 live births. Reported mortality rates are between 20 and 50%. [2] The term adult necrotizing enterocolitis (ANEC) is used to describe similar patterns of bowel necrosis in adults and is popularly known by names such as Drambrand and Pigbel. ANEC is considered as a rare disease; with only a few cases reported in literature. [3] Non occlusive mesenteric ischemia is another rare cause of intestinal necrosis with appearances similar to NEC. The surgical options in advanced cases in both these diseases are minimal and prognosis is poor.


   Case Reports Top


Case 1

A 45-year-old male, presented with acute abdominal pain of five days duration and clinical features suggestive of perforation peritonitis and shock. The patient had no other co morbidities. He gave a history of passing dark loose stools two days after the onset of pain. Blood investigations showed leucocytosis, metabolic acidosis, hyperglycemia, unconjugated-hyperbilirubinaemia and prerenal azotemia. A plain erect abdominal radiograph revealed pneumoperitoneum, thereby confirming hollow viscus perforation. At exploratory laparotomy there was fecal peritonitis associated with gangrene and sloughing of coats of intestinal segments along with multiple perforations over four feet of the terminal ileum. The cecum and the proximal part of the ascending colon were also gangrenous [Figure 1]. The mesenteric vessels were patent with good pulsations. A right hemicolectomy along with resection of three feet of contiguous small bowel was performed. The terminal ileum was brought out as an ileostomy and the proximal end of the colon was closed linearly. Post operatively, the patient developed progressive multisystem deterioration and died on the fifth post operative day. Histopathology revealed a non-specific picture of infarction necrosis of the bowel wall, with multiple ulcerations over ileum and cecum, without any evidence of major vessel thrombosis.
Figure 1: Contiguous involvement of the cecum and ileum due to necrotizing enterocolitis

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Case 2

A 24-year-old male, presented with generalized abdominal pain of two days duration associated with abdominal distension, vomiting, and dark stools. He was febrile, tachycardic, with a distended and silent abdomen. X-ray of abdomen showed multiple dilated bowel loops with multiple air fluid levels suggestive of intestinal obstruction. Exploratory laparotomy revealed fecal peritonitis and a full thickness necrosis with perforation of the ileum [Figure 2]. The cecum was congested. A limited right hemicolectomy was performed with removal of one foot of distal ileum but followed by an ileo-transverse anastomosis and a covering loop ileostomy. The post operative period was uneventful. The ileostomy was taken down after three months. Histopathology revealed transmural necrosis of the ileum with neutrophilc infiltration and mild inflammatory changes in the cecum.
Figure 2: Full thickness transmural necrosis and skip lesions

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Case 3

A 37-year-old male was referred with generalized abdominal pain of two days, bloody stools and vomiting with clinical and radiographic features of perforation peritonitis. Exploratory laparotomy revealed fecal peritonitis, two perforations over two feet of gangrenous distal ileum and a congested cecum. Right hemicolectomy along with resection of contiguous gangrenous ileum was done. The terminal ileum was brought out as a stoma, while the transverse colon was closed terminally. The post operative period was prolonged, but eventually the patient recovered. Here again histopathology revealed a non-specific picture of infarction necrosis of the bowel wall without any evidence of major vessel thrombosis. An ileo- transverse anastomosis was done seven months later and bowel continuity restored.

Case 4

A 55-year-old male, presented with severe acute abdominal pain of five days duration associated with bloody diarrhea and vomiting. Clinical and X-ray features were suggestive of perforation peritonitis. He was a known diabetic and hypertensive on irregular treatment. At exploratory laparotomy, almost the entire small bowel and ascending colon was found to be dusky, gangrenous with multiple perforations. Unlike in the previous three cases, skip lesions were absent [Figure 3]. The mesenteric vessels appeared patent with good pulsations. No resection was attempted and the patient expired the next day.
Figure 3: Involvement of continuous segment of the small bowel without skip lesions in NOMI

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   Discussion Top


The exact etiology of ANEC is uncertain. Infectious agents, inflammatory mediators and circulatory disturbances have all been implicated. The common organisms implicated are bacteria (Klebsiella,  Escherichia More Details coli, Enterobacter, Pseudomonas, Clostridia and Staphylococcus epidermidis), and viruses (Corona and Rota virus). [4] The causative factor in cases of Pigbel and Drambrand was identified to be the ί toxin produced by Clostridium perfringens type C.

Another suggested mechanism is the hypoxia-reperfusion injury due to reduced mesenteric blood flow as the initiating event, resulting in the release of oxygen free radicals thereby leading to loss of the bowel's cellular integrity. The mechanism is similar to bowel necrosis occurring in non occlusive mesenteric ischemia (NOMI). Here gut hypo perfusion occurs due to mesenteric vasoconstriction and results in intestinal necrosis, with bacterial translocation as the secondary event. [5] Reported mortality rates in NOMI are between 70 and 90%. [6]

It can be postulated that, the primary etiology of ANEC is probably different from neonatal necrotizing enterocolitis (NNEC). In children with poorly developed defence systems, an initial infective insult to the bowel leading to secondary ischemia, seems to be more likely than a primary vascular event as the cause of intestinal necrosis.

Based on clinical and radiological findings, NNEC has been classified into three progressive stages (suspected, mild and severe illness) by Bell and co-workers and later modified by Walsh and Kliegman. [7]

The clinical picture in all patients in the present study was similar to stage 3 or advanced NEC (hyponatremia, metabolic acidosis and perforation peritonitis). Little information on the diagnosis is provided by clinical, radiological and laboratory data. Findings on X-ray of these patients namely, pnuemoperitonem, thumb printing and dilated bowel loops are also seen in advanced cases of NOMI and are non specific. [8] The common findings at laparotomy include dilated and thickened loops of bowel with segments of necrosis often separated by segments of normal bowel. Histological examination is characterized by pathological features such as an intestinal necrosis beginning in the mucosa, without obstruction of the mesenteric vessels.

In this study, few factors were found universal to all the patients. They were all smokers, regularly consumed alcohol, non-vegetarians and frequented eating from unhygienic places. They all had a poor nutritional status, belonged to lower socioeconomic strata, and were from the same geographical area. It could be therefore postulated that these are probable contributory factors for ANEC in the present series. Most of them gave a history of bloody diarrhoea after onset of pain. Only one of the patients had a previous history of diabetes and cardiac disease. Skip lesions characteristic of NEC were seen in three out of four patients. In all our cases, the colon was involved probably denoting an advanced stage. Laboratory tests and X-ray findings were non-specific. It was not possible to detect Clostridium perfringens, but in all the cases the most common organisms isolated were E. coli and Klebsiella. One X-ray showed thumb printing but pnuematosis intestinalis and portal venous gas which are characteristic of NEC were not appreciated. It could be therefore suggested that the first three patients would have suffered from ANEC and the fourth patient could have had NOMI considering the age, absence of skip lesions and co-morbidities. More definitive investigations such as toxin typing, immuno-histochemical analysis and polymerase chain reaction could provide more valid information. Angiography is an useful technique to diagnose NOMI prior to occurrence of bowel infarction. [9]

Management is medical and/or surgical and includes alleviation of the symptoms, attempts at producing local vasodilatation whenever possible and resection of the affected intestinal segment. In many cases the diagnosis is made at exploratory laparotomy. However, in advanced cases surgical options are limited. Surgical intervention is necessary if there is intestinal necrosis or frank perforation or when there is clinical deterioration over a 12-24 hour period despite intensive medical support, as evidenced by persistent or worsening metabolic acidosis. The role of papaverin in producing local vasodilatation has been found to be useful in cases of NOMI and salvaging the bowel at risk. [10] Late complications include short bowel syndrome and malnutrition.


   Conclusion Top


It is strongly felt that there is a possible link between infective and vascular mechanisms involved in the pathogenesis of massive bowel necrosis, in NOMI and NEC. The infectious and circulatory mechanisms might be coexisting. The clinical findings, laboratory investigations, histopathology features and radiological evidences might be non-specific in advanced disease. A high index of suspicion is necessary in making a diagnosis.

 
   References Top

1.Fick KA, Wolken AP. Necrotic jejunitis. Lancet 1949;1:519-21.  Back to cited text no. 1
[PUBMED]    
2.Henry MC, Lawrence Moss R. Surgical therapy for necrotizing enterocolitis: Bringing evidence to the bedside. Semin Pediatr Surg 2005;14:181-90.  Back to cited text no. 2
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3.Katara AN, Chandiramani VA, Soman R, Bhaduri A, Desai DC. Necrotizing enterocolitis in adults: A study of four cases. Indian J Surg 2004,66:115-8.  Back to cited text no. 3
    
4.Schnabl KL, Van Aerde JE, Thomson AB, Clandinin MT. Necrotizing enterocolitis: A multifactorial disease with no cure. World J Gastroenterol 2008;14:2142-61.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Reinus JF, Brandt LJ, Boley SJ. Ischemic diseases of the bowel. Gastroenterol Clin North Am 1990;19:319-43.  Back to cited text no. 5
[PUBMED]    
6.Acosta S, Ogren M, Sternby NH, Berqvist D, Björck M. Fatal nonocclusive mesenteric ischemia: Population-based incidence and risk factors. J Intern Med 2006;259:305-13.  Back to cited text no. 6
    
7.Walsh MC, Kleigman RM. Necrotizing enterocolitis: Treatment based on staging criteria. Pediatr Clin North Am 1986;33:179-201.  Back to cited text no. 7
    
8.Smerud M, Johnson CD, Stephens DH. Diagnosis of bowel infarction: A comparison of plain films and CT scans in 23 cases. AJR Am J Roentgenol 1990;154:99-103.  Back to cited text no. 8
    
9.Bakal CW, Sprayregen S, Wolf EL. Radiology in intestinal ischaemia. Angiographic diagnosis and management. Surg Clin North Am 1992;72:125-41.  Back to cited text no. 9
[PUBMED]    
10.Boley SJ, Sprayregan S, Siegelman SS, Veith FJ. Initial results from an aggressive roentgenological and surgical approach to acute mesenteric ischaemia. Surgery 1977;82:848-55.  Back to cited text no. 10
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Correspondence Address:
Sanoop Koshy Zachariah
Department of Surgical Disciplines, M.O.S.C Medical College, Kolenchery, Cochin, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-2700.83881

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    Figures

  [Figure 1], [Figure 2], [Figure 3]

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