Toxic megacolon, whilst sounding like the bad guy in a children's cartoon, is in fact a life threatening condition. First described in 1950, it is best known as a complication of ulcerative colitis. Less commonly, it can occur in Crohn's disease, ischaemic colitis and infective (bacterial, viral and parasitic) colitis. It is an acute dilatation of the colon due to severe inflammation of the large intestine. For this reason, it is also referred to as 'toxic dilatation'. It occurs when the ulceration of the mucosal surface spreads to affect all layers of the bowel, including the underlying walls of smooth muscle, resulting in an impairment of its viability and contractile strength. The dilatation can involve the whole bowel, or just a segment.

The precise pathophysiology of toxic megacolon is unknown. There are a few suspected contributory mechanisms, nitric oxide being one of the prime suspects. As the inflammation spreads from the inner mucosal layer of the bowel to the surrounding smooth muscle layer, inflammatory cells (including macrophages and neutrophils) become activated and infiltrate the area. Here they release nitric oxide, which is a potent smooth muscle relaxant, which results in the loss of tone in the muscles. It is this loss of tone that allows the dilatation of the bowel.

Toxic megacolon is a complication that occurs in approximately 5% of attacks of severe ulcerative colitis. It mostly affects those with a pancolitis rather than a segmental colitis. Whilst the onset of this condition can be insidious and without apparent cause, there have been several factors that have been shown to trigger attacks. The risk of an attack is greatly increased if patients abruptly discontinue, or even just taper, their ulcerative colitis suppressant medications. Attacks can also be precipitated by the use of preparations that decrease bowel motility, such as anti-depressants or opoids. There is also a small risk that two of the procedures used to diagnose ulcerative colitis, colonoscopy and barium enemas, can induce dilatation of the bowel.

Clinical features include toxaemia; anaemia, caused by loss of blood into the bowel; acute loss of water and electrolytes; and progressive abdominal distension. The patient will also have a fever, tachycardia and raised white blood cell count. If this condition is left unchecked, it can lead to the perforation of the bowel wall. The outcome of this is a faecal peritonitis, which carries a high mortality rate.

Treatment in the first instance is conservative. The patient is placed in intensive care and receives blood transfusions, water and electrolyte replacement, parenteral nutrition and parenteral steroid and antibiotic therapy. Their condition is monitored by regular abdominal x-rays, which are used to assess the degree of colonic dilatation. If it is decided that the risk of perforation is unacceptably high, or if there is a worsening of the patient's condition, there is immediate surgical intervention to remove the colon (colectomy).

Thirty years ago, this disease carried a mortality rate of 19-27%. However, with advances in medical treatment and patient care, this has fallen to 0-2% (Seth, LaMont, 1998). This has mostly been attributed to earlier recognition of the disorder, better medical management of the disease and a lower threshold for surgical intervention.

References

• Cima R R, Pemberton J H, 2005, Medical and Surgical Management of Chronic Ulcerative Colitis, Arch Surg. 2005;140:300-310
• Sheth S G, LaMont J T, 1998, Toxic Megacolon, The Lancet 1998; 351:509-513