Annals of Burns and Fire Disasters - vol. XII - n° 2 - June 1999

Acute pseudo-obstruction of the colon (Ogilvie's syndrome) is characterized by a dramatic dilatation of the colon in the absence of any mechanical obstruction. The condition mainly affects the caecum and right colon, and can lead to life-threatening perforation.
Ogilvie's syndrome is attributed to autonomous nervous system imbalance, but the pathogenic mechanism remains unknown. It can complicate thermal injuries and several other intra- and extra-abdominal disorders (Table 1).

Although the syndrome occurs only rarely, it greatly increases burn patient mortality, and in the presence of the relative symptoms a high level of suspicion is recommended.
The incidence of the syndrome in burn patients is estimated to be I %.'In the last five years, of the 422 patients with over 15% burns treated in our burn unit, two patients developed the syndrome, with an incidence of 0.47%.

Case 1
A 62-year-old male presented with 55% T13SA partial- and full-thickness burns with associated inhalation injury. There was no past medical history of note, apart front gross obesity.
On the third day post-burn the patient developed pneumonia, associated with severe hypoxia and respiratory alkalosis, which required endotracheal intubation and supported ventilation. Additionally, he developed severe thromboeytopenia (plt = 3,000/ml).
On the same day he also developed rapidly increasing abdominal distension, pyrexia (38 'C), increased respiratory distress, and obstipation Bowel sounds were absent. Abdominal x-ray in the lateral decubitus position revealed marked distension of the entire colon (Fig. 1).

Fig. 1 - Abdominal x-ray in lateral decubitus position. Marked distension of entire colon.

Owing to the patient's poor condition a conservative approach was elected, consisting of: a. insertion of a largebore nasogastric tube, which produced a copious amount of gastric fluid; b. diagnostic and therapeutic colonoscopy, which showed no evidence of mechanical obstruction and temporarily decompressed the colon; and c. insertion of a colonic decompression tube, which was left in place in order to provide continuous mechanical relief.
On the fifth day post-burns the patient deteriorated rapidly, showing evidence of respiratory failure, generalized peritonitis, and sepsis. He died the following day. Autopsy revealed generalized peritonitis due to perforation of the markedly dilated and necrosed colon.

Case 2
A 53-year-old male presented with a 37% T13SA fullthickness burns and associated inhalation injury. He was a heavy smoker and had a history of advanced chronic obstructive pulmonary disease and hypertension.
During his hospitalization he developed hypoxia and severe hyperglycaemia. On the 16th post-burns day he presented abdominal distension, vomiting, pyrexia (38.3 °C), mild abdominal pain, and diarrhoea. Erect abdominal x-ray revealed excessive dilatation of the colon with concomitant air fluid levels (Fig. 2). Immediate treatment included: a. insertion of a nasogastric aspiration tube; b. colonoscopy, which failed to reveal mechanical obstruction and to decompress the bowel; and c. insertion of a colonic decompression tube.

Fig. 2 - Abdominal x-ray in erect position. Excessive dilatation of colon with concomitant air fluid levels.

The patient was checked with frequent abdominal xrays, which showed increasing colonic distension. When the caecal diameter exceeded 12 cm, an immediate laparotomy was performed.
The operative findings included an enormously dilated colon with a small area of focal necrosis in the caecum, but no perforation (Fig. 3). Consequently, a subtotal colectomy with temporary ileostomy was performed. Apart from three surgical operations for resurfacing the burn area with partial -thickness skin grafts the patient's further hospitalization was uneventful. He was discharged on the 53rd post-burn day. The ileostomy was reversed two months later, since when he has been fit and well.

Fig. 3 - Operative findings. Enormously dilated colon with small area of focal necrosis in caecum, but no perforation.

Acute colonic pseudo-obstruction as a syndrome was first described by Ogilvie in 1948.'It is characterized by colonic dilatation in the absence of mechanical obstruction or any obvious causes of paralytic ileus. The syndrome's pathogenic mechanism remains unknown.
Until 1986 only 400 cases had been reported. The condition can occur in patients with various metabolic, surgical, and medical problems. It can also be idiopathic in a small percentage of patients.
With regard to the syndrome's common presenting symptoms (Table II), both our patients had sudden and rapidly increasing abdominal distension, respiratory distress, and moderate fever. The first patient had obstipation and reduction of bowel sounds, while the second had diarrhoea, mild abdominal discomfort, and increased bowel sounds. Both patients received total enteral nutrition, prior to the development of the syndrome, via a nasoduodenal tube and a controlled administration pump. Enteral nutrition is not considered to contribute to the manifestation of the syndrome, as proved by its uneventful administration to burns patients in our clinic with TBSA exceeding 15%. Both had inhalation injury, infection, and severe hypoxia, which may have triggered the development of the syndrome.

The common symptoms and signs of the syndrome (e.g., tympany, increased or decreased bowel sounds, tachycardia, pyrexia, increased number of leucocytes in peripheral blood, and severe abdominal pain) may be difficult or impossible to evaluate in severely burned patients.
The appearance of sudden and rapidly increasing abdominal distension therefore necessitates subsequent frequent evaluation with a series of abdominal x-rays, preferably in the erect position, if the condition of the patient permits. The presence of diffuse colonic dilatation, with or without air fluid levels or free air, in the event of perforation, can be detected. Treatment consists of conservative measures, colonoscopy, and surgery.
Conservative treatment should include insertion of a nasogastric aspiration tube, cessation of food ingestion, insertion of a colonic decompression tube, discontinuation of narcotic analgesics, early correction of fluid and electrolyte imbalance, and control of systemic disturbances.
Colonoscopy at the earliest possible time can be of both diagnostic and therapeutic value as it provides: a. exclusion of obstruction and establishment of the diagnosis among other possible causes of colonic dilatation (Table III) and b. successful decompression of the colon in up to 81% of the patients.

The recurrence rate of dilatation is high, as happened in our first case. In an enormously dilated colon, colonoscopy can be hazardous and should therefore be avoided.
There is no consensus regarding the value of gastrointestinal motility drugs such as neostigmine, metinclopramide, urecholine, and cicapride.
Indications for immediate operative intervention are: a. signs of bowel wall necrosis or peritonitis; b. caecal diameter greater than 12 cm in erect x-rays; failure of conservative management; d. severe respiratory embarrassment; and e. impossibility of excluding mechanical obstruction of the colon.
In cases with no rupture or in the absence of massive colonic dilatation with ischaernia, surgical decompression of the colon can be accomplished via caecostomy or Colostomy. In cases with perforation or ischaernia, which can lead to perforation of the colonic wall, partial or subtotal colectomy is indicated with immediate or delayed restoration of intestinal continuity, depending on the patient's condition.
In conclusion, Ogilvie's syndrome is a rare but serious complication in burns patients. The outcome depends mainly on early detection and prompt treatment of the syndrome.