494

INFARCTION OF THE COLONBy C. I. COOLING, F.R.C.S.

and R. H. B. PROTHEROE, M.D.Westminster Hospital Teaching Group, London, S.W. i

IntroductionVascular lesions of the lower gastro-intestinal

tract have recently been receiving some attention,both as a source of unexplained bleeding, and alsoin relation to fulminating ulcerative colitis, peri-arteritis nodosa and lupus erythematosis. Massiveinfarction of the colon is, however, rare andcarries a high mortality. Dzialoswynski (1925)reported what he believed to be the first case ofrecovery from resection of the entire gangrenoustransverse colon. A case of infarction of thetransverse colon due to occlusion of the middlecolic arteries is described, which was successfullytreated surgically. The changes in the mucousmembrane will be discussed in relation to ulcera-tive colitis and periarteritis nodosa and systemiclupus erythematosis (S.L.E.).

Case ReportMrs. M. F., aged 69 years, was admitted to the

Gordon Hospital on May I3, 1956, complainingof sudden onset of abdominal pain at 8.30 a.m.The pain was generalized and continuous. Shehad vomited on four occasions; the bowels hadacted three times, the stools being loose and con-taining blood. Normally the bowels acted oncedaily apart from recent constipation. Four dayspreviously she had been discharged from anotherhospital where treatment for bronchitis had beengiven.On examination the temperature was 99.60 F.,

the pulse rate 120 per minute and respiration ratenormal. The patient was in obvious distress, thetongue coated, and coarse rales were present inall lung areas. The heart was within normallimits but the blood pressure was 170/90 mm. Hg.

Examination of the abdomen revealed general-ized tenderness and guarding with very infrequentbowel sounds. Rectal examination confirmed thepresence of bright red blood, but the rectalmucosa appeared normal. The diagnosis wasconsidered to be mesenteric thrombosis, or.possibly an intussusception.

Laparotomy was performed under spinal and

general anaesthesia 12 hours after the onset ofsymptoms. The wall of the transverse colon wasthickened and dark red in colour and its mesenterywas congested and odematous. Resection of theaffected bowel was performed, continuity restoredand a portion of caecum exteriorized in caseof need.

Progress. Recovery from the operation wassatisfactory, but the exteriorized caecum wasopened on the fourth day due to abdominal dis-tension and failure of the bowel to evacuate.The caecostomy acted freely and normal bowelactions commenced on the eleventh post-operativeday. On the sixteenth day evidence of deep veinthrombosis appeared in the left leg and a courseof anticoagulants was commenced using heparinin the first instance followed by Dindevan. Bythe eighteenth day the prothrombin time hadrisen alarmingly to 8o seconds, the normal valuebeing I4 seconds. Further treatment was stoppedbut on the twentieth day she collapsed, becamevery shocked and complained of abdominal pain.Examination revealed a mass 6 inches in diameterdeep to the wound. This was explored underlocal anaesthesia and large blood clots evacuatedand the cavity drained.

Further progress was satisfactory and thecaecostomy was formally closed. The patient isnow in robust health.The specimen consisted of 33 cm. of transverse

colon, 4 cm. in diameter. There was intensemucosal congestion of the specimen over almostits entire length and also linear ulceration, theulcers being parallel to the taenia coli (see Fig. i).The peritoneal coat was also congested and noobvious thrombosed vessels could be seen. Therewas no dilatation of the colon. Microscopyshowed numerous thrombosed arterioles in thesubmucosa of the colon with haemorrhagic infarc-tion of the mucous membrane (see Fig. 2). Therewas loss of the normal architecture with intensehaemorrhage into the lamina propria and necrosisof the cells of the crypts of Lieberkuhn (see Fig. 2),together with linea frank ulcers lined by fibrin

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September I 958 COOLING and PROTHEROE: Infarction of the Colon 495

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FIG. I.-Resected transverse colon showing throughout almost its length mucosal congestionand linear ulceration due to infarction of its wall.

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FIG. 2.-Numerous thrombosed arterioles in the sub-mucosa with infarction of the mucous membraneand necrosis of the cells of the crypts of Lieberkiihn.Haematoxylin and eosin x 8o.

and an acute inflammatory exudate. The sub-mucosa was thickened due to vascular congestionand also extravasation of blood into the tissues.The muscle coats were intact except for areas ofvascular congestion and infarction due to scatteredthrombosis of arterioles. The peritoneal coat wasthickened and congested.

DiscussionOcclusion of the mesenteric vessels is not rare.

The condition may occur at any age, but the agesof the majority are in the third to seventh decades.Cases in childhood are usually associated withintra-abdominal infection. The male sex pre-dominates in the ratio 3: 2. Trotter (I9I3)found in a series of 360 cases that 41 per cent. ofcases of intestinal infarction were due to venousocclusion, 53 per cent. to arterial occlusions and6 per cent. to simultaneous occlusions of bothvessels. The vessels most commonly affected arebranches of the superior mesenteric vessel supply-ing the small intestine. It is rare for the colonto be involved and the commonest site is theascending colon which is involved twice as fre-quently as the transverse colon and this twice asfrequently as the descending and sigmoid colon.The recto-sigmoid junction has been thought tohave an inadequate collateral circulation (Sudeck,1907). However, McGowan (1955) considers thatintramural anastomotic channels are the meanswhereby the collateral circulation is maintained inthis area following ligation or obstruction of theinferior mesenteric artery below its last sigmoidbranch. It is of interest that although this portionof the large intestine has been thought to have theweakest collateral circulation, that infarction isleast cornmon in the distal colon (Thomson, 1948).

F1

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FIG. 3.-Total colectomy specimen of fulminating ulcerative colitis with dilatation of theascending colon and hepatic flexure.

The effects of mesenteric vascular occlusiondepend on its site and extent. Trotter (19I3)records a case of complete occlusion by ananeurysm of the superior mesenteric vessels, yetthe bowel remained healthy as a sufficient col-lateral circulation had time to develop. Should theocclusion be sudden the result is infarction of aportion of the bowel since the superior mesentericvessel is functionally an end artery under suchconditions. Arterial occlusion may b6 due to anembolus from the heart or athero-sclerosis or evenan aneurysm of the mesenteric vessels. In thecase under discussion there was no clinical evi-dence of a cardiac lesion and the most likelycause was thought to be thrombosis of the middlecolic artery due to athero-sclerosis with subse-quent peripheral spread to involve the intramuralarterioles of the colon. Venous occlusion may bea primary thrombosis from no apparent cause, ormay be secondary to intra-abdominal sepsis suchas a gangrenous appendicitis, or portal venousthrombosis and cirrhosis of the liver, or malignantinfiltration of the mesenteric veins.The prognosis in mesenteric infarction is poor.

In the series of 6o cases at the Mayo Clinic re-viewed by Whittaker and Pemberton (I938) themortality was 95 per cent. and of those treatedsurgically it was 84.2 per cent. Gordin andLaurent (1956) reviewed 47 cases, of which onlythree left hospital alive. This may be due to thefatal extent of intestinal damage, poor health fromthe causative disease in the heart, intra-abdominalsepsis, malignancy or spread of the thrombosisfollowing treatment. Smith (I95i) consideredinfarction of the large intestine to be particularlylethal. However, some cases probably recoverwithout surgical treatment and remain undiag-nosed. The introduction of anticoagulants heldgreat promise and if the damage to the bowel isextensive, may offer the only hope. Its use afterresections theoretically prevents further throm-bosis and has been recommended by Murray(939). Laufman (I949), in experimental workin animals, was unable to show any difference inthe results after resection whether anticoagulantswere used or not.

Recently a most interesting case was describedby Lister and Jungmann (I956) in which infarction

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September 1958 COOLING and PROTHEROE: Infarction of the Colon 497

of the transverse colon and splenic flexure occurreddue to mesenteric thrombosis. Resection wasnot performed and barium enema studies revealedpictures analogous to those seen in chronic ulcera-tive colitis. Ultimately a faecal fistula developedand the infarcted bowel sloughed through thefistula.

Mucosal InfarctionVascular lesions have been suggested as a

cause of mucosal damage in ulcerative colitis bya number of authors (Proc. Int. Congress ofGastroenterology, 1956). It is of interest, there-fore, to compare the changes due to colonicinfarction with those of fulminating ulcerativecolitis.The macroscopic appearances of the mucous

membrane in the two conditions are very similar,as mucosal ulceration and congestion are a featureof the two diseases. Also in ulcerative colitis theulceration is frequently linear and related to thetaenia coli (Lium, 1939) (see Fig. 3). However,in fulminating ulcerative colitis whilst the historymay be short, two to three months on occasions,it is never as short as that in mesenteric infarction.Frequently there is an antecedent history of mildsymptoms (Lumb, Protheroe and Ramsay, I955)with evidence of recent mucosal spread to involvethe majority of the colon. Also dilatation of thecolon due to muscle damage is a common finding(see Fig. 4). This was not found in the case ofinfarction described by Lister and Jungmann(1956) or in the present case.

Vascular lesions of the intramural vessels havebeen suggested as the cause of the mucosaldamage in ulcerative colitis. Gallart Mones (1954and 1956) believes that submucosal thrombosisoccurs with subsequent infarction and miliaryabscess formation. Warren and Sommers (1949)felt that the changes in I9 of i 8o specimens re-sulted from mucosal degeneration following aninadequate blood supply caused by necrosis andthrombosis of blood vessels in the submucosa andmesentery. Similar findings in a smaller serieswere reported by Ihre (1956).

Vascular lesions of the colon are found in peri-arteritis nodosa. Gastro-intestinal symptoms andlesions are found in 62 per cent. of cases (Nizumand Nizum, 1954), but they are usually confinedto the upper gastro-intestinal tract. However,the mesenteric arteries are involved in 25 per cent.of cases (Diaz Rivera and Miller, I946), butthrombosis of the principal branches of themesenteric arteries is rare (Felsen, 194I). It isusually the intramural branches which are in-volved and arborization is sufficient to preventmassive infarction.The lesions in the colon, however, are usually

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FIG. 4.-Vascular congestion of the ulcerated mucousmembrane and destruction of muscle coats in ful-minating ulcerative colitis. Haematoxylin andeosin x 96.

overshadowed by others in more important organs.Lawrie (I955) described two cases with wide-spread small ulcers in the colon the result of smallsubmucosal infarcts, and in one of the seven casesreported by Diaz Rivera and Miller (I946) therewas widespread involvement of the colon withsmall ulcers separated by intact mucosa. Accord-ing to Felsen (I94I) the sigmoidoscopic appear-ances of periarteritis nodosa are very characteristic,and different from ulcerative colitis. Indeed, heconsidered that periarteritis nodosa could be diag-nosed by sigmoidoscopic examination as horizontallinear dark red streaks in parallel lines can be seenbeneath the intact mucosa of the rectum.

Interest has recently been revived in the gastro-intestinal manifestations of systemic lupus ery-thematosis (S.L.E.). Harvey et al. (1954) reviewed138 patients with S.L.E. and found that I4 percent. complained of nausea, i i per cent. of vomit-ing, 8 per cent. of diarrhoea, 5 per cent. of gastro-intestinal haemorrhage, io per cent. of abdominalpain and 6 per cent. of dysphagia. They reported

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FIG. 5.-Thrombosed submucosal arteriole in ful-minating ulcerative colitis. Note absence of infarc-tion. Haematoxvlin and eosin X 30.

involvement of the large bowel in five patientswith S.L.E.; in four of whom there was anarteritis, with ulceration of the mucosa. Theydid not report whether the findings were similarto those seen in ulcerative colitis.Brown et al. (i956b) reviewed the gastro-

intestinal manifestations in 87 patients havingS.L.E. Seven had severe gastro-intestinal symp-toms which constituted major problems in diag-nosis and treatment. Two patients had S.L.E.and ulcerative colitis. One patient (Brown et al.,I956a) had a long history of colitis and the entirecolon was involved with superimposed rheumatoidarthritis and cardiac involvement. The secondpatient had atypical ulcerative colitis with hepatitisand lupus erythematosis. This association is un-common and only three cases, including a caseseen by Boone and McKee (1955) have beenreported. The two conditions have much incommon. The systemic complications of ulcera-tive colitis (arthritis, erythema nodosum, iritis,pyoderma gangrenosum, stomatitis, etc.) suggestthat it might be a collagen disease similar toS.L.E. Some authors (Levine et al., 195I, andJacobson and Kirsner, 1956) have shown thatthere is a deficiency of ' ground glass substance 'of the basement membrane of the mucosal cellsin chronic ulcerative colitis. However, this hasnot been confirmed in the uninvolved mucousmembrane (Lumb and Protheroe, I957). TheL.E. test will clearly be of use in differentiatingthe two conditions provided it is rememberedthat the L.E. test is not entirely specific for S.L.E.(Holman, I95I).One of the authors has recently had the oppor-

tunity of examining I 52 surgical specimens ofulcerative colitis (Lumb and Protheroe, I958).In the fulminating cases of the disease, vascular

dilatation and congestion and haemorrhage intothe inflamed tissues is a marked feature leading tointense mucosal reddening, and isolated throm-bosed or thickened arterioles are seen due, wethink, to spread of the inflammation to involve thewalls of blood vessels (see Fig. 5). No case ofcolonic infarction or sloughing was seen, dueprobably to the abundant anastomoses and overlapbetween the small arterioles supplying the wall ofthe colon. Further study is needed to determinewhether the earliest changes in this disease occurin the capillaries of the lamina propria of themucous membrane, as suggested by Busson,Delarue and le Quintrec (I954), or in the base-ment membrane (Jacobson and Kirsner, I956), orin the lining epithelium (Lumb and Protheroe,I957). In the meantime it seems best to separateulcerative colitis from the group of so-calledcollagen diseases.

SummaryA case of massive infarction of the transverse

colon due to thrombosis of the middle colic arteryis described.The case was successfully treated surgically.The aetiology of massive colonic infarction is

discussed.Colonic infarction is discussed in relation to

periarteritis nodosa, systemic lupus erythematosisand ulcerative colitis. Notwithstanding the fre-quency of thrombosis of submucosal vessels inthese conditions, massive infarction is rare pre-sumably due to abundant intramural anastomoses,Our thanks are due to Mr. A. Lawrence Abel,

M.S., F.R.C.S., for permission to publish thecase of colonic infarction and also to Dr. PeterHansell for photographs of the specimens.

BIBLIOGRAPHYBOONE, J., and McKEE, J. A. (I955), 'Hospital for Sick Children,

Toronto, Ontario, Canada.' Unpublished communication.-BROWN, C. H., HASERICK, J. R., and SHIREY, E. K. (1956a),

Cleveland Clin. Quart., 23, 43.BROWN, C. H., SHIREY, E. K., and HASERICK, J. R. (1956b),

Gastroenterology, 3I, 649.BUSSON, A., DELARUE, J., and LE QUINTREC, Y. (I954),

Arch. Mal. Appar. dig., 43, 1154.BUSSON, A., and DELARUE, J. (i956), 'Proc. Int. Cong. Gastro-

enterology,' London, June I956. Gastroenterologia, 86, 656.DIAZ-RIVERA, R. S., and MILLER, A. J. (1946), Ann. intern.

Med., 24, 420.DZIALOSWYNSKI, H. (1925), Zbl. Chir., 52, 2120.FELSEN, J. (I94I, Ann. intern. Med., 15, 25I.GALLART MONPS, F. (I954), Minerva chir. (Torino), 9, 477.GALLART MONPS, F. (1956), 'Proc. Int. Cong. Gastroentero-

logy,' London, June 1956. Gastroenterologia, 86, 632.GORDIN, R., and LAURENT, L. E. (1956), Acta med. scand.,

154, 267.HARVEY, A. M., SHULMAN, L. E., TUMULTY, P. A.,

CONLEY, C. L., and SCHOENRICH, E. H. (1954), Medicine,33, 2931.

HOLMAN, S. (95s), J. clin. Path., 4, 290.IHRE, B. J. E. (I956), ' Proc. Int. Cong. Gastroenterology,' London,

June 1956. Gastroenterologia, 86, 666.

Bibliography continued on next page

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Bibikography continuedfrom preceding page-C. I. Coolinga. F.R.C.S.. and R. H. B. Protheroe. M.D.JACOBSON, M. A., and KIRSNER, J. B. (I956), Gastroenterology,

30, 279.LAUFMANN, H. (1942), Surg. Gynec. Obstet., 74, 479.LAWRIE, T. D. (i955), Glasg. med. J., 36, 220.LEVINE, M. D., KIRSNER, J. B., and KLOTZ, A. P. (195I),

Science, 1I4, 552.LISTER, E. F., and JUNGMANN, H. (1956), Brit. J. Radiol.,

29, 341-LIUM, R. (1939), Arch. intern. Med., 63, 210.LUMB, G. D., PROTHEROE, R. H. B., and RAMSAY, G. S.

(Iq95), Brit. J. Surg., 43, I82.LUMB, G. D., and PROTHEROE, R. H. B. (I958), Gastro-

enterology, in press.LUMB, G. D., and PROTHEROE, R. H. B. (1957), Gastro-

enterology, 33, 457.

McGOWAN, J. R. (I955), Arch. Surg. (Chicago), 71, 531.MURRAY, G. D. W. (1939-40), Brit. J. Surg., 27, 567.NUZUM, J. W. (Jnr.), and NUZUM, J. W. (Snr.) (I954), Arch.

intern. Med., 84, 942.SMITH, R. (I95I), Postgrad. med. J., 27, 502.SUDECK, P. (1907), Munch. med. Wschr., 54, 1314.THOMSON, F. B. (1949), Canad. med. Ass. J., 58, I83.TROTTER, L. B. C. (1913), 'Embolism and Thrombosis of the

Mesenteric Vessels,' Cambridge University Press.WARREN, S., and SOMMERS, S. C. (I949), Amer. Y. Path.

25, 657.WHITTAKER, L. D., and PEMBERTON, J. J. (I938), Y. Amer.

med. Ass., III, 2I.

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