TREATMENT OF ACUTE LARGE BOWEL OBSTRUCTION 1

Large bowel obstruction is caused by: Carcinoma or Carcinoma or Diverticular disease, Diverticular disease, & presents in acute or chronic form. The condition of pseudo-obstruction should always be considered and excluded by a limited contrast study or CT scan. 2

* When a removable lesion is found in the: caecum, caecum, ascending colon, ascending colon, hepatic flexure or hepatic flexure or proximal transverse colon, proximal transverse colon, an emergency right hemicolectomy is performed * If the lesion is irremovable: proximal stoma (colostomy or ileosotomy) or ileotransverse bypass. 3

* Obstructing lesions at the splenic flexure: should be treated by: should be treated by: extended right hemicolectomy with ileo- descending colonic anastomosis. 4

* For obstructing lesions of the left colon or rectosigmoid junction, immediate resection should be considered unless there are clear contraindications: 1- Inexperienced surgeon. 2- Moribund patient. 3- Advanced disease. 5

It is safest to bring the proximal colon to the surface as a colostomy. When possible, the distal bowel should be brought out at the same time (Paul–Mikulicz procedure) to facilitate subsequent closure. In the majority of cases, the distal bowel will not reach and is closed and returned to the abdomen (Hartmann's procedure). 6

Decompression of the obstructed left colon using endoscopically placed stents often as a bridge to surgery has been widely reported. 7

Treatment of caecal volvulus: At operation, is usually ischaemic & needs resection. If, viable, the volvulus should be reduced & fixation of the caecum to RIF (caecopexy) &/or caecostomy. Recurrence after caecopexy is up to 40 %. 8

Treatment of sigmoid volvulus: - Flexible or rigid sigmoidoscopy and insertion of a flatus tube out to allow deflation of the gut. - The tube should be secured in place with tape for 24 hours & a repeat x-ray taken to ensure that decompression has occurred. - Successful deflation, as long as ischaemic bowel is excluded, will resolve the acute problem. 9

- In young patients, an elective sigmoid colectomy is required but in the elderly endoscopic decompression may be enough. Failure results in an early laparotomy, with untwisting of the loop and per anum decompression. When bowel is viable, fixation of the sigmoid colon to the posterior abdominal wall may be a safer or sigmoid colectomy. 10

11

CHRONIC LARGE BOWEL OBSTRUCTION 12

The symptoms of chronic intestinal obstruction may arise from 2 sources: – cause & subsequent obstruction. – cause & subsequent obstruction. causes of obstruction may be: A: organic: 1- intraluminal (rare) – faecal impaction. 2- intrinsic intramural – strictures (Crohn's disease, ischaemia, diverticular), anastomotic stenosis; 3- extrinsic intramural (rare) – metastatic deposits (ovarian), endometriosis, stomal stenosis; 13

B: functional: Hirschsprung's disease, idiopathic megacolon, pseudo- obstruction. The symptoms of chronic obstruction differ in their predominance, timing and degree from acute obstruction. In functional cases, the symptoms may have been present for months or years. Constipation appears first, It is initially relative and then absolute, associated with distension. 14

In large bowel disease, the point of greatest distension is in the caecum, and this is heralded by the onset of pain. Vomiting is a late feature and therefore dehydration is less severe. Examination is unremarkable, only distension (which can be profound) & the peritonism is late. Rectal examination may confirm the presence of faecal impaction or a tumour. 15

Investigation : Plain abdominal radiography confirms the presence of large bowel distension. single-contrast water-soluble enema, CT scan or endoscopic assessment to rule out functional disease. Organic disease requires decompression with either a laparotomy or stent. Functional disease requires colonoscopic decompression in the first instance and conservative management. 16

ADYNAMIC OBSTRUCTION: 17

Paralytic ileus: Is a state in which there is failure of transmission of peristaltic waves secondary to neuromuscular failure (i.e. in the myenteric (Auerbach's) and submucous (Meissner's) plexuses). The resultant stasis leads to accumulation of fluid & gas within the bowel, with associated distension, vomiting, absence of bowel sounds & absolute constipation. with associated distension, vomiting, absence of bowel sounds & absolute constipation. 18

Types of paralytic ileus: 1- Postoperative: A degree of ileus occurs after any abdominal procedure and is self-limiting, with a variable duration of 24–72 hours. Postoperative ileus may be prolonged in the presence of hypoproteinaemia or metabolic abnormality 2- Infection: Intra-abdominal sepsis 3- Reflex ileus: following fractures of the spine or ribs, retroperitoneal haemorrhage. 4- Metabolic: Uraemia and hypokalaemia 19

Clinical features: Paralytic ileus takes on a clinical significance if 72 hrs after laparotomy: - there has been no return of bowel sounds. - there has been no return of bowel sounds. - there has been no passage of flatus. - there has been no passage of flatus. Abd distension becomes more marked & tympanitic. Colicky pain is not a feature. In the absence of NG, effortless vomiting may occur. Radiologically: the abdomen shows gas-filled loops of intestine with multiple fluid levels. 20

Management: - If a primary cause is identified, this must be treated. - GIT distension must be relieved by decompression by NG suction and restriction of oral intake. - Close attention to fluid & electrolyte balance. 21

- There is no place for the routine use of peristaltic stimulants. Rarely, in resistant cases, medical therapy with a gastroprokinetic agent, such as domperidone or erythromycin may be used. - If paralytic ileus is prolonged, CT scanning is the most effective investigation; it will demonstrate any intra- abdominal sepsis or mechanical obstruction and therefore guide any requirement for laparotomy, the need for a laparotomy becomes increasingly likely if it lasts for more than 7 days. 22

Pseudo-obstruction This condition describes an obstruction, usually of the colon, that occurs in the absence of a mechanical cause or acute intra-abdominal disease. It is associated with a variety of syndromes in which there is an underlying neuropathy &/or myopathy and a range of other factors: 23

1- Metabolic: DM, Hypokalaemia, Uraemia, Myxodoema. 2- Severe trauma: to the lumbar spine and pelvis. 3- Shock: Burns, MI, Stroke, Idiopathic, Septicaemia. 4- Retroperitoneal irritation: Blood, Urine, Enzymes (pancreatitis), Tumour. 5- Drugs: antidepressants, Phenothiazines, Laxatives. 6- Secondary gastrointestinal involvement: Scleroderma. 24

Small intestinal pseudo-obstruction: The clinical picture consists of recurrent subacute obstruction. The diagnosis is made by the exclusion of a mechanical cause. Treatment consists of initial correction of any underlying disorder. Metoclopramide & erythromycin may be of use. 25

Colonic pseudo-obstruction: either acute or a chronic. The acute (Ogilvie's syndrome) presents as acute LBO. Abdominal radiographs show evidence of colonic obstruction, with marked caecal distension. Caecal perforation is a well-recognised complication. The absence of a mechanical cause requires urgent confirmation by: Colonoscopy or Single-contrast water-soluble barium enema or CT. 26

Once confirmed, pseudo-obstruction requires treatment of any identifiable cause. If this is ineffective, intravenous neostigmine should be given (1 mg intravenously) If neostigmine is not effective, colonoscopic decompression should be performed. 27

Caecal perforation can occur in pseudo-obstruction. Abdominal examination should pay attention to tenderness & peritonism over the caecum & as with mechanical obstruction, caecal perforation is more likely if the caecal diameter is 14 cm or greater. Surgery is associated with high morbidity and mortality & should be reserved for those with impending perforation when other treatments have failed or perforation has occurred. 28

29