Obliterative appendicitis: a study.
1. Serosal vessel congestion.
2. Sub mucous lymphoid hyperplasia.
3. Dilated lumen filled with fecal material.
4. Occasionally cross section of parasite enterobius vermicularis.
5. The entire lumen is obliterated and filled with varying proportions of fibrocollagenous, neural, adipose tissue and lymphoid aggregates.
6. Rarely carcinoid.
Any intra-abdominal hollow viscus on expansion of the cavity can produce pain.
OBSERVATIONS: 366 cases of appendix were operated in Rajah Muthiah Medical College during the study period from January 2013 to March 2014-out of which 12 cases were reported as obliterative appendicitis, 183 cases were reported as acute appendicitis, 169 cases were reported as serosal congestion with sub mucosal lymphoid hyperplasia and 2 cases were reported as appendiceal carcinoid.
Total number of appendicectomy specimen - 366 Number of cases of Obliterative appendicitis -12
SI. No Diagnosis Number 1 Obliterative Appendicitis 12 2 Acute Appendicitis 183 3 Serosal congestion + sub mucosal 169 lymphoid hyperplasia 4 Carcinoid 2 TOTAL 366
Serosal congestion Acute with lymphoid Obliterative carcinoid appendicitis hyperplasia appendicitis appendix 0-20 75 60 4 2 20-40 01 110 4 0 40-60 10 6 4 0
DISCUSSION: A common feature of the appendix in obliterative appendicitis is luminal obliteration by a fibrotic process that tends to start at the tip and progresses proximally to involve the entire lumen. [1, 2]
The lumen is obliterated in one of the following two ways:
1. By the pressure atrophy of the mucosa resulting from encroachment of the increasing hyaline connective tissue originating from inflammatory stimulated sub mucosal tissues and from preexisting hyaline connective or endothelial tissue elements.
2. By an additional acute inflammation which finally destroys so much of the mucosa that it cannot be regenerated by the decreased number of functioning crypts of Lieberkuhn, before adhesion to the opposite wall occurs. 
Various modifications of these two processes may be encountered in a large group of specimen; however the mechanism of formation of the lumen occlusion is fundamentally the same . Some cases could be due to post inflammatory scarring.  However, most if not all examples of appendiceal luminal obliteration appears to be caused by a neurogenic occlusive proliferation called neurogenic hyperplasia or neurogenic appendicopathyJ [6,7,8, 9] When this process obliterates the lumen, the lesion may be called an axial neuroma. Axial neuromas are associated with the loss of the normal mucosa and lymphoid tissue. Neurogenous hyperplasia may also cause intramucosal or submucosal proliferations resulting in tumor like nodules or diffuse expansion of lamina propria. These sub mucosal and intramucosal neuromas show histologic features similar to those of the more obliterative lesions. 
Many factors play an important role in the production of obliteration of the appendiceal lumen:
1) As various stages in mammalian development are ascended, the appendix becomes more and more a vestigial structure, which has an increasing tendency to stenosis.
2) Any process which causes a narrowing and diminishment in the lumen of the appendiceal artery causes deprivation of adequate nourishment and the stenosing process extends progressively towards base of appendix.
3) Slow and retrogressive involution of all body tissues including appendix after attaining maturity; also progressive and definite obliteration of capillary beds of all parenchymatous organs after physical maturity.
4) Human appendix is notoriously unable to cope with a mild infection due to inadequacy of the terminal blood supply.
5) The fat of the mesoappendix apparently migrates along the course of the perforating blood vessels as they ramify from the mesoappendix to the sub mucosa.
6) All structures containing excess of lymphoid tissue normally have a tendency to undergo involution after maturity has been reached. (3)
Situated in the axial region of obliterated appendices are small nodules of spindled nuclei with scant, indistinct cytoplasm that tend to aggregate in onion skin like lamellae. The cells lie in a lace-like eosinophillic pericellular material and produce a tactoid whorling pattern. These nodules may be rimed by denser connective tissue, a feature better highlighted by the Masson trichrome stain. These nodules are thought to arise from pericellular mucosal nerve plexuses, possibly owing to stimulation by argentaffin cells that had migrated from the crypts of Lieberkuhn. Most often these nodules are not grossly evident, but on occasion large ganglioneuromatous nodules may be grossly visible.  These tend to involve Meissner and Auerbach plexuses and may extend to the periappendiceal fat. A syndrome of chronic recurrent right lower quadrant pain without evidence of peritoneal irritation is reported in some of these patients, and appendicectomy apparently relieves the symptoms.  It has been suggested that the neuroendocrine proliferation in neurogenic appendicopathy could be a cause of appendiceal pain, thus producing symptoms mimicking appendicitis . However, luminal obliteration is encountered in incidental appendicectomy specimens more often than in appendixes removed from patients with symptoms of appendicitis,  and it is a common finding in appendixes at autopsy. [1, 8]
CONCLUSIONS: From this study it is found that apart from the usual cases of acute appendicitis, the appendix can also harbor some histological curiosity where the lumen can be filled with adipose tissue, fibro fatty tissue, neural tissue, lymphoid aggregate. Carcinoid tumor can also obliterate the lumen.
[1.] Andreou P, Blain S, du Boulay CEH: A histopathological study of the appendix at autopsy and after surgical resection. Histopathology 17: 427-431, 1990.
[2.] Chang AR: An analysis of the pathology of 3003 appendices. Aust NZJ Surg 51: 169-178, 1981.
[3.] Donald C.Collins, Obliterative appendicitis, Annals of surgery, vol. 104, 2: 204-209, 1936.
[4.] Maale C.U: Histopathological studies over processus vermiformis 266Pp. Kobenhaven, Jacob Lund, 1908.
[5.] Carr NJ, Montgomery E: Patterns of healing in the appendix: the morphologic changes in resolving primary acute appendicitis and a comparison with crohn's disease. Int J Surg pathol 2: 23-30, 1994.
[6.] Segal GH, Petras RE: Vermiform appendix. In Sternberg S (ed): Histology for pathologists. New York, Raven, 1997, PP 539-550.
[7.] Stanley MW, Cherwitz D, Hagen K, et al: Neuromas of the appendix: a light microscopic, immunohistochemical and electron microscopic study of 20 cases. Am J Surg Pathol 10: 801815, 1986.
[8.] Olsen BS, Holck S: Neurogenous hyperplasia leading to appendiceal obliteration: an immunohistochemical study of 237 cases. Histopathology 11: 843-849, 1987.
[9.] Stead RH, Franks AJ, Goldsmith CH, et al: Mast cells, nerves and fibrosis in the appendix: a morphological assessment. J Pathol 161: 209-219, 1990.
[10.] Noel Weidner, cote, suster, weiss, Modern surgical pathology, 1st edn, 2003; 2: 867
[11.] Zarabi M, LaBach JP: Ganglioneuroma causing acute appendicitis. Hum pathol 13: 1143-1146, 1982.
[12.] Howie. JGR: The Prussian blue reaction in the diagnosis of previous appendicitis. J pathol bacteriol 91: 85-92, 1966.
[13.] Stephenson J, Snoddy WT: Appendiceal lesions: Observation in 4000 appendectomies ArchSurg 83; 661-666, 1961.
The various illustrate depicts different proportions of the tissue that fills the lumen:
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Lumen of the appendix is obliterated with adipose tissue, fibrocollagenous tissue, neural tissue and lymphoid tissue along with congested blood vessels.
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Lumen is obliterated with adipose tissue, fibrocollagen, neural tissue and lymphoid tissue.
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[FIGURE 9 OMITTED]
Lumen is obliterated with adipose tissue, fibro collagen and neural tissue.
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Lumen is obliterated with fibro- collagen and lymphoid tissue.
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Lumen is obliterated with adipose tissue, fibro- collagen and neural tissue.
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Lumen of the appendix is obliterated with adipose tissue and fibrocollagenous tissue with congested blood vessels.
CARCINOID OF APPENDIX:
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Lumen is filled with carcinoid tumor nodules.
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Tumor cells are small, round and darkly stained.
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Entire appendix replaced with carcinoid tumor.
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Appendix wall contain carcinoid tumor nodule.
(1.) K. Murali
(2.) K. V. Hariprasad
(3.) Nimmy Venu
(4.) J. Kabalimurthy
(5.) C. S. Subramanian
(6.) Rehana Tippoo
(7.) P. Viswanathan
(8.) B. Krishnaswamy
PARTICULARS OF CONTRIBUTORS:
(1.) 2nd Year Post Graduate, Department of Surgery, Rajah Muthiah Medical College, Annamalai University.
(2.) 2nd Year Post Graduate, Department of Pathology, Rajah Muthiah Medical College, Annamalai University.
(3.) 2nd Year Post Graduate, Departmentof Pathology, Rajah Muthiah Medical College, Annamalai University.
(4.) Professor, Department of Surgery, Rajah Muthiah Medical College, Annamalai University.
(5.) Professor & HOD, Department of Surgery, Rajah Muthiah Medical College, Annamalai University.
(6.) Professor, Department of Pathology, Rajah Muthiah Medical College, Annamalai University.
(7.) Professor, Department of Pathology, Rajah Muthiah Medical College, Annamalai University.
(8.) Professor, Department of Pathology, Rajah Muthiah Medical College, Annamalai University.
NAME ADDRESS EMAIL ID OF THE CORRESPONDING AUTHOR:
Dr. P. Viswanathan, Professor, Department of Pathology, Faculty of Medicine, Rajah Muthiah Medical College, Annamalai University, Chidambaram, PIN--608002, Tamilnadu, India.
Date of Submission: 27/05/2014.
Date of Peer Review: 28/05/2014.
Date of Acceptance: 04/06/2014.
Date of Publishing: 16/06/2014.
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|Title Annotation:||ORIGINAL ARTICLE|
|Author:||Murali, K.; Hariprasad, K.V.; Venu, Nimmy; Kabalimurthy, J.; Subramanian, C.S.; Tippoo, Rehana; Visw|
|Publication:||Journal of Evolution of Medical and Dental Sciences|
|Article Type:||Case study|
|Date:||Jun 16, 2014|
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