Retief, P.J.

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23 July 1966 S.A. MEDICAL JOURNAL 649common factor which is almost certainly the rapidity withwhich faeces from one individual reach the intestine ofanother.TABLE IV. ASSOCLATION BETWEE ' DIFFERE T PARASITESX' PAscaris v. Trichuris 0·90 15·3 <0·001Ascaris v. Hookworm and/orstrongyloides 0·30 4·3 0,02-0·05E. coli v. Hookworm and/orstrongyloides 0·07 0·7 0·70-0·80E. coli v. I. burschlii 0·83 25·9 <0·001E. hisrolytica v. E. coli 0·41 7·59 O·ool-{)·OlE. hislOlytica v. Ascaris and/ortrichuris 0·32 2·42 0·10-0·20E. hisrolyrica v. Hookworm and/orstrongyloides 0·07 0·19 0·50-0·70E. hisro!ytica v. All other protozoa 0·77 11·9 <0·001SUMMARYComparison of the prevalence of intestinal parasites in non-dysenteric African and Indian patients at King Edward VIIIHospital, Durban, shows a high incidence of soil-transmittedhelminths in both races, although the degree of infection islight in the vast majority. In contrast, the incidence of intes-tinal protozoa is much higher among Africans, being highestin those harbouring cysts of E. histolytica. It is suggested thatthese differences are due to different patterns of transmission,and statistical analysis of these findings supports this view. Therapid transfer of fresh faeces can explain the higher incidenceof E. histolytica among Africans and a gain in virulence dueto repeated passage may account for the frequency of invasiveamoebiasis. The underlying mechanism accounting for increasein virulence is briefly discussed.We wish to thank Dr. R. Nupen, formerly Acting MedicalSuperintendent of King Edward VIll Hospital, Durban, forfacilities. The Amoebiasis Research Unit is sponsored by theCSIR, the University of Natal, the Natal Provincial Adminis-tration, and the US Public Health Service (Grant AI-01592).REFERENCESI. Freedman, L. and Elsdon-Dew, R. (1959): Amer. J. Trop. Med. Hyg.,8, 327.2. Elsdon-Dew, R. (1958): Proceedings of the World Congress on Gastro-etlterology, p. 770. Baltimore: Williarns & Wilkins.3. Elsdon-Dew. R. and Maddison. S. E. (1964): S. Afr. J. Sei., 61, 172.4. Westphal, A. (1937): Arch. Sehiffs- u. Tropenhyg.. 41, 262.5. Powell, S. J. and EIsdon-Dew, R. (1961): S. Mr. J. Med. Sei., 26, 89.6. Elsdon·Dew, R. (1947): S. Afr. J. Sei., 43, 305.7. Powell, S. J., Hennessy, E., Wilmot, A. J. and E1sdon-Dew, R. (1961):Amer. J. Trop. Med. Hyg., 10, 22.8. Elsdon-Dew, R. (1946): S. Mr. Med. J., 20, 580.9. Blende. O. J. (1955): Northw. Med. (Seattle), 54, 609.10. Brooke. M. M. (1964): J. Amer. Med. Assoc., 188, 519.I I. Faust, E. C. (1930): Amer. J. Trop. Med .• 10, 137.12. Brooke, M. M .• Melvin, D. M., Sappenfield, R .. Payne, F., Carter. F.R. N., Offutt, A. C. and Feye, W. W. (1955): Amer. J. Hyg .• 62, 214.13. Brooke. M. M .• Gleason. N. and Montero-Gei, F. (1963): Rev. BioI.trop. (S. Jose), 11, 47.14. Beaver, P. C. J. (1949): Parasitology, 35, 125.15. Walker, E. L. (1913): Philipp. J. Sei., 8. 253.16. Freedman, L. (1958): S. Afr. Med. J .• 32, 797.17. Maddison, S. E., Powell. S. J. and Elsdon-Dew, R. (1965): Amer. J.Trop. Med. Hyg .. 14, 554.18. Neal, R. A. (1957): Trans. Roy. Soc. Trop. Med. Hyg .. SI, 313.19. Neal, R. A. and Vincent, P. (1956): Parasitology. 46, 173.20. Wiles, H .. Maddison, S. E .. Powell, S. J. and Elsdon-Dew, R. (1963):Ann. Trop. Med. Parasit.. 57, 7 I.21. Tornasz, A. (1965): Nature (Lond.), 208, 155.NON-SPECIFIC ULCERAnON OF TIIE SMALL BOWELP. J. RErIEF, M.B., CH.B. (PRET.), Department of Surgery, Pretoria Hospital and University of PretoriaNon-specific ulceration of the small bowel is a rare condi-tion. Only 130 cases were described before 1948.' TheMayo Clinic treated 18 cases during the period 1946-1955,' while Craighead3 reports 7 cases out of 1,035,943admissions. At the General Hospital, Pretoria, 3 cases wereadmitted and treated during a 6-month period (February-July 1965). The purpose of this paper is to review our ex-perience with these cases and to briefly discuss the condi-tion.CASE REPORTSCaseIG.N., a 16-yeal-old Bantu male, was admitted on 28 July1965. The patient had been in excellent health until 2 weeksbefore admission. He then developed abdominal pain whichhe described as a 'vague discomfort' and it cleared up spon-taneously after 24 hours. Three days before admission thepain recurred, this time more severely; it came on 12 hoursafter a drinking party. No stools or flatus had been passedfor the previous 24 hours and vomiting occurred.On examination the patient was acutely ill and shocked. Thetemperature was 101 OF, and the pulse 112/minute. The abdo-men was distended, and bowel sounds were present althoughdiminished; rebound tenderness was present. WBC 10,000/cu.mm. Faecal cultures were negative.Radiography showed distended loops of small bowel as welIas fluid levels. Air was present under the diaphragm.At laparotomy a large quantity of sero-purulent fluid wasfound in the peritoneal cavity. There were 2 perforations inthe distal ileum, 6 in. apart. The perforations, situated on theantimesenteric border, were round and 1 - 1t cm. in diameter.The surrounding ileum appeared oedematous and there wasregional lymph node enlargement After biopsy specimens ofthe margin of the ulcers had been taken, both perforationswere oversewn.Histology. Sections of the margin of the perforation showedwidespread infiltration by acute inflammatory cells. No specificaetiological factor could be demonstrated.The patient made an uneventful recovery, and was dis-charged on the 10th postoperative day.Case 2S.P., a 34-year-old Bantu male, was admitted on 26February 1965. The patient had been in excellent health until3 days before admission, when he suddenly developed an acuteabdominal pain. The pain originated around the umbilicus butlater spread towards the RIP. Vomiting was present on theday of admission, but the bowels were normal.On examination the patient was acutely ill and severelyshocked. The blood pressure was 95/60 mm.Hg, the pulse waslOO/min. and temperature 100-4OF. There was generalized ten-derness and distension of the abdomen, more marked in theRIF, and there was rectal tenderness high up and to the right.Radiography showed a few distended loops of small boweland fluid levels were present.Laparotomy showed the presence of sero-purulent fluid. Asingle round perforation was found in the terminal ileum 6ft. from the ileo-caecal valve on the antimesenteric border.This perforation was approximately 1 cm. in diameter. Re-gional lymphadenopathy was also present. A biopsy of theulcer was taken and the perforation oversewn.Histology. Non-specific acute enteritis.o complications arose and the patient was discharged onthe 10th day.Case 3W.S., a 24-year-old Bantu male, was admitted on 13 April1965. This patient was in good health until 2 days beforeadmission, when he developed an acute abdominal pain whichwas situated mainly over the lower abdomen and was cramp-like in character. Persistent vomiting was present and the mo-tions were loose and watery.On examination the patient was ill and restless. His pulsewas 114/min., the temperature l00·6°F and the blood pressure100/65 mm.Hg. Pronounced tenderness was present over the650 S.A. TYDSKRIF VIR GENEESKUNDE 23 Julie 1966whole abdomen and rebound tenderness could be elicited.Bowel sounds were diminished. Rectally, tenderness was pre-sent.Radiography showed the presence of air under the rightdiaphragm. Distended loops of small bowel and fluid levelscould be seen.At laparotomy a large amount of purulent fluid was found.There was a single perforation in the terminal ileum, approxi-mately 1 cm. in diameter. Regional lymphadenopathy was pre-sent. The surrounding ileum was found to be oedematous. Nobiopsy was taken in this case, and the perforation was over-sewn.Postoperative period. Bowel sounds became normal after 36hours. On the 5th postoperative day the patient developedacute dyspnoea with pain in the chest, collapsed and diedshortly afterwards. The relatives unfortunately refused a post-mortem examination but the cause of death was probably amassive pulmonary embolism.AETIOLOGYThe aetiology of non-specific ulceration of the small bowelis unknown, and no proven cause has been found at pre-sent.Peptic UlcerationAlthough this condition can mImIC peptic ulcer, mostpatients have normal or low gastric acid secretion: Fur-thermore, once the ulcers are excised, these patients are re-markably free from recurrence. No proof of ectopic gastricmucosa has been found on histological examination. Zol-linger and Ellison's case" had peptic ulceration of thejejunum due to islet cell tumours of the pancreas.InfectionStaphylococci, streptococci, salmonellae, amoebae, cho-lera, tuberculosis and syphilis may all produce ulcers ofthe small bowel. No specific organism was found in thecases reported by Seddon et al." nor could we demonstrateany specific organism or a histological picture resembling,for example, typhoid, in our series.DrugsAspirin, phenylbutazone, corticosteroids and cincophenmay cause ulceration, but a history of ingestion of thesedrugs must indeed be fortuitous. In our series no evidencewas found of a drug causing the ulceration.TraumaThe ulcers do not resemble ulcers caused by trauma.These lesions are usually round, with oedema and have theappearance of a chronic ulcer.Vascular LesionsEmbolism, thrombosis and collagen disorders may causeulceration," but none of these factors was found in ourcases.PATHOLOGYDistribution and MorphologyAlthough the proximal jejunum and distal ileum aremostly affected, any part of the small intestine may be in-volved." The disease is found in all age-groups, includingneonates,' and there is a preponderance of males: In thecases presented here all the patients were young males. Theulcers may he single or multiple; in our series 1 patienthad 2 ulcers. These are usually situated on the antimesen-teric border.HistologyThe histological picture is of non-specific inflammationwith varying degrees of lymphocytic infiltration andfibrosis.DISCUSSIONThe 3 cases presented here, were all young Bantu males(aged 16, 34 and 24 years respectively).Two cases were in excellent health before commence-ment of their symptoms (cases 2 and 3). Case 1, on theother hand, had a similar attack 2 weeks previously. Thispain was almost certainly caused by the ulcer in the distalileum. Horwitz et al.· described a case having severalattacks of abdominal pain similar to the pattern of painfound in a peptic ulcer before the ulcer of the ileum waseventually diagnosed at laparotomy. In one of our cases(case 1), it is possible that the heavy drinking could haveprecipitated the perforation.DiagnosisThe diagnosis is always made at laparotomy. We believe,however, that with advances in the technique of smallbowel investigation, a pre-operative diagnosis will be mademore frequently in the future.TreatmentThe treatment of choice, according to the availableliterature (e.g. Horwitz et al.,· Shea," Morlock et al.'), is re-section of the affected segment. The perforations couldalso be oversewn-our 3 cases and a case described bySeddon et al." were treated in this way. The brief follow-up in our series does not allow us to draw definite conclu-sions in this respect, although the postoperative periodappeared to be uneventful.PrognosisThe prognosis, especially after resection, is good. Mor-lock et al.' have a follow-up of up to 25 years with norecurrence of symptoms.SUMMARY AND CONCLUSION1. Three cases of non-specific ulceration of the small bowelare presented. This diagnosis should always be kept in mind,in patients with a history of peptic ulceration, where thebarium meal is negative. Similarly, in cases of peritonitis ofunknown origin, a careful examination for minute perforationsin the small bowel should be made at laparotomy.2. No case has yet been diagnosed before the onset of com-plications. The complications are perforation, haemorrhage andobstruction.3. Resection seems to be the treatment of choice though ina few cases the perforations were oversewn, with apparentgood results.I wish to express my appreciation and thanks to Prof. C. H.Derksen, Head of the Department of Surgery, for his en-couragement. I am also' grateful to Dr. P. N. Swanepoel, Medi-cal Superintendent, for permission to report details of thesecases.REFERENCESI. Evert, J. A., Black, B. M. and Dockerty, M. B. (1948): Surgery, 23,185.2. Morlock, C. G., Goeurs, H, R. and Dockerty, M. B. (1956): Gastro-enterology, 31, 667.3. Craighead, C, C. (1952): Amer. J. Surg., 84, 47.4. Morrin, F. J, (1931): Irish J, Med. Sci .. 6,. 198.5. Zollinger, R. M. and Ellison, E. U. (1955): Ann. Surg., 142, 709.6. Seddon, J, A., Hamilton, D. W, and Downie, R. J. G, (1965): Brit.J. Surg .. 52, 367.7. Schiff, C. A, (1955): Arch. Surg., 70, 439.8. Horwitz, F., Parathy, R. and Baronofsky, I. (1960): J. Mt Sinai Hosp.,27, 308.9. Shea, P. C. (1951): J. Amer, Med, Assoc., 146, 1490.

Non-specific ulceration of the small bowel

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Non-specific ulceration of the small bowel

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