Usually, the gastrointestinal tract handles 8–9 l of fluid every day, most of which is reabsorbed by the small bowel. If the occlusive status persists, simple SBO develops into decompensated SBO. The increasing intraluminal tension causes a change of parietal microcirculation, which hampers the ability of the bowel. This happens only when the intraluminal pressure is greater than the pressure in the capillary vessels, causing an alteration of ­vascular permeability. The bowel loop, progressively, becomes decompensated. A definite flow of fluids forms out of the intestinal wall, into the lumen, and in the peritoneal cavity. Nevertheless, the wall does not become thicker, because the tension of the lumen squeezes it like a sponge. The stretched and squashed wall becomes thin and tight.

IV contrast-enhanced CT shows thin walls with preserved and homogeneous CE.

The wall transudates liquid into and out of the loop; the transudate appears in the peritoneal cavity. As in all states of imbalance, the decompensated bowel may be acute or chronic, and it may resolve or deteriorate. In simple and decompensated SBO, the mortality is about 3 %.

Simple and decompensated SBO (Fig. 29.2) may resolve after medical therapy and placement of a nasogastric tube.

Complicated SBO means an occlusive state complicated by vascular changes of the bowel wall. These complications may present with two different modalities:

Regardless of the type, in the initial phase vascular change in the loop is a reversible phenomenon with recovery of the intestinal vitality and function still possible. Nevertheless, without a timely resolution, the final condition of this acute secondary venous ischemia is necrosis, gangrene, perforation, and peritonitis.

In the progression of SBO, vascular suffering due to reaction may appear. The origin of this event is multifactorial and unpredictable.

Main factors include:

IV contrast-enhanced CT shows high contrast enhancement in the wall with normal or borderline thickness. The continuous vascular afflux causes repeated engorgement and a vascular dilation with intramural congestion: the wall becomes thick.

Usually, a reactive loop is near the obstructive site. The venous congestion of the loop may cause passage of blood into the peritoneal cavity. Mesenteric involvement is absent or minimal.

The mechanism of strangulation involves the loop and its mesentery. In these cases, the perfusion deficit involves the venous circulation which is more easily compressible and collapsible. Impairment of the arterial circulation is very late. The obstacle to the blood outflow causes:

Strangulation has been observed in 10–15 % of patients who underwent surgery for SBO. Frager and Baer (1995) report a mortality of about 8 % if the surgical intervention is performed within 36 h from the beginning of symptoms. Over 36 h, the mortality increases to about 25 %.

The term volvulus derives from the Latin verb “volvere” – to roll or twist – and defines loop torsion on its mesenteric axis; the mesentery wraps itself into coils (Fig. 29.3). This mechanism causes abnormal location of loops and vessels, which appear to converge toward the torsive point. Loops assume a spiral configuration. Vessels are stretched and twisted until the artery and vein are inverted.

Volvulus may spontaneously resolve. For­mation of volvulus does not necessarily imply strangulation of the feeding vessel pedicle. This ultimate event verifies only in cases of a particularly serrated strangulation.

Closed loop means an obstructed loop at two adjacent points along its course (Fig. 29.4). Formation mechanism of closed loop is a single obstructed focus which interacts on two points of the same intestinal tract. Numerous formation mechanisms of SBO may generate closed loops. Actually, it may be caused by an adhesive band, entrapped-incarcerated hernia or laparocele, or also volvulus. Warning: evidence of a closed loop is not synonymous with strangulation.

It is an unusual cause of bowel obstruction consisting of an invagination of a proximal segment of bowel (intussusceptum) into the lumen of a distal, adjacent segment of bowel (intussuscipiens). Intussusception may involve only the small bowel (ileoileal intussusception, typically in adults), the small and the large bowel (ileocolic intussusception, typically in children), or just the colon (colocolic intussusception). In adults, intussusception must be considered as a complication of a neoplasm, until proven otherwise. On the basis of canalization, three types of intussusception are identifiable: (1) cold intussusception (asymptomatic), (2) incomplete and reversible hot intussusception (with recurrent and transient episodes of intestinal obstruction), and (3) complete and irreversible hot intussusception (complicated obstruction due to simultaneous involvement of both the bowel and its vascular supply) (Fig. 29.5).