Ulcerative colitis (UC) belongs to the group of inflammatory bowel diseases (IBD). It has a multifactor aetiology and various clinical presentation. UC occurs everywhere in the world; however, the highest incidence is observed in the Caucasian population, particularly in Europe (UC: 505/100,000 in Norway; Crohn’s disease: 322/100,000 in Germany) and North America (UC: 286/100,000 in the USA; Crohn’s disease: 319/100,000 in Canada). UC incidence in Europe is approximately 10/100,000. The prevalence of inflammatory bowel diseases has exceeded 0.3% in North America, Oceania and many European countries (1). The highest incidence of UC is observed between 20 and 40 years of age; however, the disease can occur both in children and in the elderly as well. Women and men are affected by UC at a similar rate, unlike Crohn’s disease, which is more common in women (2). Inflammatory bowel diseases are more common in individuals living in the city and performing office work (3).

Depending on the affected portion of the bowel patients can report different symptoms. The first symptom which may raise the suspicion of ulcerative colitis is most often diarrhoea (lasting usually over 6 weeks) with traces of blood. The number of bowel movements can be as high as 20 daily. When lesions do not extend beyond the rectum, the rate of bowel movements can be unaffected and the only symptom present can be constipation with traces of blood and sometimes abdominal pain as well. The disease is chronic, with periods of exacerbations and remissions.

The main procedure performed to diagnose the disease, monitor its course and conduct oncological surveillance is colonoscopy.

A clinical division of UC types is necessary to determine the point when local treatment is insufficient and systemic treatment needs to be introduced. In 2005, during the World Congress of Gastroenterology in Montreal a classification of UC based on the extensiveness of lesions in the colon was proposed (4).

This scale differentiates between:

– E1: proctitis, in which the disease is limited to the rectum (the proximal extent of inflammation is distal to the rectosigmoid junction). In this form of the disease the patients mainly complain of urgency to defecate, lower gastrointestinal tract bleeding and sometimes constipation,

– E2: distal/left-sided UC, in which the disease is limited to a proportion of the colorectum distal to the splenic flexure,

– E3: extensive UC, in which the disease extends proximally to the splenic flexure, sometimes involving even the whole colon (pancolitis) and sometimes reaching the distal part of the ileum.

In the case of extensive UC, the manifestations of the disease are more severe and lower gastrointestinal tract bleeding can occur. Patients experience urgency to defecate and traces of mucus and pus can occur in the stool. Patients also complain of nocturnal defecation and girdle abdominal pain, often located in the left iliac fossa, intensifying directly before and subsiding after defecation.

The clinical presentation of UC patients can be various. The authors present the case of a 61-year-old man in whom the disease had a short and very rapid course requiring aggressive treatment.

A 61-year-old patient was admitted to the Department of General and Oncological Surgery, Health Centre in Tomaszów Mazowiecki, Poland, with a diagnosed ulcerative colitis and colonic stricture in the splenic flexure reported on colonoscopy (suspected proliferative lesion) for further diagnostic investigation and possible surgical treatment. The patient complained of significant weakness, the loss of approximately 20 kilograms over two months and persistent diarrhoea with traces of blood lasting already three months with sometimes as many as 9 bowel movements a day. He denied any abdominal pain and vomiting, but did report a few episodes of nausea.

The patient underwent a cardioverter-defibrillator implantation surgery three years earlier due to second-degree atrioventricular block with pre-MAS syndrome. The patient also had a history of type 1 diabetes and cholecystectomy.

One month earlier, due to persistent bloody diarrhoea lasting over ten days the patient was hospitalised at the Department of Infectious, Tropical and Parasitic Diseases of the Department of Infectious Diseases and Hepatology. Based on tests infectious aetiology of the diarrhoea was excluded. An abdominal CT scan revealed the following: “The splenic flexure with irregularly thickened walls and irregular lumen, no peristalsis observed in this segment: a proliferative process suspected. Colonic wall thickening along the whole segment is visible with signs of inflammation”. Conclusion from the examination: “proliferative lesions in the gastrointestinal tract cannot be excluded”. A decision was made to perform another colonoscopy in order to collect a sample of the mucosa for histopathological examination. Due to poor preparation the colonoscope was inserted only up to 55 cm. Upon endoscopy, the colon was stiff and the mucosa of the descending and sigmoid colon and partly of the rectum was highly hyperaemic, reddened, friable and prone to bleeding upon contact with the examination device. Multiple sigmoid polyps of 2-5 mm in diameter could be seen. Multiple shallow diverticula were also found in the sigmoid colon. Histopathological examination of samples taken from the sigmoid colon, the descending colon and the rectum revealed lesions characteristic for active ulcerative colitis. Preliminary conservative treatment was applied: sulphadiazine and steroids. Due to anaemia 2 units of packed red blood cells were administered. Remarkable laboratory findings included an elevated level of carcinoembryonic antigen (CEA): 8.88 ng/ml (n: 0.00-3.40). After the treatment the patient was transferred to a gastroenterology department for further diagnostic investigation.

There, the patient underwent another colonoscopy in which the mucosa of the rectum, sigmoid and descending colon was oedematous on the whole surface, which was uneven and cobblestone-like and had numerous ulcerations of 5-6 mm in diameter, covered with fibrin and prone to bleeding upon contact at some spots. The mucosa in the splenic flexure was highly oedematous; for this reason, it was impossible to pass the colonoscope through. Once a smaller-diameter device was used, the proximal part of the transverse colon was reached and similar lesions were revealed. Samples were collected for histopathological examination, which confirmed the diagnosis of active-phase ulcerative colitis. Pharmacological therapy was introduced: oral and enema mesalazine, oral azathioprine, metronidazol, albumins, iron supplementation, a high-protein product to supplement the diet and an intestinal bacteria formulation. Glucocorticosteroid therapy was continued (Encorton 30-20-0 mg). The patient was discharged from hospital and he reported the next day to a surgical department for treatment.

There, following bowel preparation, the patient underwent another colonoscopy which revealed lesions characteristic for active ulcerative colitis. The endoscopy technician passed the device through the splenic flexure without problems, finding no significant stricture that made it impossible to perform full colonoscopy on the previous occasion (fig. 1, 2).

Additional tests revealed the following remarkable findings: WBC = 3.1 x 10³/mm³, RBC = 2.67 x 10⁶/mm³, HGB = 8.0 g/dl, potassium = 2.9 mmol/l. The total serum protein level was 5.2 g/dl, therefore, due to cachexia, parenteral nutrition was included. The level of C-reactive protein (CRP) was 62.1 mg/l (n: 0.0-9.0). Due to the lesion reported in CT examination, a blood sample was also taken to check the level of CA 19-9: 34.28 IU/ml (n: 0.00-37.00) and CEA: 0.9 ng/ml (0-2.5 ng/ml); however, both were within the normal range. Based on the examination results and the severity of the patient’s complaints leading to rapid weight loss and progressing cachexia, a decision was made to perform urgent colectomy with end ileostomy. Due to the patient’s asthenia, the surgery was performed following patient preparation and a week-long total parenteral nutrition. Before surgery, the WBC level was 3.6 x 10³/mm³; RBC was 3.43 x 10⁶/mm³; HGB was 10.6 g/dl and the total protein level rose to 5.4 g/dl. A total of 4 units of packed red blood cells were administered to the patient before the operation.