Introduction
Mega-colon refers to a condition where the colon is hypomotile manifesting in obstipation, with dilation or hypertrophy of the colon leading to fecal impaction and is caused by either congenital or acquired diseases (Byers, Leasure, and Sanders 2006).
Congenital forms include aganglionosis (reported in an 11-week old kitten), Manx deformity or a feature of situs inversus (White 2002; Roe, Syme, and Brooks 2010).Acquired mega-colon is either, secondary to chronic mechanical or functional bowel obstruction, or primary, also known as idiopathic. Obstructive mega-colon manifests as hypertrophic mega-colon, whereas a primary dysmotility disorders such as idiopathic mega-colon cause the colon to become dilated in the end-stage of the disease (Byers et al. 2006). Of cases, 62% are idiopathic, with 23% due to pelvic canal stenosis due to malunion of a pelvic fracture, or deformity, 6% nerve injury related to Manx sacral spinal cord deformity (Washabau 2003). Other reasons cited include complications from col- opexy, colonic neoplasia, neuromuscular dysfunction caused by dysautonomia, rectal stricture, and metabolic or endocrine disease. The vast majority of cats with megacolon, that is, idiopathic mega-colon will not have primary neurological disease. The unknown pathology afflicts colonic smooth muscle leading to generalized dysfunction and absence of motility.
Idiopathic mega-colon is most commonly described in the domestic shorthair, Siamese, and domestic long-hair cats with the mean age of onset being 7 years and 11 months (range 9 months to 17 years) but mostly observed in middle aged male cats (Trevail et al. 2011; Washabau 2003). Cats will have a history of tenesmus, dyschezia, occasional systemic signs including anorexia, weight loss, and vomiting. Clinical findings include dehydration, abdominal pain, and mesenteric lymphadenopathy (Washabau 2003).
A potential sequel to the anorexia from mega-colon in the cat is hepatic lipidosis (Salas 2003).Mega-colon, both dilated and hypertrophic mega-colon in dogs, is rarely described. Reported breeds include, German Shepherd Dog, Rottweiler, Giant Schnauzer, Sharr Mountain dog, Hungarian Kuvasz, Caucasian Shepherd, Sarplaninanc, and the English Mastiff. The most common form is secondary, with only 25% of cases being idiopathic (Prokic et al. 2010). A case series described this condition as more common in male dogs, dogs that received low levels of exercise, and had a history of chronic constipation, in the preceding five to 26 weeks (Nemeth, Solymosi, and Balka 2008). The underlying causes include, pelvic canal stenosis, lumbar and sacral spinal injuries, hindlimb fractures.
The highest risk factor in dogs include a bone diet and low levels of physical activity (Nemeth et al. 2008; Prokic et al. 2010). Common historical complaints documented were persistent tenesmus, dyschezia, and obstipation refractory to medical management. Clinical signs included distended colon filled with hard feces, and abdominal pain (Nemeth et al. 2008). The histopathology is characterized by severe hypertrophy of the smooth muscle.