Ischaemic Bowel Disease

J Clin Pathol: first published as 10.1136/jcp.s3-11.1.68 on 1 January 1977. Downloaded from J. clin. Path., 30, Suppl. (Roy. Coll. Path.), 11, 68-77 Ischaemic bowel disease T. ALSCHIBAJA AND B. C. MORSON From the Department ofPathology, St Mark's Hospital, London A supply of oxygenated blood appropriate to the tis- Natural history sue needs of the gut is essential to the maintenance of its vital functions. The splanchnic vascular system The natural history of ischaemic bowel disease can serves this purpose and much of our knowledge of be described as a complex but related series of cel- ischaemic bowel disease has developed from studies lular and tissue reactions to anoxic injury produced ofradiological and pathological abnormalities of this by interruption of a supply of oxygenated blood system. The purpose of this paper is to summarize sufficient for the functions of the bowel, no matter current information concerning the histopathology of what the cause. The extent and the forms of these intestinal ischaemia in the light of our better under- reactions vary with the severity and duration of the standing of the micro-circulation of the gut in health ischaemia, the adequacy of collateral avenues of and disease; also to describe the difficulties we have blood supply and the capability of the affected cells in understanding the pathogenesis of ischaemic and tissues to survive and regenerate. The alterations bowel disease because of the growing spectrum of provoked in this cycle of reaction to injury range systemic disorders with which it is associated. from minor degrees of change in the most vulnerable cells of the mucosal villi through major but reversible Nomenclature degrees of destruction of the mucosa and submucosacopyright. to irreversible full-thickness gangrene of the bowel Until recent times ischaemic bowel disease was a wall. There are many gradations and overlaps clinical entity recognized usually in its irreversible in the stages of survival and restoration of tissues and fatal forms and less frequently in its reversible many variations in the resultant gross and micro- chronic forms. Protean clinical manifestations and scopic features, all reflected to varying degrees in a resemblance to inflammatory disorders of the bowel spectrum of clinical events and radiological findings. led to a multiplicity of names for presumably The section of gut affected, the extent and multi-http://jcp.bmj.com/ separate entities with common pathological features plicity of the sites involved, the patterns of involve- -names such as haemorrhagic necrosis, necrotizing ment and secondary alterations such as stenosis, enterocolitis, membranous or pseudomembranous megacolon, ulceration, 'cobblestoning', etc, add to enterocolitis, infarction, gangrene, ischaemic stric- the morphological diversity of the disorder and tend ture, clostridial or staphylococcal enterocolitis, to obscure the identity of its cause. uraemic enterocolitis, necrotizingenterocolitis, phleg- Major vascular occlusion is not required to pro- monous enterocolitis, etc (table I). This report duce a serious degree of ischaemia in the bowel. The on September 25, 2021 by guest. Protected occurrence of intestinal gangrene without demon- strable vascular occlusion is recognized clinically and Ischaemic enterocolitis Infarction of the intestinal tract experimentally (Williams et al, 1967; Marston, 1972; Intestinal gangrene Whitehead, 1972; Marcuson, 1974). Occlusion due Haemorrhagic enterocolitis low- Neonatal necrotizing enterocolitis to functional constriction, cardiogenic shock, Uraemic enterocolitis flow states or remote partial organic obstruction is Phlegmonous or croupous enterocolitis usually operative in these instances. The essence of Clostridial enterocolitis Pseudomembranous or antibiotic enterocolitis the matter is that the gut is equally susceptible to ischaemic necrosis from a summation of minor Table I Nomenclature of ischaemic bowel disease vascular deficiencies as well as from single demon- strable major occlusions. describes ischaemic bowel disease in general no mat- The reaction to moderately severe ischaemia fol- ter what its cause and describes gross and micro- lows a predictable course of inflammation and repair scopic pathological features differentiating this divisible into three general phases: (1) acute, with entity in particular from inflammatory bowel disease. haemorrhage and necrosis; (2) reparative, with 68 J Clin Pathol: first published as 10.1136/jcp.s3-11.1.68 on 1 January 1977. Downloaded from Ischaemic bowel disease 69 granulation tissue formation and fibrosis and (3) later been shown that the blood supply at this point is forms of residual pathology with bowel constriction precarious as the anastomosis is frequently deficient and chronic complications (table II). The pre- (Marston, 1972). Ischaemic stricture of the right dominant gross and microscopic features charac- colon is rare perhaps because this part of the gut has teristic of these phases are described in the following a rich blood supply. sections. A transient, 'self-healing' form of intestinal Whilst rectal involvement was considered initially ischaemia is known experimentally and is thought to rare or even non-existent, rectal lesions are now occur in humans also when the initial injury is slight recognized with increasing frequency (Kilpatrick et or of short duration and collateral blood flow is al, 1968). The distribution and the pattern of involve- adequate. Severe and prolonged ischaemia causes ment bear no relationship to the severity of the segmental infarction of the bowel and subsequent ischaemia, but specific precipitating causes of gangrene leading to perforation and peritonitis ischaemic damage appear to show a predilection for (Marston et al, 1966). certain areas. Thus ligation of the inferior mesenteric artery usually results in ischaemic lesions of the Phases of Injury and Repair sigmoid colon, while low-flow state affects primarily the splenic flexure. Similarly the length of bowel Category Types of Response Tissue Alterations involved varies with the aetiology: atheromatous 1 Acute Oedema, haemorrhage, occlusion produces short segmental damage, while necrosis lesions 2 Repair Epithelial regeneration, low-flow states result in much longer granulation tissue (Marston et al, 1966). formation, chronic Analysis of 358 clinical examples of ischaemic inflammation, mural fibrosis colitis in which segmental location of the lesion was 3 Residual pathology Panmural fibrosis, described gives the following distribution (fig 1) Stenosis (McGovern and Goulston, 1965; Marston et al, Table II Natural history of ischaemic bowel disease 1966; Moller and Stjernvall, 1971; Marcuson, 1972, 1974; Kaminski et al, 1973; Williams and Willenberg, copyright. Location of ischaemic bowel disease 1975). Right colon ....................... 27 The location and extent of ischaemic lesions of the Transverse colon .................... 54 intestine reflect the anatomy and physiology of the Splenic flexure ...................... 84 blood supply and the anastomosing network of Descending and sigmoid colon ........ 99 secondary vessels which supply the various divisions of the alimentary tract. The ischaemic lesions them- selves vary from focal forms such as the sharply http://jcp.bmj.com/ localized annular ulcers of the ileum associated with the intake of enteric-coated potassium tablets to the massive forms of infarction seen with acute mesenteric arterial thrombosis or venous occlusion. In some instances the location of the ischaemic injury is determined by the anatomy of the blood supply and the precipitating cause, ie, compression on September 25, 2021 by guest. Protected of the superior mesenteric artery by an adhesive bond or occlusion of the inferior mesenteric artery by aortic aneurysm. In other cases the injury is so extensive that it can only be the manifestation of a generalized vascular disorder such as heart failure or hypotension, Es occurs in myocardial infarction or by a widespread small vessel occlusion due to spasm or intravascular coagulation. Ischaemia may involve any portion of the colon. However, the area of maximum susceptibility is the watershed area between the superior and inferior mesenteric vessels and thus the common site of ischaemic lesions is the region of the splenic flexure. The splenic flexure is the point where the superior and inferior mesenteric arteries anastomose; it has Fig 1 Distribution of358 cases of ischaemic colitis. J Clin Pathol: first published as 10.1136/jcp.s3-11.1.68 on 1 January 1977. Downloaded from 70 T. Alschibaja and B. C. Morson The blood supply of the small intestine benefits from the abundant system of anastomosing arcades which are less numerous in the colon and which perhaps explain the less frequent occurrence of vascular damage in the small bowel. Segmental ischaemic lesions of the small intestine are usually confined to the jejunum and ileum and most often result from external vascular obstruction due to compression or twisting (adhesive band, volvulus, internal hernias, neoplasms, trauma). Ischaemia due to intramural vascular occlusion is caused by small vessel thrombosis or stenosis and is usually associated with systemic vascular disorders, hypotension or the use of the enteric-coated potassium or thiazide treatment for hypertension. In 27 cases of ischaemic en;erocolitis reported by McGovern and Goulston there were 12 instances of involvement of the small intestine (McGovern and Goulston, 1965). The ileum alone was involved

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