About 5% of patients who have symptomatic diverticula experience complications such as perforation, bleeding, fistulation and stricture formation which can necessitate surgical intervention.

A giant colonic diverticulum (GCD) is defined as a diverticulum larger than 4 cm in diameter [4]. Some as large as 40 cm have been reported in the literature [5]. The mean age of presentation of GCD mirrors that of diverticular disease with the majority presenting after the sixth decade [1,4].

The presentation of GCD is variable, ranging from the asymptomatic patient (4%) to a host of non-specific gastrointestinal (GI) symptoms with only 10% of patients presenting with an abdominal mass [4]. GCD carries a substantial risk of complications and elective surgical removal is recommended [6].

Examination revealed a well circumscribed, mobile mass in the left hypochrondrium extending above the level of the ribs raising the possibility of an enlarged spleen. There was no palpable lymphadenopathy.

A blood film showed atypical myelomonocytic cells but a subsequent bone marrow aspiration was normal. All other routine blood tests were within normal limits. An abdominal ultrasound scan demonstrated a normal spleen and a separate gas-filled cyst in the left hypochondrium.

Over the next few weeks, the patient developed diarrhoea and lost 3 kg in weight. He reported that the mass appeared to be fluctuating in size.

An abdomen computed tomography (CT) scan (Figure 1) demonstrated a large gas-filled structure measuring 11 cm × 12 cm, appearing to arise from the sigmoid colon, displacing the adjacent small and large bowel loops. The features were consistent with a giant sigmoid diverticulum.

He was referred to colorectal surgeons and a barium enema was performed to further assess the extent of the diverticular disease. This confirmed moderate sigmoid diverticulosis but did not demonstrate direct communication between the colon and the giant cyst (Figure 2). The diagnosis of GCD was discussed with the patient and definitive surgical management was advised. Initially, the patient was reluctant to have surgery, but over the next 6 months, he experienced two further episodes of acute abdominal pain necessitating hospital admission. Both episodes were similar in nature with pain as the predominant symptom; an abdominal X-ray (AXR) taken on admission demonstrated the gas-filled structure and in the absence of raised inflammatory markers, a normal white cell count and no fever, the diagnosis of enlarging GCD was made. Both episodes settled quickly with bowel rest and intravenous fluids. The patient then agreed to surgical intervention.

A laparoscopic-assisted sigmoid colectomy was performed 6 weeks later. Four 12 mm ports were inserted and pneumoperitoneum achieved. Three of the ports were positioned along the lateral edge of the right rectus abdominus muscle and triangulated to provide optimum access to the left colon. The fourth port was in the left iliac fossa. The large cystic structure was clearly visible in the left hypochondrium at the apex of a long mobile loop of sigmoid colon on the anti-mesenteric border (Figure 3). The remaining sigmoid colon had macroscopic evidence of mild diverticulosis. The diverticulum was attached to the lateral abdominal wall adjacent to the spleen by adhesions. These adhesions were divided laparoscopically by a combination of scissor diathermy and ultracision. The sigmoid colon was then fully mobilised from lateral to medial but no attempt was made to divide the mesenteric vessels intracorporeally in view of the fact this was benign disease and the sigmoid was long and tortuous. The mobilised sigmoid colon was externalised through a 7 cm incision in the left iliac fossa. A wound protector was used during extraction of the cyst and a decision was made not to decompress it before removal in order to keep possible contamination down to a minimum. The sigmoid colon was resected along with the diverticulum and a hand-sewn primary anastomosis was performed extracorporeally.

The patient made an excellent postoperative recovery and was discharged on the fourth postoperative day.

Macroscopic assessment of the segmental colonic resection confirmed the presence of diverticular disease with an associated giant cyst measuring 11 cm in maximal diameter. The wall of the cyst measured 0.6 to 1 cm in thickness. Microscopically, it did not contain any elements of bowel wall and instead was composed of reactive scar tissue with foreign body type giant cell reaction. The presence of plant material admixed with inflammatory debris was thought to be indicative of faecal matter and suggested a direct communication between the cyst and bowel lumen. However, this was not identified histologically. There was no evidence of dysplasia or malignancy. In accordance with the classification suggested by Steenvoorde et al. [4], the histological features were consistent with Type II GCD (Table 1).

GCDs are defined as those that are larger than 4 cm in diameter [4,5] and with the increasing incidence of diverticular disease [3,8], it is likely that the incidence of these giant lesions will increase further. Awareness of the presenting symptoms, investigations, differential diagnosis and management is therefore important.

As in our patient, it is not unusual for these patients to undergo multiple investigations before making the correct diagnosis. Plain supine abdominal X-ray is the simplest and most readily available investigation and should be used as the first line in suspected cases. If a large air filled structure with or without fluid levels is visualised then an abdominal CT scan would be indicated. Barium enema failed to demonstrate a communication between the giant diverticulum and the colon in approximately one-third of reported cases [1,4]. It is therefore not surprising that no communication was identified in our patient. Barium enema can be useful at providing valuable information regarding the extent of further diverticula.

The use of abdominal ultrasound has been reported to be helpful in only 25% of cases [4]. Early colonoscopy is advised in the setting of persistent or frequent acute diverticulitis to rule out concurrent pathology [9]. Our patient was admitted acutely on two occasions a few months apart, however, the symptoms and signs were not suggestive of acute diverticulitis but were felt to be in keeping with enlarging GCD therefore colonoscopy was not performed.

The role of colonoscopy in diagnosing GCD is limited. The ostium between the diverticulum and the colon is frequently too small to be detected [1,2,4] and even in cases with wide necked GCD, the ostium is not detected on sigmoidoscopy [1]. The combination of a large soft, mobile mass in an elderly patient and a lucent cystic structure related to the sigmoid colon on AXR should suggest the diagnosis of a GCD [6].

Other causes for intra-abdominal gas-filled cysts, radiologically mimicking GCD [2], along with their principal distinguishing features, are summarised in Table 2. Steenvoorde et al. suggested a histological classification of GCD based on three subtypes (Table 1). The distinction between type I and II has not always been made with both categories being discussed as one entity in many papers [5]. Theories behind the formation of GCD type I and II are speculative and not mutually exclusive. The suggested aetiology of type I is based on the premise that the communication between the GCD and the colon is small enough to preclude the escape of air from the diverticulum [1]. The two most widely accepted theories are, a unidirectional ball-valve mechanism causing gas entrapment and infection with gas producing organisms leading to progressive diverticula enlargement [5]. However, such theories do not convincingly explain the existence of type I GCD with wide necks.

Type II is postulated to form following a subserosal perforation resulting in a walled off abscess cavity that gradually enlarges to giant size [7]. Type III contains all layers of bowel wall and structurally resembles a duplication cyst [7] but is in continuity with the gut lumen and occurs in adults. Approximately 20% of GCD show no evidence of a communicating ostium between the colon and the diverticulum and it is thought that this tract may be lost due to inflammatory changes [5].

Surgical management of a GCD involves either removing the diverticulum in isolation or colectomy. Diverticulectomy is not recommended as the mouth of the diverticulum may be wide and the surrounding inflammation could increase the potential for breakdown of the colonic closure [2]. Giant diverticula appear mostly (81%) in the sigmoid colon [5] with 50% of patients having concurrent sigmoid diverticula [4], thus sigmoid colectomy with primary end-end anastomosis [7] is the preferred operation. Resection is frequently difficult due to the inflammatory diverticulum and it is often densely adherent to surrounding structures [2]. In complicated or emergency cases, the safest surgical solution may be a Hartmann’s procedure [7].

The presence of a GCD carries substantial risk of complications (12% to 19%) including inflammation, perforation, abscess formation, fistula formation, urinary obstruction [7], volvulus, small bowel obstruction and rarely, the development of adenocarcinoma [1,4].

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