Chapter 12 Dyschezia and Tenesmus
Definition
Dyschezia and tenesmus are clinical signs usually associated with colorectal disease. Dyschezia is the term applied to difficult or painful defecation, which is most commonly observed with anorectal disorders. Tenesmus is the clinical sign associated with straining to defecate (more common) or urinate (less common). Tenesmus is usually caused by large bowel disease, particularly colitis. Straining is usually evident as an animal maintaining a posture of defecation for an extended period, or as repeated, nonproductive attempts to defecate are observed. Tenesmus is often associated with other clinical signs of colonic disease including large bowel diarrhea (e.g., increased frequency of defecation, the production of scant fecal volume), hematochezia (fresh red blood on the feces), and/or excessive fecal mucus. Tenesmus is a clinical sign and not a disease; consequently, an underlying cause must be identified. In general, tenesmus and dyschezia are more commonly associated with colorectal disorders in dogs than in cats. Dysuria in cats with lower urinary tract disease may be misinterpreted as dyschezia and tenesmus.
Pathophysiology and Mechanisms
Inflammation of the colonic or rectal mucosa is the most common cause of tenesmus and dyschezia in dogs and cats.1–4 Tenesmus may also occur with colonic, rectal, or anal obstruction, and constipation. Dyschezia is usually caused by diseases involving anal and perianal structures.3,4 Severity of inflammation causing tenesmus or dyschezia is generally dictated by the magnitude of the host immune response. For example, mucosal inflammation of colonic inflammatory bowel disease (IBD) may be explained by (a) aberrant host responses to the colonic microbiota and (b) disturbances in colonic motility.5 A generic inflammatory response involving infiltrating immune cells (e.g., B and T lymphocytes, macrophages), secretomotor neurons (e.g., vasoactive intestinal polypeptide, substance P), cytokines (both T-helper type 1 [Th]1 and Th2 derived), and various inflammatory mediators (e.g., leukotrienes, prostanoids, reactive oxygen species, and nitric oxide metabolites) drive the chronic inflammatory process.5 Inflammation can cause suppression of normal colonic motility patterns, which may contribute to onset and severity of clinical signs. Other factors that may contribute to large bowel signs include previous therapies (especially antibiotics), bacterial fermentation (e.g., short-chain fatty acids [SCFA], lactate) products, altered composition of the colonic microbiota, and perturbed mucus secretion.
Other inflammatory conditions causing tenesmus and dyschezia can include helminths (Trichuris spp., Ancylostoma spp.), protozoa (Giardia spp., Trichomonas spp.), fungi (Histoplasma spp.), oomycetes (Pythium spp.), algae (Prototheca spp.), bacteria (Campylobacter spp., Clostridia spp., enteropathogenic/enterotoxigenic Escherichia coli), colorectal tumors, and rectal/anal strictures.2 Mechanism for mucosal inflammation with these disorders varies and includes local mucosal irritation (e.g., nematode parasites), robust host immune responses (e.g., histoplasmosis, pythiosis), and direct mucosal association (e.g., adherent and invasive E. coli [AIEC] as seen with granulomatous colitis).
Constipation is another important cause of tenesmus and dyschezia in animals.2 Constipation is defined as difficult, reduced, or painful evacuation of feces that occurs secondary to colonic hypomotility or dysmotility disorders, mechanical obstruction, or colorectal diseases. Dry, hardened feces are difficult to pass, and chronically constipated cats have intermittent episodes of tenesmus, hematochezia, or diarrhea due to the mucosal irritant effect of impacted feces. Fiber-responsive colitis is a unique large bowel diarrheal syndrome of dogs in which altered colonic motility causes clinical signs of excessive fecal mucus, hematochezia, and tenesmus.
Differential Diagnosis
Box 12-1 presents causes for tenesmus and dyschezia in companion animals. Although diseases affecting colon and rectum are the predominant source of clinical signs, it is important to exclude disturbances in other organs (e.g., urogenital disease) that can also cause tenesmus. Cats are notorious for stranguria associated with FLUTD, which can confound accurate assessment of ineffective straining associated with colorectal disease. A thorough patient history and observation of the animal’s elimination process are essential for avoiding misdiagnosis.
Evaluation of the Patient
History
Always obtain a history pertaining to both urinary and gastrointestinal tracts in animals with tenesmus. A careful history and complete physical examination are required to determine which organs are affected and to assess potential severity of the dysfunction. Besides tenesmus, lower urinary tract disorders (especially cystitis or urethritis) often result in hematuria and pollakiuria, which are readily apparent to most clients. Normal urinary habits are most suggestive of tenesmus caused by colorectal disorders. Tenesmus preceding defecation usually indicates an obstructive lesion, whereas inflammatory disorders are often associated with persistent tenesmus following evacuation. A history of large bowel signs may be evident in patients with colonic disease alone and in animals having more extensive colorectal disease. Systemic signs of disease, such as anorexia, weight loss, vomiting or diarrhea, may be reported especially in animals having concurrent systemic disease or disorders involving other segments of the gastrointestinal tract. Animals are generally alert, active, and well-fleshed with normal appetites on presentation. The following historical concerns are of significance in animals with tenesmus and dyschezia:
• Is the diarrhea (if present) acute or chronic? Acute, self-limiting large bowel diarrhea is common and rarely requires an in-depth diagnostic evaluation.
• Are clinical signs static, progressive, or cyclical? Colorectal neoplasia may cause progressive signs whereas colonic IBD is characterized by a waxing/waning clinical course.
• Is there evidence of dietary, environmental, parasitic, or infectious causes for large bowel signs? Dietary and parasitic causes may constitute up to 50% of clinical cases dependent upon the geographic area.
• What type of diet is the animal being fed? Note recent dietary changes (this might incriminate responsible nutrients), the amount and frequency of feeding, and the administration of medications (e.g., antibiotics, narcotics, motility modifiers, laxatives) that might alter colonic function.
• Do clinical signs resolve when the animal is fed either an intact protein or hydrolysate elimination diet? This might suggest the presence of an adverse food reaction (i.e., dietary sensitivity or intolerance).
• A positive response to glucocorticoid therapy may indicate inflammatory or immune-mediated diseases, such as IBD or perianal fistula.
• Does the animal roam freely? If so, parasitic, toxic, and infectious causes for colorectal diseases may be more likely.
• Does the animal’s travel history suggest an increased risk of disease with a regional incidence, such as histoplasmosis (Midwest United States) or intestinal parasites (Southern United States)?
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