Diverticulosis and Diverticulitis

Colonic diverticula do not arise randomly from the circumference of the large intestine but tend to originate in four distinct rows (Fig. 15-48): (a) on either side of the TM and (b) near the mesenteric borders of the TO

and TL.5,21 These are related to the points of intramural penetration through connective tissue septa of the co-lonic wall.21 Their sites of origin from the TM-TL and TM-TO haustra can be identified clearly on routine radiographic studies (Fig. 15-49).

Bona fide diverticula do not arise from the TO-TL antimesenteric row of sacculations. At surgery or autopsy, only pinhead protrusions may be noted occasionally in association with this row, but they are not identifiable on contrast studies, and no clinical significance has been attributed to them. On frontal and even oblique views, diverticula may project laterally from the lower descending and sigmoid colon. This appearance is related to the fact that the TO and TL anatomically approach each other in this region, reducing the dimensions of their intervening haustra. Lateral views, however, consistently show that these diverticula actually arise from the posterior wall (TM-TO).

Colonic Diverticular Angioarchitecture and Hemorrhage

Colonic diverticulosis increases in incidence with each decade of adult life and occurs in as many as 35-50% of individuals over 60 years ofage.22 Diverticula ofthe large intestine constitute a common source of lower gastrointestinal bleeding, both occult and massive, and are a particularly common cause of right-sided colonic hemorrhage.21,23,24 Colonic diverticulosis is the most frequent

Diverticulitis Bleed

Fig. 15-46. Duplication of colon.

Barium enema study demonstrates a tubular communicating duplication (D) within the mesentery of the transverse colon. Its lower border conforms to the superior haustral row of the transverse colon.

Fig. 15-46. Duplication of colon.

Barium enema study demonstrates a tubular communicating duplication (D) within the mesentery of the transverse colon. Its lower border conforms to the superior haustral row of the transverse colon.

Microcolon

Fig. 15-47. Duplication of colon.

(a) Barium enema study demonstrates a narrow, tortuous duplication in the mesentery of the descending colon.

(b) Following selective opacification of the duplication, the "microcolon" is outlined throughout the mesenteric border of the large intestine, ending blindly at the level of the cecum.

(Reproduced from Beyer et al.19)

Fig. 15-47. Duplication of colon.

(a) Barium enema study demonstrates a narrow, tortuous duplication in the mesentery of the descending colon.

(b) Following selective opacification of the duplication, the "microcolon" is outlined throughout the mesenteric border of the large intestine, ending blindly at the level of the cecum.

(Reproduced from Beyer et al.19)

cause of severe rectal bleeding.25 The hemorrhage is typically acute, massive, and life threatening, in contrast to the mild and often intermittent bleeding secondary to diverticulitis, which apparently originates from highly vascularized granulation tissue lining inflamed diverticula.26

Angioarchitecture and Pathogenesis of Bleeding. Meyers et al. have defined the characteristic angioarchitecture of colonic diverticula21 and shown their structural predisposition to massive bleeding.27,28 The four distinct longitudinal rows from which diverticula arise (Fig. 15-50) correspond closely with the four sites of penetration of

Fig. 15-48. Sites of origin of colonic diverticula.

Note that the antimesenteric TO-TL haustral row does give rise to diverticula. (Reproduced from Meyers et al.5)

Diverticula Vasa RectaDiverticulum Vasa Recta

Fig. 15-49. Diverticula (arrowheads) arise from the TM-TO and TM-TL rows, but none originates from the antimesen-teric TO-TL haustra. (Reproduced from Meyers et al.5)

Diverticulosis Vasa Recta

the major branches of the vasa recta, the colonic branches of the marginal artery (Fig. 15-51).

Injection studies have shown that a prominent long vasa recta courses in an intimate subserosal position over the dome of every colonic diverticulum (Figs. 15-52 and 15-53a) to reappear as either a single or multiple submucosal branches along the antimesenteric side of its orifice (Fig. 15-53b). Rather than the point of vascular penetration directly leading to a weakness (locus minoris resistentiae) in the bowel wall predisposing to the for mation of diverticula,29 we have shown that it is the obliquely oriented connective-tissue septa separating the circular smooth muscle bundles of the colonic walls that constitute the common plane of least resistance. It is clearly through these septa that both the vasa recta consistently penetrate the colonic wall from the serosa to the submucosa (Fig. 15-54) and the diverticula form from mucosal protrusions.21 Segmentation of the colon produced by muscular contraction leads to localized increased intraluminal pressure that results in herniation

Taenia Mesocolica

Fig. 15—51. (a) Sites of origin of colonic diverticula in relation to taenia.

Diverticula point toward mesenteric border. (b) Intramural blood supply of colon.

Vasa recta reach bowel wall and divide into long subserosal branches that then penetrate obliquely through bowel wall. Short branches penetrate near the taenia mesocolica (TM). They continue in submucosa, finally ramifying into rich plexus.

(Reproduced from Meyers et al.27)

Fig. 15—51. (a) Sites of origin of colonic diverticula in relation to taenia.

Diverticula point toward mesenteric border. (b) Intramural blood supply of colon.

Vasa recta reach bowel wall and divide into long subserosal branches that then penetrate obliquely through bowel wall. Short branches penetrate near the taenia mesocolica (TM). They continue in submucosa, finally ramifying into rich plexus.

(Reproduced from Meyers et al.27)

Fig. 15—52. Radiograph of sigmoid colon with injected arterial supply.

The circumferential branches of the vasa recta are deflected immediately over the domes of diverticula (D), and short branches of these are displaced around their necks. (Reproduced from Meyers et al.21)

Gross RelationshipVasculitis Diverticulitis

Fig. 15-53. Gross vascular relationships of colonic diverticula.

(a) Photograph of serosal surface of ascending colon. Prominent injected vasa recta (arrows) course from the mesenteric side on the right over the domes of two diverticula. In penetrating the colonic wall, they disappear from view on the antimesenteric borders of the diverticula, near a taenia (T).

(b) Enlarged photograph of the mucosal surface of two diverticula. The branches of the injected vasa recta reappear in the submucosa on the antimesenteric side of the orifices of the diverticula (D). (Reproduced from Meyers et al.21)

Fig. 15-53. Gross vascular relationships of colonic diverticula.

(a) Photograph of serosal surface of ascending colon. Prominent injected vasa recta (arrows) course from the mesenteric side on the right over the domes of two diverticula. In penetrating the colonic wall, they disappear from view on the antimesenteric borders of the diverticula, near a taenia (T).

(b) Enlarged photograph of the mucosal surface of two diverticula. The branches of the injected vasa recta reappear in the submucosa on the antimesenteric side of the orifices of the diverticula (D). (Reproduced from Meyers et al.21)

Vasa Recta Colon Diverticula

Fig. 15-54. Penetration of vasa recta (VR) from serosa to submucosa.

Transverse histologic section shows that it occurs through a widened, obliquely oriented connective-tissue cleft between fascicles of circular muscle (CM). (Reproduced from Meyers et al.21)

Fig. 15-54. Penetration of vasa recta (VR) from serosa to submucosa.

Transverse histologic section shows that it occurs through a widened, obliquely oriented connective-tissue cleft between fascicles of circular muscle (CM). (Reproduced from Meyers et al.21)

of mucosa and submucosa through these natural weaknesses in the colonic wall.30'31

These anatomic relationships result in a remarkably constant angioarchitecture of colonic diverticula (Figs. 15-55 and 15-56). An artery of considerable relative size, the vas rectum, intimately courses in the serosa over the dome of the diverticulum; at this point, it is separated from the lumen of the diverticulum by only mu-

cosa and a few strands of attenuated muscle fibers. The vas rectum then penetrates the colonic wall along the antimesenteric margin of the diverticulum, lying close to its neck and orifice.

The pathogenesis of massively bleeding diverticulosis is primarily determined by their distinctive angioarchi-tecture.27 28 Histologic changes at the precise site of bleeding show asymmetric rupture of the vas rectum

Fig. 15—55. Structural dynamics of diverticular formation and vascular relationships.

(a) The vas rectum normally penetrates the colonic wall from the serosa to the submucosa through an obliquely oriented connective-tissue septum in the circular muscle (CM). This occurs near the mesenteric side of a taenia (T).

(b) The mucosal protrusion marking the development of a diverticulum occurs through, and consequently widens, the connective-tissue cleft. In doing this, it begins to lift up the artery.

(c) With transmural extension of the diverticulum, the vas rectum is displaced over its dome and therefore penetrates to the submucosa on the antimesenteric border of its neck and orifice.

(Modified from Meyers et al.21)

COLONIC LUMEN

COLONIC LUMEN

Antimesenteric Border Diverticulum

Fig. 15—56. Characteristic angioarchitecture of colonic diverticula.

Radiograph of colonic diverticulum with injected vas rectum. The vas rectum (VR) approaches the diverticulum (D) from its mesenteric border, arches in the serosa immediately over its dome, and penetrates the colonic wall on its antimesenteric margin (arrow). CM designates the approximate location of circular muscle. (Original magnification, X 8.)

(Modified from Meyers et al.21)

Antimesenteric SerosaDiverticulocis Com

toward the lumen of the diverticulum precisely at its dome or antimesenteric margin. The changes are associated with conspicuous eccentric intimal thickening of the vas rectum, often with medial thinning and duplication of the internal elastic lamina (Figs. 15-57 through

15-59). The mechanism involves injurious factors arising within the diverticular or colonic lumen that induce eccentric intimal proliferation and weakening of the associated vasa recta, predisposing to rupture and massive bleeding (Fig. 15-60). It is important to recognize that

Vasa Recta Rectum

Fig. 15-57. Eccentric mural changes in vas rectum in case of bleeding diverticulum.

Vas rectum in area of hemorrhage demonstrates duplication of internal elastic lamina (arrows) with lamellar arrangement and marked eccentric thickening of intima. D = mucosa of diverticulum. (Elastic van Gieson; original magnification, X65.)

(Reproduced from Meyers et al.28)

Fig. 15-58. Histologic section through the bleeding point in a case of colonic diverticular hemorrhage.

The vas rectum (arrows) courses over the dome of the diverticu-lum from the right, extends along its antimesenteric margin, and has ruptured (curved arrow) near the neck of the diverticu-lum. (Elastic van Gieson; original magnification, X65.) (Reproduced from Meyers et al. )

Fig. 15-58. Histologic section through the bleeding point in a case of colonic diverticular hemorrhage.

The vas rectum (arrows) courses over the dome of the diverticu-lum from the right, extends along its antimesenteric margin, and has ruptured (curved arrow) near the neck of the diverticu-lum. (Elastic van Gieson; original magnification, X65.) (Reproduced from Meyers et al. )

Fig. 15—59. Histologic section through the bleeding point in a case of colonic diverticular hemorrhage.

A thrombus (T) projects from the lumen of the ruptured vas rectum (VR) through a small mucosal erosion into the lumen of the diverticulum (D). The vas rectum shows marked intimal thickening (arrows) that is visible deep to the darkly stained internal elastic lamina. The thickening is strikingly eccentric toward the lumen of the diverticulum, and the media of the artery is absent in this area. (Elastic van Gieson; original magnification, x65.) (Reproduced from Meyers et al.28)

Diverticulocis Com

Injurious

Pictures Diverticulitis That Rupture

Initial damage Eccentric Concentric Eccentric rupture intimal intimal thickening thickening with luminal accentuation

Fig. 15—60. Pathogenesis of colonic diverticular hemorrhage.

Progressive eccentric changes weaken the wall of the vas rectum, which finally ruptures into the lumen of the diverticulum. (Reproduced from Meyers et al. )

smooth muscle cells of the media develop the intimal layer, so that intimal proliferation results in attenuation and weakening of the muscular component of the vas rectum. This explains why rectal hemorrhage, rather than intraperitoneal or extraperitoneal bleeding, is a consequence of this condition.

The predominance of hemorrhage from right-sided diverticula is noteworthy since the majority of divertic-ula are located in the descending and sigmoid colon, and only about one-third of patients with diverticulosis have diffuse involvement of the large intestine. One anatomic feature distinguishes right-sided from left-sided diverticula, which may explain their increased frequency of bleeding. Because the diverticula arising in the right colon have wider necks and domes, their vasa recta are exposed over a greater length to injurious factors arising from the colon.27,28

Arteriography Diagnosis and Management. In the diagnosis and management of massive diverticular hemorrhage, the primary problem is accurate localization of the bleeding point. Selective arteriography may readily accomplish this, allowing a trial of nonoperative control of hemorrhage by infusion of vasopressin, permitting more specific and limited colonic resection when bleed-

24 32 33

ing is uncontrolled or recurrent. ' ' Extravasation is shown in virtually all cases of acutely bleeding diverticula23,24 as a circular accumulation of the contrast medium within the confines of the diverticulum (Fig. 15-61) that, in the presence of extremely brisk bleeding, may overflow to opacify the lumen of one or several haustral sacculations. The feeding vas rectum itself can be iden tified and, at times, its precise point of rupture21 (Fig. 15-61).

Vasoconstrictive therapy immediately following arteriography diagnosis and localization provides an effec-

23,32,33

tive method that may make operation avoidable.

Bleeding may recur within hours or days of the initial control,23,33 but the temporary cessation of bleeding provides time for stabilization of the patient's clinical condition before segmental colectomy. Occasionally, rebleeding has been encountered within several months,23 which may be a consequence of dislodgment of the thrombus that characteristically extends into the lumen

21,27,28

of the diverticulum. ' ' Recurrent bleeding from a second distant diverticulum has been documented only rarely.34

If vasopressin fails to control diverticular bleeding in a patient who is a poor surgical risk, embolization of the bleeding artery may be carried out,34 but this incurs the risk of potential ischemic injury to the colon35,36 because of the relative lack of collateral blood supply.

Colonoscopic treatment by bipolar electrocoagula-tion of the identified bleeding vessel in the neck of the diverticulum37 or by peridiverticular epinephrine injec-tion38 has been recently reported.

Diverticulitis

The majority of diverticula are related to extraperitoneal tissues (Fig. 15-48). Diverticulitis may thus result in a localized inflammatory process involving only the TM-TL or TM-TO haustra (Fig. 15-62). Mesenteric abscesses and extraperitoneal gas or abscesses are well-

Extraperitoneal Rectal Injury

Fig. 15—61. Extravasation into an acutely bleeding right colon diverticulum shown by selective superior mesenteric arteriography.

A vas rectum (arrowheads) courses typically over the dome of the diverticulum and appears intact in this segment, indicating its point of arterial rupture to be on the antimesenteric margin of the diverticulum.

(Reproduced from Meyers et al.21)

Fig. 15—61. Extravasation into an acutely bleeding right colon diverticulum shown by selective superior mesenteric arteriography.

A vas rectum (arrowheads) courses typically over the dome of the diverticulum and appears intact in this segment, indicating its point of arterial rupture to be on the antimesenteric margin of the diverticulum.

(Reproduced from Meyers et al.21)

recognized complications of diverticulitis39 (Fig. 15-63). Many cases of intestinovesical fistulas are secondary to extraperitoneal extension of an inflammatory or suppurative process from the diverticulum and then perforation through the base of the urinary bladder (Fig. 1564). Rarely, communication from a perforated divertic-

Sigmoid Colon Laying Bladder

Fig. 15—62. Diverticulitis of the hepatic flexure.

Left posterior oblique projection. Localized inflammatory changes involve the TM-TO haustra. (Reproduced from Meyers et al.5)

ulum may be established to the inferior mesenteric venous drainage, leading to intrahepatic portal venous gas40 (Figs. 15-65 and 15-66). Furthermore, the absence of diverticular origin from the lateral haustral rows facing

Diverticulitis

Fig. 15-64. Sigmoid diverticulitis with fistulization to urinary bladder.

CT documents inflammatory adherence of the sigmoid colon (SC), demonstrating mural thickening and several gas containing diverticula to the urinary bladder (B), which has air in its lumen.

Fig. 15-64. Sigmoid diverticulitis with fistulization to urinary bladder.

CT documents inflammatory adherence of the sigmoid colon (SC), demonstrating mural thickening and several gas containing diverticula to the urinary bladder (B), which has air in its lumen.

Muscular Hypertrophy Sigmoid Colon

Fig. 15—63. Extraperitoneal diverticular abscess.

(a) Gas-containing diverticular abscess (A) is characteristically localized to the extraperitoneal fatty tissue within the pelvis, having arisen from (b) underlying diverticula-bearing sigmoid colon involved with circular muscle hypertrophy.

Fig. 15—63. Extraperitoneal diverticular abscess.

(a) Gas-containing diverticular abscess (A) is characteristically localized to the extraperitoneal fatty tissue within the pelvis, having arisen from (b) underlying diverticula-bearing sigmoid colon involved with circular muscle hypertrophy.

the intraperitoneal lateral paracolic gutters provides an explanation for the low incidence of subhepatic and sub-phrenic abscesses secondary to diverticulitis. Thus, localized involvement of the TO-TL haustra alone cannot be secondary to diverticulitis. Inflammatory reaction of these haustra consequent to diverticulitis affecting one or both of the mesenteric rows indicates an extensive paracolic abscess.

Diverticulitis Complicating Granulomatous Colitis

Granulomatous colitis (Crohn's disease of the colon) is not unusual in patients over the age of 50 years and may affect any segment of the colon. The sigmoid colon is involved in 72% of primary Crohn's colitis and in 35% of granulomatous ileocolitis.42 Diverticulosis is also a a

DiverticulitisDiverticulocis Com
c
Appearance Diverticulosis

Fig. 15—65. Sigmoid diverticulitis leading to intrahepatic portal venous gas.

(a) Several diverticula are present within the thickened wall of the sigmoid colon. Mild inflammatory stranding of the paracolic fat is present. The findings reflect diverticulitis.

(b) At a higher level, gas within the inferior mesenteric vein is evident (arrow).

(c) This leads to distal portal venous gas within the liver.

Fig. 15—65. Sigmoid diverticulitis leading to intrahepatic portal venous gas.

(a) Several diverticula are present within the thickened wall of the sigmoid colon. Mild inflammatory stranding of the paracolic fat is present. The findings reflect diverticulitis.

(b) At a higher level, gas within the inferior mesenteric vein is evident (arrow).

(c) This leads to distal portal venous gas within the liver.

Crohns Disease Barium Enema

Fig. 15-66. Colovenous fistula complicating sigmoid diverticulitis.

(a) Abdominal radiograph following an attempted barium enema study demonstrates opacification of a long linear structure in the left abdomen, representing the inferior mesenteric vein (arrowheads). Multiple sigmoid diverticula are present.

(b) A delayed film reveals barium within the inferior mesenteric vein (open arrow), splenic vein (arrowhead), the superior mesenteric vein (large arrow), and portal venous radicles (small arrow).

(c) Noncontrast CT shows barium entering the splenic vein from the inferior mesenteric vein (arrowhead), passing into the portal venous confluence (open arrow), and within portal venous radicles in the right hepatic lobe (closed arrow).

(Reproduced from Rossman and Burr. )

Granulomatous Colitis

Fig. 15-66. Colovenous fistula complicating sigmoid diverticulitis.

(a) Abdominal radiograph following an attempted barium enema study demonstrates opacification of a long linear structure in the left abdomen, representing the inferior mesenteric vein (arrowheads). Multiple sigmoid diverticula are present.

(b) A delayed film reveals barium within the inferior mesenteric vein (open arrow), splenic vein (arrowhead), the superior mesenteric vein (large arrow), and portal venous radicles (small arrow).

(c) Noncontrast CT shows barium entering the splenic vein from the inferior mesenteric vein (arrowhead), passing into the portal venous confluence (open arrow), and within portal venous radicles in the right hepatic lobe (closed arrow).

(Reproduced from Rossman and Burr. )

common in this age group, particularly involving the sigmoid colon. The clinical and radiologic difficulty in distinguishing between segmental granulomatous colitis and diverticulitis has been described.43,44 Clinically, either may present with pain, partial obstruction, a lower abdominal mass, rectal bleeding, fever, and leukocytosis. Often, however, "the diagnostic problem is not primarily the distinguishing of Crohn's colitis from diverticular disease, but recognizing when the diseases coexist."45 I have shown, however, that the relationship is not one of chance coexistence, but rather that the involvement of diverticula by granulomatous colitis causes a 2- to 10fold increased incidence of diverticulitis.46

Granulomatous colitis is characterized by transmural inflammation, mucosal ulceration, and fissuring of the bowel wall, typically accompanied by the presence of a granulomatous tissue response.47 In contrast, diverticu-litis results from a microperforation or macroperforation of a diverticulum with sequelae such as deep sigmoiditis, perisigmoiditis (peridiverticulitis), or frank peritonitis.48 Because diverticula represent protrusions of mucosa and submucosa into and through the bowel wall, their involvement by Crohn's disease facilitates the transmural extension and paracolic complications of this disease process. The mucosal lining of diverticula may be the site of giant cell granulomas (Fig. 15-67) and aphthous ulcerations overlying lymphoid follicles, which may extend as dissecting intramural tracts (Fig. 15-68) and lead to the formation of pericolic abscesses.

The radiologic signs of peridiverticulitis complicating granulomatous colitis usually show clear evidence of the underlying pathologic changes. These include (a) the presence of aphthous ulcers, superficial ulcerations overlying areas of lymphoid hyperplasia, within diverticula that may indicate a predisposition to their rupture (Fig. 15-69); (b) localized diverticular perforation, perhaps with multiple communications (Figs. 15-70 and 15-71); and (c) mass pressure on the sigmoid colon from the paracolic abscess. Any extraluminal longitudinal sinus tract is thus almost invariably on the mesenteric border of the colon (Fig. 15-72).

Based on these histologic and radiologic observations, the pathogenic mechanisms of diverticulitis complicating granulomatous colitis are established (Fig. 15-73):

1. The earliest lesion of Crohn's disease is lymphoid hyperplasia followed by superficial ulceration.49,50 When this type of aphthous ulcer involves the mucosa of a diverticulum, it may undergo infection to result in per-idiverticulitis.

2. The deep fissuring characteristic of Crohn's disease may establish communication with one or several diverticula that may then be followed by peridiverticu-litis and/or abscess formation.

3. A paracolic abscess secondary to transmural fissuring ulcerations of severe Crohn's disease may penetrate through the domes of adjacent diverticula with further dissecting peridiverticulitis.

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