One of the most common GI abnormalities encountered in the critical care setting is the disruption of normal intestinal motility. Loss of motor function may occur in the small intestine as well as the colon. A variety of terminologies have been used to describe disrupted intestinal motility. Ileus is a physiologic term referring to the complete discontinuation of neuromuscular function in the small and large intestine. The term acute intestinal pseudo-obstruction refers to nonmechanical causes of small intestinal and colonic dysfunction. Intestinal obstruction describes a mechanical blockade of the small or large intestine. Postoperative ileus is a term for the normal gut response that occurs for up to 72 hours following abdominal and other types of surgery. Often the clinician will be faced with a diagnostic dilemma in differentiating between mechanical intestinal obstruction, which may require surgical intervention, and pseudo-obstruction, which generally responds to medical therapy.
Acute Intestinal Obstruction in the Critically Ill
More than 90% of all cases of mechanical obstruction of the intestine involve the small intestine alone. Intestinal obstruction is generally caused by adhesions within the abdominal and pelvic cavities; hernias, carcinoma, and intestinal volvulus are other less common causes. Intestinal obstruction may also occur as a consequence of congenital anomalies such as intestinal malrotation; inflammatory bowel disease, especially Crohn's disease; intestinal ischemia; or impaction of the intestinal lumen by foreign bodies such as gallstones.11
Adhesions develop after abdominal surgery and following prior intra-abdominal sepsis.12 Intestinal obstruction secondary to adhesions may occur as early as 3 days after the original surgery. However, delayed effects of adhesive small bowel disease are common, with some patients having recurrent bouts of small intestinal obstruction up to 20 years after their initial surgery.13
The pathophysiologic consequence of a mechanical small intestinal obstruction is distention of the region of the small intestine proximal to the blockade. High pressures develop within the intestinal lumen that may ultimately compromise the blood flow to affected areas. Bowel edema with fluid secretion into the small intestinal lumen occurs as well. This phenomenon, in conjunction with fluid losses secondary to vomiting, causes fluid and electrolyte derangements. As luminal pressure increases, strangulation of the bowel may occur. Bacterial translocation into the circulatory system with resulting bacteremia as well as perforation, peritonitis, and shock are the sources of mortality associated with this condition.
The clinical presentation of patients with acute intestinal obstruction includes intermittent abdominal pain, nausea, and vomiting. Fever, leukocytosis, and electrolyte disturbances commonly occur. Colicky abdominal pain, distension, and abnormal bowel sounds in a patient with previous abdominal surgery are highly sensitive and specific for the presence of mechanical small intestinal obstruction.14
Radiographs of the abdomen with supine and upright views as well as an upright chest x-ray are commonly used to confirm the diagnosis of small intestinal obstruction. Whereas dilated loops of small intestine and colon with the presence of air in the rectum are seen in acute intestinal pseudo-obstruction, mechanical intestinal obstruction is characterized by small intestinal dilation alone without much air in the colon or rectum. Air-fluid levels may be present and represent separation of gas and fluid within fluid-filled, static portions of the small intestine (Fig. 81-4). Absence of air beyond a dilated segment of the small intestine is seen in a complete small intestinal obstruction. Air under the diaphragm on the upright chest x-ray is indicative of an intestinal perforation.
Radiograph of an acute mechanical small intestinal obstruction showing multiple dilated loops of small intestine. (Courtesy of Dr. Arunas Gasparaitis.)
Computed tomography (CT) scanning with oral contrast has been demonstrated to have better sensitivity in diagnosing complete small intestinal obstruction than plain abdominal radiography.15 CT with contrast may also be used to pinpoint the location of a mechanical small intestinal obstruction by identifying decompressed bowel that is distal to the obstruction and may be used to diagnose the presence of intestinal ischemia.16 CT scanning is also used to identify the source of obstruction such as an intra-abdominal or pelvic mass. Small intestinal radiography with contrast may be used to differentiate intestinal obstruction from pseudo-obstruction and for cases not resolving with conservative management. Caution is advised with the use of contrast studies, since barium entering the abdominal cavity through a perforated organ may cause a chemical peritonitis, whereas aspirated water-soluble contrast can result in pneumonitis. The therapeutic role of water-soluble contrast agents for the relief of intestinal obstruction has been investigated and remains controversial.17
Partial small intestinal obstruction is initially treated conservatively with nasogastric suction, administration of intravenous fluids, and correction of electrolyte abnormalities. Nasogastric suction is used for bowel decompression. Serial abdominal examinations and x-rays are vital in the ongoing management of partial intestinal obstruction. The development of sepsis, complete obstruction, or clinical signs of perforation are indications for immediate surgery. Nonresolution of partial mechanical small bowel obstruction is another indication for surgery.18
Conservative management for partial small intestinal obstruction is effective in about 70% of patients. Patients failing conservative management require laparotomy and lysis of adhesions with resection of nonviable intestine. Hospital mortality for small intestinal obstruction is about 10%. Recurrences are common, and more than 50% of patients undergoing surgery for intestinal obstruction can expect a recurrence during their lifetime.13
Intestinal pseudo-obstruction results from disruption of the extrinsic or intrinsic neuronal pathways of the intestine. The mechanism for the development of this disruption varies. In some patients, such as those who have recently undergone abdominal surgery, sympathetic overdrive is present, thus diminishing cholinergic output to the intestine. In others, the direct anticholinergic activity of drugs and neurohumoral mediators inhibits gut function.19 A variety of conditions may result in acute intestinal pseudo-obstruction (Table 81-1). Small intestinal motility in patients with acute idiopathic intestinal pseudo-obstruction is markedly reduced. For example, manometric studies performed in patients with these disorders show marked abnormalities of the fasted motility pattern, including the MMC.20
Table 81–1. Common Causes of Acute Intestinal Pseudoobstruction ||Download (.pdf)
Table 81–1. Common Causes of Acute Intestinal Pseudoobstruction
| Surgery (especially abdominal)|
| Acute pancreatitis|
| Retroperitoneal hemorrhage|
| Intestinal ischemia|
| Cyclic antidepressants|
| Calcium channel blockers|
| Ganglionic blockers|
| Myocardial infarction|
| Shock of any cause|
| Bone fractures|
| Surgery (postoperative—nonabdominal)|
| Chronic intestinal motility disorders|
The clinical symptoms of acute intestinal pseudo-obstruction closely resemble those of mechanical small intestinal obstruction. Most patients have abdominal distention and absence of bowel sounds. Abdominal pain is usual but may not be recognized in the patient who is sedated, delirious, or encephalopathic. Vomiting may also be present, placing patients with this condition at risk for aspiration pneumonia.
Treatment consists of correction of electrolyte abnormalities and administration of intravenous fluid. Pharmacologic agents that may be causing or aggravating the condition should be discontinued. Nasogastric suctioning may result in symptomatic improvement and may alter the pathophysiologic consequences of bowel distention in these patients. Limited therapeutic trials of pharmacologic agents for acute intestinal pseudo-obstruction or prolonged postoperative ileus with metoclopramide and erythromycin have shown few beneficial effects.20 Recent studies of opiate antagonists including methylnaltrexone and alvimopan21,22 have shown promise as potential therapies for postoperative ileus. Movement of the patient and ambulation when possible are encouraged.
Ogilvie's Syndrome: Acute Colonic Pseudo-Obstruction
This syndrome, first described by Sir Heneag Ogilvie in 1948, is generally seen in the ICU or in postoperative patients. It is characterized by abdominal distention accompanied by colonic dilation, particularly involving the cecum and right colon. A variety of medical conditions are associated with the development of Ogilvie's syndrome. It is generally accepted that this disorder results from decreased parasympathetic tone to the distal colon from the sacral nerves with normal vagal impulses to the right side of the colon resulting in a pseudo-obstruction of the distal colon with associated proximal colonic dilation.23 Sympathetic hyperactivity of the right colon has also been postulated as a potential mechanism for the development of this disorder.
The most common medical conditions associated with Ogilvie's syndrome include sepsis, respiratory failure, organic brain disorders, and malignancy. Trauma to the spine, retroperitoneum, and pelvis, as well as burns, may also result in the development of Oglivie's syndrome.24,25 Electrolyte disturbances, including hyponatremia, hypernatremia, hypokalemia, and hypocalcemia, are seen in the majority of patients.26 A variety of medications have been implicated as potential etiologic agents in Ogilvie's syndrome, including narcotics, phenothiazines, calcium channel blockers, and cyclic antidepressants. For example, in one review of Ogilvie's syndrome, 56% of patients had received opiates on the day of diagnosis, 42% had received phenothiazines, and 15% ingested cyclic antidepressants.27 Other medications associated with the development of Ogilvie's syndrome include clonidine and anticholinergic agents. Ogilvie's syndrome may also occur in the postoperative period, most commonly after cesarean sections, orthopedic surgery, and urologic procedures.24
Physical examination of patients with Ogilvie's syndrome always reveals abdominal distention. Bowel sounds remain present in most patients, but may be hypoactive or high pitched. Leukocytosis may be seen in up to 30% of patients, even prior to the development of associated bowel ischemia or perforation. Abdominal x-rays are the diagnostic test of choice, showing dilation of the cecum, usually with associated dilation of the right colon (Fig. 81-5). A decrease in the gas pattern of the left colon is often seen. At the time of diagnosis of colonic pseudo-obstruction, the transverse diameter of the cecum often measures 9 cm or greater on an unmagnified abdominal film.28
Plain radiograph of a patient with Ogilvie's syndrome showing massive cecal and transverse colon dilation. (Courtesy of Dr. Geraldine Newmark.)
Ogilvie's syndrome may be complicated by ischemia and perforation of the distended cecum. As the colon becomes increasingly enlarged (and its radius of curvature increases), less additional pressure is needed to further distend it, and its wall tension rises dangerously (as described by the law of Laplace).28 Case series have shown that the spontaneous cecal perforation rate in Ogilvie's syndrome is approximately 13%, and mortality from this occurrence is 43%. However, the absolute cecal diameter does not correlate specifically with the risk of perforation. The duration of cecal dilation and the rate at which it dilates appear to be the most important factors related to perforation.29
The goal of therapy for Ogilvie's syndrome is decompression of the colon. Some have advocated an initial conservative approach, including nasogastric suction, intravenous hydration, correction of electrolyte abnormalities, discontinuation of offending medications, and treatment of predisposing medical or surgical conditions.27 Others suggest early colonoscopic decompression of the cecum and right colon as an effective and safe therapy for the disorder.26 The colonoscope is advanced to the cecum or the right colon, an often technically challenging procedure because no colonic cleansing preparation is used. Minimal air is insufflated during the procedure to prevent iatrogenic cecal perforation. The reported success rate for initial colonoscopic decompression ranges from 61% to 76%.23,26 The success rate increases after repeat colonoscopic decompression which is required in 20% to 50% of cases. Complication rates for colonoscopic decompression in Ogilvie's syndrome are modest and range from 0% to 3% in published series. Overall the condition carries a mortality rate of approximately 15% in uncomplicated cases, with patients generally dying from their underlying condition. If bowel becomes ischemic or perforates, mortality increases to about 40% as previously described.27
A variety of pharmacologic treatments have been attempted for Ogilvie's syndrome, including cisapride and erythromycin.30,31 These treatments have been reported as case studies only. Neostigmine, a cholinesterase inhibitor, stimulates neuromuscular activity. Several case studies involving a total of 58 patients have demonstrated the efficacy of neostigmine administered slowly by the intravenous route.32–34 Most recently, Trevisani and associates treated 28 patients with 2.5 mg neostigmine administered over 3 minutes. Twenty-six patients (93%) had resolution of the condition with therapy.34 Abdominal cramping, nausea, and diaphoresis were common side effects, although no patients experienced severe bradycardia or cardiovascular collapse, complications that have been described with the use of neostigmine.
Colonoscopic decompression fails in approximately 15% to 20% of patients, even after multiple attempts. These patients require surgical decompression, generally accomplished with a cecostomy and placement of a catheter. A 50% morbidity and 15% mortality is anticipated following cecostomy placement for Ogilvie's syndrome.29 Complications include pericatheter leakage, superficial wound infections, catheter herniation, catheter dislodgment, and prolonged cecal-cutaneous fistula. Nonetheless, this procedure is reportedly successful in 96% of patients. Occasionally patients will require a colonic resection for treatment of this disorder, with an expected 30% surgical mortality.27