**7. Chagasic megacolon**

As previously described, this disease occurs in two phases, an acute one characterized by cell destruction, extensive inflammatory foci, and a large number of circulating parasites, and a chronic phase that can cause potentially fatal cardiac and digestive disorders [19]. It has been described that up to 40% of people who suffer from it will develop one of these complications or a combination of both [20]. Megacolon is defined as irreversible dilation of the colonic segment, predominantly in the chronic phase of Chagas disease, where the dilated segment presents histopathological changes characterized by a significant loss of neurons of the myenteric or Auerbach and submucosal or Meissner plexus and although not the mechanisms of this destruction are well elucidated, it has been proposed that it could be due to the release of toxins during the fragmentation of the parasite, direct cellular damage, or inflammatory damage [20, 21].

Recently it has been described that the progress to the chronic phase is determined mainly by an inflammatory state, to which the virulence of the parasite and its tropism for the tissues contribute. During Chagasic cardiomyopathy, there is an extensive production of pro-inflammatory cytokines, such as interferon γ (INF γ), Tumor Necrosis Factor α (TNF α), as well as other mechanisms that cause tissue damage, such as the cytotoxic activity of CD8 T lymphocytes [10]. Similarly, in Chagasic megacolon, the myenteric plexus is severely affected by an inflammatory process that leads to neuronal degeneration, ganglionitis, peri-ganglionitis, neuritis, and peri-neuritis. The inflammatory infiltrate has been characterized by the presence of eosinophils, mast cells, CD68 + macrophages, Natural Killer CD57 + cells, and TIA-1 + cytotoxic lymphocytes that maintain the inflammatory process and neuronal destruction [21]. It has also been described that the neuronal destruction process derives from an autoimmune response mediated mainly by TNF α and INF γ. Both cytokines are involved in the control of the parasite during acute infection, however, an imbalance in the response of these cytokines can lead to progression to chronicity and eventually to the cardiac and intestinal complications characteristic of the chronic phase of the disease [21]. The role of the megacolon in the context of intestinal neoplasms is controversial. It is suggested that derived from the dilation of the organ and the presence of food stasis, there is prolonged contact between the intestinal mucosa and potentially carcinogenic agents. In this context, the role of Galectin 3, a protein whose increased expression is related to tumor progression and which is used by *T. cruzi* to enter cells, has been studied, which suggests that there could be a relationship between this protein and neoplastic progression [22]. However, other studies have

sought to demonstrate that patients with chronic-phase Chagas disease have a lower risk of colon tumors at least in the megacolon region, probably derived from denervation in this area, since it has been proposed that neuronal invasion could promote tumor invasion [23].

According to current estimates, up to 10,000 deaths associated with this disease could occur annually [24], since between 15 and 20% of all cases will present digestive complications, including megaesophagus and megacolon [25]. The prevalence of megacolon in patients with Chagas disease may be higher in those who presented symptoms during the acute phase than in those in whom there were no manifestations in this phase [26].

Chagasic megacolon presents clinically with chronic constipation due to pathological dilation of the organ wall, mainly in the sigmoid portion of the colon, a site where *T. cruzi* is commonly found [27]. This is considered to be the most frequent symptom in patients with Chagasic megacolon, however, it has been reported that there are patients with normal evacuations, as well as patients with Chagas disease who present constipation not associated with megacolon.

Although this sequel is well known in the context of Chagas disease, few studies have described the clinical manifestations of its presentation, having little information on digestive visceromegaly caused by *T. cruzi*. In some case reports, constipation is reported as well as other associated signs and symptoms, such as bloating [28]. Likewise, it has been described those subjects with megacolon present a decrease in basal motility and wave frequency in manometry, absence of an inhibitory rectus-anal reflex, and it is noteworthy that in patients with diverticular disease and Chagasic megacolon, the diverticula appear in non-dilated portions of the colon [29].

The approach to patients with megacolon associated with Chagas disease is complex because most infected patients do not present symptoms in the acute phase; so, it is very likely that they will seek care when the typical manifestations of megacolon appear (constipation, abdominal pain, diarrhea, changes in defecatory habits, or bloody stools); in this situation, if the patient is not known to have trypanosomiasis and lives in an endemic area, it will be essential to make a proper diagnosis of this disease [30, 31]. When questioning these patients, other associated symptoms and signs should be identified, since heart disease coexists in up to 30% of cases. Likewise, it is necessary to question the patient about other digestive symptoms, since some of these are not associated with Chagas disease [30]. In the study of patients in the chronic phase, the diagnostic methods are indirect, that is, laboratory techniques that identify antigens of *T. cruzi* (direct hemagglutination) or antibodies against the parasite (Enzyme Immuno Assay, Indirect Immunofluorescence, Western Blot) [31].

The diagnosis of megacolon depends on clinical, radiological, endoscopic, and surgical findings. One of the most widely used radiological studies is the Barium enema or colon enema (**Figure 5**), with which the diagnosis can be confirmed if the rectosigmoid diameter at the pelvic border is greater than 6.5 cm or the diameter of the middle sigmoid is 10 cm or more. Computed tomography colonography can also be used as it allows measurement of the diameters and length of the colon from different views [32]. Colonoscopy is not the ideal study for the identification of megacolon, since it depends on the interpretation of the person who performs it, in this sense, the diagnosis can be made through the result of incomplete colonoscopy [32].

The management of megacolon will depend on the degree of constipation of the patient, his/her nutritional status, and his/her comorbidities. Treatment options are clinical or symptomatic and surgical. There is no consensus on the surgical management of choice, however, the most widely used procedure is the Duhamel-Haddad

*Digestive Disorders in Chagas Disease: Megaesophagus and Chagasic Megacolon DOI: http://dx.doi.org/10.5772/intechopen.102871*

#### **Figure 5.**

*Nervous plexuses of the digestive system.*

#### **Figure 6.** *Megaesophagus seen with barium esophagram.*

procedure (rectosigmoidectomy with retrocecal interposition) or rectosigmoidectomy with low end-to-side colorectal anastomosis (see **Figures 6**–**8**) [30].

It has been reported that complications derived from chronic constipation such as rectal prolapse or acute volvulus may occur [32, 33] (imagen 8). Of these, the most

**Figure 7.** *Barium enema showing megacolon.*

**Figure 8.** *Intraoperative image of sigmoid volvulation in chagasic megacolon.*
