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Megacolon is a state of permanently increased diameter of the large bowel. This change in intestinal structure leads to abnormal function, including reduced colonic motility and chronic constipation.

The condition most commonly occurs in cats and dogs, but pigs can also be affected. White foals suffering congenital colonic agangliosis, an autosomal recessive trait, may develop secondary megacolon.

In small animals, megacolon may be congenital or acquired, which may be idiopathic. Although well described in human medicine, congenital megacolon has not been convincingly described in animals despite first being reported in 1988[1]. In man, Hirschsprung's disease manifests at a very young age is caused by an absence of inhibitory neurons in Meissner’s submucosal plexus and Auerbach’s myenteric plexus in the distal colon or rectum[2]. This gives persistent smooth muscle contraction in the affected region and proximal dilation of the colon. A similar pathogenesis is proposed in cats.

Acquired megacolon is more common than the congenital form, and in cats this is most often idiopathic. The true cause of "idiopathic" megacolon is thought to be an intrinsic defect in colonic smooth muscle function[3]. Acquired megacolon can occur in both cats and dogs as a sequel to any disease or lesion that interferes with normal defecation: faecal retention causes dilatation of the colon and impairs colonic motility.

Causes could include:

neuromuscular abnormalities (spinal cord disease, intervertebral disk disease, dysautonomia, trauma)
metabolic disorders (severe dehydration, hypokalaemia)
drug therapy (vincristine, anticholinergics, barium)
mechanical obstruction (pelvic fracture malunion, foreign bodies, stricture, anal/rectal atresia)
conditions causing dyschezia (anal sacculitus, perianal fistula, trauma preventing posturing, proctitis).

After megacolon has persisted for several months, it is unlikely that normal colonic motility will be restored after resolution of the underlying cause. In many cases, the aetiology of megacolon is not determined.


Manx Cat. Source: Wikimedia Commons; Author: Jonik (2004)

Megacolon much more commonly affects cats than dogs, but any age, breed or sex of animal may develop acquired megacolon.

Idiopathic megacolon is more common in middle-aged to older cats, and there is some evidence for an increased risk in Manx cats due to a sacral spinal cord deformity.


Clinical Signs

Idiopathic megacolon is likely to be a long-term, recurring problem, with clinical signs presenting over months to years. In acquired megacolon, signs can be acute or chronic in onset. The primary sign of megacolon is constipation or obstipation (severe constipation caused by intestinal obstruction). Animals suffer tenesmus when defaecating and produce little or no faeces. Faeces that is expelled is very hard and dry, and animals defaecate less frequently. After prolonged tenesmus, a small amount of often mucoid diarrhoea may be expelled. Vomiting, anorexia and weight loss are other key features.

On clinical examination, an enlarged colon packed with hard faeces is palpated within the abdomen. The animal may be dehydrated, and the hair coat rough. Digital anorectal examination is necessary, and confirms faecal impaction as well as potentially revealing an underlying obstructive cause.

Megacolon must be differentiated from other causes of palpable colonic masses. These could include adenocarcinoma, lymphoma or intussusception and can be distinguished on the basis of texture, rectal examination and diagnostic imaging. Tenesmus can be caused by colitis as well as megacolon, and palpation, rectal examination and imaging can again be used to exclude this. Dysuria or stranguria may also look similar to the tenesmus caused by megacolon. Palpation of the bladder and colon and urinalysis will help eliminate this differential diagnosis.

Laboratory Tests

Haematology and biochemistry may give evidence of dehydration, such as raised packed cell volume, total protein and urea/creatinine. A stress leukogram may also be seen. The duration of constipation may result in changes to blood electrolytes, and dehydration can lead to pre-renal azotaemia.

Urinalysis should always be performed to rule out lower urinary tract disease as a differential diagnosis and to check renal function in dehydrated animals.

There are no laboratory tests specific for megacolon.

Diagnostic Imaging

Plain radiographs should be taken of the abdomen and pelvis in an attempt to confirm megacolon and to investigate underlying causes. The enlarged, faeces-filled colon is easily seen on these x-rays. Subsequent contrast studies or abdominal ultrasound may help identify an underlying cause, such as mural or obstructive masses.


Colonoscopy may be necessary to rule out obstructive masses in the large intestinal wall or lumen.


The colon is found to be dilated and impacted with faeces, with the most sever dilatation occurring in the transverse and descending colon[4]. Histologically, the colon is usually normal: the only cases in which histological abnormalities have been reported were mature adult cats, which is an atypical signalment for a congenital condition[1][4][5]. The histological findings in these cats were aganglionosis and absent myenteric ganglia.


Megacolon may be managed medically, or surgically if the condition is severe or recurrent.

Medical therapy aims to restore the patient's hydration and then clear the faecal impaction. Intravenous fluid therapy should be continued until the animal is willing to eat and drink independently. Under anaesthesia, the colon is manually evacuated using warm water enemas, lubrication and gentle extraction of faeces with forceps or a finger. Care must be taken not to damage the colonic mucosa during this procedure, and prophylactic antibiotics are recommended before commencement. Once the patient's colon is clear, the focus is shifted to preventing recurrence.

Dogs and cats must have adequate access to litter or the outdoors to encourage regular defaecation, and regular exercise may be beneficial. Diets containing bulk-forming fibre may contribute to the recurrence of impaction, but a high-fibre diet may occasionally be useful in prevention. Stool softeners such as lactulose, and prokinetic drugs such as cisapride can promote motility and defaecation. Medical management is usually an ongoing, life-long commitment which may be frustrating for the owner, and relapse is common.

Sub-total colectomy can be used to correct megacolon in the cat. However, this technique is very poorly tolerated in the dog. The term refers to the removal of the majority of the colon, and the ileocaecocolic valve may be preserved or removed. The ileocaecocolic valve prevents reflux of colonic contents into the small intestine and so some surgeons believe that removing this structure can predispose to small intestinal bacterial overgrowth, steatorrhoea and deconjugation of bile salts[2]. However, removing the ileocaecocolic valve minimises the recurrence of megacolon.

As yet, there is no established figure for how much colon to remove. If the ileocaecocolic valve is removed, an enterocolostomy is performed; if not, the colon is transected 3 cm from the caecum to ensure the following colocolostomy is not under tension from the short mesocolon. Any longitudinal tension on the anastomosis site is likely to lead to dehiscence postoperatively. In surgeries where the valve is resected, an oblique incision of the ileal portion and a short antimesenteric incision of the distal colon will allow for disparities in lumen diameter. The intestine is closed in a single layer using full-thickness appositional, simple interrupted suture in an absorbable material. Staples may similarly be used.

Although sub-total colectomy is an effective way of correcting megacolon, removal of majority of the colon has the potential to cause metabolic effects in the animal. For example, the colon normally functions to absorb water. This is achieved by the creation of an osmotic gradient by active sodium absorbtion. Additionally, extracellular potassium is lost and bicarbonate ions are exchanged for chloride ions in the colon. It could therefore be implied that sub-total colectomy disrupts water and electrolyte homeostasis, but paradoxically cats undergoing sub-total colectomy have been found to show no clinical evidence of abnormal bowel function[6]. However, other, non-clinical changes were found: small intestinal enterocytes and villi were increased in height, the absorptive area of the small intestinal mucosa was increased, serum cobalamin and faecal sodium were increased and faecal potassium was low. The significance of these results is unknown.

After surgery faeces are loose and defaecation is associated with tenesemus, but faecal consistency improves over the following months. Complications associated with the surgery itself are rare and tend to be related to the anastomotic procedure[2]. For example, the abdomen may become contaminated during surgery, leading to peritonitis, or the anastomosis site may break down. For this reason, the patient should be monitored for three to five days post-surgery.

Long-term complications usually involve recurrence of constipation, which can be managed medically in most cases. Stricture formation and persistent diarrhoea have also been reported.

Some cases of megacolon may be prevented by identification and correction of the underlying cause before faecal retention occurs. Fractures that narrow the pelvic canal should be carefully reconstructed, and exposure to foreign bodies and feeding of bones should be avoided.


Historically, medical management has been unrewarding in the long term. The inclusion of cisapride in medical therapies appears to improve the prognosis, but this drug can currently be difficult to obtain.

Following sub-total colectomy, recurrence of constipation is uncommon in cats. Post-operative diarrhoea typically resolves by 6 weeks post-surgery but may persist for several months while the ileum adapts by increasing its ability to absorb water and its reservoir capacity.

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  1. 1.0 1.1 Rosin, E et al (1988) Subtotal colectomy for treatment of chronic constipation associated with idiopathic megacolon in cats: 38 cases (1979-1895). Journal of the American Veterinary Medical Association, 193, 850-853.
  2. 2.0 2.1 2.2 Pratschke, K (2005) Surgical disease of the colon and rectum in small animals. In Practice, 27, 354-362.
  3. Washabau, R J and Stalis, I H (1996) Effects of cisapride on feline colonic smooth muscle function. American Journal of Veterinary Research, 57, 541-546.
  4. 4.0 4.1 Yoder, J T, Dragstedt, L R 2 and Starch, C J (1968) Partial colectomy for correction of megacolon in a cat. (Report of a case). Veterinary Medicine: Small Animal Clinics, 63, 1049-1052.
  5. Ly, J T (1977) Surgical correction of megacolon in a cat. Australian Veterinary Practitioner, 7, 210.
  6. Gregory, C R et al (1990) Enteric function in cats after subtotal colectomy for treatment of megacolon. Veterinary Surgery, 19,216-220.

Petrus, D J, Nicholls, P K and Gregory, S P (2001) Megacolon secondary to autonomic ganglioneuritis in a dog. The Veterinary Record, 148(9), 276-277.

Tilley, L P and Smith, F W K (2007) The 5-minute Veterinary Consult (Fourth Edition) Blackwell Publishing.

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