phosphate deficiencies increase intestinal plasma membrane calcium pump gene expression. Proc

Natl Acad Sci U S A 1993; 90(4):1345–1349.

24. Walters JR. Calbindin-D9k stimulates the calcium pump in rat enterocyte basolateral membranes.

Am J Physiol 1989;256(1 Pt 1):G124–D128.

25. Said HM. Recent advances in carrier-mediated intestinal absorption of water-soluble vitamins. Annu

Rev Physiol 2004;66:419–446.

26. Leser TD, M⊘lbak L. Better living through microbial action: the benefits of the mammalian

gastrointestinal microbiota on the host. Environ Microbiol 2009;11(9):2194–2206.

27. Joyce SA, Gahan CG. The gut microbiota and the metabolic health of the host. Curr Opin

Gastroenterol 2014;30(2):120–127.

28. Elamin EE, Masclee AA, Dekker J, et al. Ethanol metabolism and its effects on the intestinal

epithelial barrier. Nutr Rev 2013;71(7):483–499.

29. Everard A, Cani PD. Diabetes, obesity and gut microbiota. Best Pract Res Clin Gastroenterol

2013;27(1):73–83.

30. Keshavarzian A, Fields JZ, Vaeth J, et al. The differing effects of acute and chronic alcohol on

gastric and intestinal permeability. Am J Gastroenterol 1994;89(12):2205–2211.

31. Wang HB, Wang PY, Wang X, et al. Butyrate enhances intestinal epithelial barrier function via upregulation of tight junction protein Claudin-1 transcription. Dig Dis Sci 2012;57(12):3126–3135.

32. Willemsen LE, Koetsier MA, van Deventer SJ, et al. Short chain fatty acids stimulate epithelial

mucin 2 expression through differential effects on prostaglandin E(1) and E(2) production by

intestinal myofibroblasts. Gut 2003;52(10):1442–1447.

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Chapter 49

Ileus and Bowel Obstruction

David I. Soybel and Ariel P. Santos

Key Points

1 Peritoneal adhesions account for more than half of small bowel obstruction (SBO) cases.

2 In simple obstruction the intestinal lumen is partially or completely occluded without compromise of

intestinal blood flow. Simple obstructions may be complete, meaning that the lumen is totally

occluded, or incomplete, meaning that the lumen is narrowed but permitting distal passage of some

fluid and air. In strangulation obstruction, blood flow to the obstructed segment is compromised and

tissue necrosis and gangrene are imminent.

3 Four key symptoms that are associated with acute mechanical bowel obstruction include abdominal

pain, vomiting, distention, and obstipation; abdominal pain out of proportion to physical findings

should raise concern about rapidly evolving closed-loop obstruction and the need for urgent

resuscitation and operation.

4 Use of water-soluble contrast may be both diagnostic and therapeutic.

5 Increasingly, computed tomography (CT) is the “go-to” imaging modality to detect and identify the

likely site and source of obstruction.

6 Conservative management consisting of intravenous hydration, nasogastric decompression, and

restoration of electrolyte balance is a cornerstone of initial management of any patient suspected of

having intestinal obstruction.

7 Open exploratory laparotomy is the gold standard in treating unresolved SBO but laparoscopic

management should be considered in select group of patients. Types of intestinal obstruction that are

more likely to lead to strangulation and the need for urgent/emergent operation include closed-loop

obstructions, obstruction that occurs without a prior history of operation, and obstructions that occur

after laparoscopic procedures.

8 Ileus denotes underlying alterations in motility of the gastrointestinal tract, leading to functional

obstruction.

9 Postoperative ileus (POI) can be differentiated from SBO with the use of contrast CT and

enteroclysis imaging techniques.

10 POI is often self-limiting; less frequent interventions are required for prolonged POI, if proper

precautions have been taken during surgery.

INTRODUCTION AND HISTORICAL PERSPECTIVE

The purpose of this chapter is to provide an overview of the pathophysiology, natural history, diagnosis,

and management of acute obstruction and ileus of the small and large intestines. The development of

the modern approach to intestinal obstruction and ileus paralleled the development of techniques for

safe abdominal surgery. Chief among these accomplishments were the discovery of safe general

anesthetics, the popularization of aseptic methods in the operating rooms and management of wounds,

and the development of techniques for intestinal resection, intestinal anastomosis, and colostomy. The

foundations of the recognition and management of intestinal obstruction and ileus are attributed to

Frederick Treves.1–3 In 1884, he published a detailed discussion of the etiologies (including adhesions)

and surgical management of mechanical intestinal obstruction.1 Treves also distinguished mechanical

from nonmechanical (i.e., paralytic) causes of intestinal distention, classifying the latter causes under

the term ileus. From 1880 to 1925, proximal intestinal decompression was recognized to provide relief

from the symptoms of mechanical obstruction or ileus.3 In 1933, Wangensteen and Paine reported the

efficacy of gastrointestinal intubation in relieving symptoms of intestinal distention caused by intestinal

obstruction or from the ileus that resulted from laparotomy.4,5 Subsequently, Wangensteen and Rea

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provided experimental evidence that the source of gaseous distention in cases of obstruction or ileus

was swallowed air.6 The value of intravenous fluid resuscitation in experimental models of intestinal

obstruction was recognized as early as 19127 and became a principle of care of the patients with

intestinal obstruction in the late 1920s. By 1920, plain abdominal radiographs were used in diagnosis of

intestinal obstruction.3 Thus, the principles of early diagnosis, rapid intravenous fluid resuscitation,

gastrointestinal decompression, and early operation to avoid intestinal gangrene and peritonitis, were

established well before the advent of antibiotic therapy, invasive hemodynamic monitoring, and

parenteral nutrition.8 These early developments were most important in reducing morbidity and

mortality of mechanical intestinal obstruction and ileus.9

MECHANICAL OBSTRUCTION OF THE INTESTINES

Terminology and Classification

The term mechanical obstruction means that luminal contents cannot pass through the gut tube because

the lumen is blocked. This obstruction is in contrast with neurogenic or functional obstructions in which

luminal contents are prevented from passing because of disturbances in gut motility that prevent

coordinated peristalsis from one region of the gut to the next. This latter form of obstruction is

commonly referred to as ileus in the small intestine and pseudo-obstruction in the large intestine. In

simple obstruction the intestinal lumen is partially or completely occluded without compromise of

intestinal blood flow. Simple obstructions may be complete, meaning that the lumen is totally occluded

(Fig. 49-1), or incomplete, meaning that the lumen is narrowed but permitting distal passage of some

fluid and air. In strangulation obstruction, blood flow to the obstructed segment is compromised and

tissue necrosis and gangrene are imminent. Strangulation usually implies that the obstruction is

complete, but some forms of partial obstruction can also be complicated by strangulation.

Figure 49-1. Schematic illustration of different forms of simple mechanical obstruction. Simple obstruction is most often due to

adhesion (A), groin hernia (B), or neoplasm (C). The hernia can act as a tourniquet, causing a closed-loop obstruction and

strangulation.

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1 The various forms of mechanical intestinal obstruction can be classified according to different but

overlapping schemes. Most commonly, obstruction is classified according to etiology. As detailed in

Table 49-1, distinctions are drawn between intraluminal obturators such as foreign bodies or gallstones,

intramural lesions such as tumors or intussusceptions, and extrinsic or extramural lesions such as

adhesions. Adhesions are the most common cause of intestinal obstruction, accounting for more than

half of all cases. In order to highlight the pathophysiology, presentation, and natural history, however,

it is useful to classify obstruction according to the location of the obstructing lesion. Proximal or “high”

obstructions involve the pylorus, duodenum, and proximal jejunum. Intermediate levels of obstruction

involve the intestine from the midjejunum to the midileum. Distal levels of obstruction arise in the

distal ileum, ileocecal valve, and proximal colon whereas the most distant or “low” obstructions would

arise in regions beyond the transverse colon. As shown in Table 49-2, clinical symptoms and signs of

obstruction (pain, vomiting, abdominal distention, and gas pattern on abdominal radiographs) vary with

the level of obstruction.

It is also important to distinguish between open-loop and closed-loop obstructions. An open-loop

obstruction occurs when intestinal flow is blocked but proximal decompression is possible through

vomiting. A closed-loop obstruction occurs when inflow to the loop of bowel and outflow from the loop

are both blocked. This obstruction permits gas and secretions to accumulate in the loop without a means

of decompression, proximally or distally. Examples of closed-loop obstructions are torsion of a loop of

small intestine around an adhesive band (Fig. 49-2), incarceration of the bowel in a hernia, volvulus of

the cecum or colon, or development of an obstructing carcinoma of the colon with a competent ileocecal

valve. The primary symptoms of a closed-loop obstruction of the small intestine are sudden, severe

midabdominal pain and vomiting whereas symptoms of the large intestine are pain and sudden

abdominal distention. This pain often occurs before associated findings of localized abdominal

tenderness or involuntary guarding. When signs of peritoneal irritation or frank peritonitis develop,

there is a high level of suspicion that the viability of the bowel is compromised.

Table 49-1 Classification of Adult Mechanical Intestinal Obstructions

Pathophysiology of Intestinal Obstruction

Local Effects of Bowel Obstruction

When a loop of bowel becomes obstructed, intestinal gas and fluid accumulate. Stasis of luminal content

favors bacterial overgrowth, alters intestinal fluid transport properties and motility, and causes

variations in intestinal perfusion and lymph flow. Luminal contents and volume, bacterial proliferation,

and alterations in motility and perfusion work in concert to determine the rate at which symptoms and

complications develop. Each of these factors merits discussion in some detail.

Intestinal Gas. Approximately 80% of the gas seen on plain abdominal radiographs is attributable to

swallowed air.6 Approximately 70% of the gas in the obstructed gut is inert nitrogen.10 Oxygen accounts

for 10% to 12%, CO2

for 6% to 9%, hydrogen 1%, methane 1%, and hydrogen disulfide 1% to 10%. In

the setting of acute pain and anxiety, patients with intestinal obstruction may swallow excessive

amounts of air. Passage of such swallowed air distally is prevented by nasogastric suction.

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Intestinal Flora. An important contribution to normal digestive function comes from its bacterial

population.11 In patients with normal gastric acid secretion, the chyme entering the duodenum is sterile.

The small numbers of bacteria that are found in stomach and proximal intestine are aerobic, grampositive species found in the oropharynx. Distally, in the ileum and colon, gram-negative aerobes are

present and anaerobic organisms predominate. Total bacterial counts in normal feces reach 1011

organisms per gram of fecal matter. Control of the bacterial populations depends on intact motor

activity of the intestines and the interactions of all species present. This ecology can be disturbed by

antibiotic therapy or by surgical reconstructions that result in stasis within intestinal segments.

Intestinal bacteria serve several functions, including metabolism of fecal sterols, releasing the smallchain fatty acids that are an important food source for colonocytes; metabolism of fecal bile acids, fatsoluble vitamins (e.g., vitamin K) and vitamin B12; and breakdown of complex carbohydrates and

organic matter, leading to formation of CO2

, H2

, and CH4 gases.9 Considerable evidence suggests that

the normal flora may contribute to baseline levels of intestinal secretion and, perhaps, normal intestinal

motility. Under baseline conditions, the small intestines in germfree animals are frequently dilated, fluid

filled, and without peristalsis.12,13

Table 49-2 Symptoms and Signs of Bowel Obstruction

Figure 49-2. Schematic illustration of a closed-loop obstruction. The small intestine twists around its mesentery, compromising

inflow and outflow of luminal contents from the loop. Also, the vascular supply to the loop may be compromised due to the

twisting of the mesentery. The risk of strangulation is high.

In recent years, the role of bacterial toxins in mediating the mucosal response to obstruction has

received increasing attention. In germfree dogs, luminal accumulation of fluid is not observed and

absorption continues.13 In addition, it is well recognized that bacterial endotoxins can stimulate

secretion, possibly via release or potentiation of activity of neuroendocrine substances and

prostaglandins.12 Finally, since a substantial part of systemic microvascular and hemodynamic responses

to endotoxemia appear to be attributable to heightened synthesis of nitric oxide,14,15 it seems likely that

mucosal response to local inflammation and endotoxin release will also be altered by conditions

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modifying the synthesis or activity of nitric oxide. The role of nitric oxide in mucosal fluid and

electrolyte movements is currently under active investigation.16,17

Intestinal Fluid. Classical experimental studies established that fluid accumulates intraluminally with

open- or closed-loop small intestinal obstruction.9,11,18 Factors contributing to the accumulation of fluid

include intraluminal distention and pressure, release of prosecretory and antiabsorptive hormones and

paracrine substances, changes in mesenteric circulation, and elaboration and luminal release of bacterial

toxins. Experimental studies and clinical investigation19,20 demonstrated that elevation of luminal

pressures above 20 cm H2O inhibits absorption and stimulates secretion of salt and water into the lumen

proximal to an obstruction. In closed-loop obstructions, luminal pressures may exceed 50 cm H2O and

may account for a substantial proportion of luminal fluid accumulation.21 In simple, open-loop

obstructions, distention of the lumen by gas rarely leads to luminal pressures higher than 8 to 12 cm

H2O.22 In open-loop obstructions, the contributions of high luminal pressures to hypersecretion may not

be important.

The release of endocrine/paracrine substances remains relatively uncharacterized in states of

mechanical bowel obstruction.23,24 Suggestions have been made that vasoactive intestinal polypeptide

(VIP) may be released from the submucosal and myenteric plexuses within the gut wall, promoting

epithelial secretion and inhibiting absorption.24,25 Use of prostaglandin synthesis inhibitors has also

implicated excess release of prostaglandins.23 Further work may be expected to focus on the role of

luminal factors such as irritative bile acids, proinflammatory agents such as endotoxin and plateletactivating factor,26–28 and messengers such as nitric oxide29,30 in coordinating responses of mucosal

secretory and absorptive functions during intestinal obstruction.

Intestinal Blood Flow. Microvascular responses to intestinal obstruction may also play an important

role in determining the hydrostatic gradients for fluid transfer across the mucosa into the lumen. In

response to heightened luminal pressure, total blood flow to the bowel wall may initially increase.31

The breakdown of epithelial barrier structures and enzymatic breakdown of stagnant intestinal contents

leads to increased osmolarity of luminal contents. In addition to secretory stimulation and absorptive

inhibition of the mucosa, the simultaneous changes in hydrostatic and osmotic pressures on the blood

and lumen sides of the mucosa favor flow of extracellular fluid into the lumen. Perfusion is then

compromised as luminal pressures increase, bacteria invade, and inflammation leads to edema within

the bowel wall.11

Intestinal Motility. Obstruction of the intestinal lumen does not simply block distal passage of luminal

contents. The accumulation of fluid and gas in the obstructed lumen also elicit changes in myoelectrical

function of the gut, proximal and distal to the obstructed segment. In response to this distention, the

obstructed segment itself may dilate, a process known as receptive relaxation.32 Such changes ensure that,

despite accumulation of air and fluid, intraluminal pressures do not amplify easily to the point of

compromising blood flow to the intestinal mucosa. At sites proximal and distal to the obstruction,

changes in myoelectrical activity are time dependent. Initially, there may be intense periods of activity

and peristalsis. Subsequently, myoelectrical activity is diminished and the interdigestive migrating

myoelectrical complex pattern, is replaced by ineffectual and seemingly disorganized clusters of

contractions.33–35 Similar alterations have been observed in experimental models of large bowel

obstruction. Subsequent patterns of myoelectrical quiescence may correspond to increasing

accumulation of fluid and air proximally and the attempt to prevent luminal pressures from rising. It is

likely that many factors contribute to the rate at which these changes in myoelectrical activity occur.36

These factors would include neurohumoral milieu, bacterial products, and luminal constituents.

Complications and Systemic Effects of Bowel Obstruction

Closed-Loop Obstructions. The complications of closed-loop obstructions evolve rapidly. The reasons

for this rapid evolution are best understood by considering the simplest and most common form of

closed-loop obstruction, appendicitis. When a fecalith obstructs the blind-ended appendix, secretion of

mucus and enhanced peristalsis represent the initial attempt to clear the blockage. Intense crampy

abdominal pain focused at the umbilicus results. Nausea and vomiting are not uncommon as a result of

luminal obstruction but as a reflexive response to hyperperistalsis and stretching of the mesentery. Over

the next 8 to 18 hours, continued secretion of mucus to high intraluminal pressures, stasis, bacterial

overgrowth, mucosal disruption, and elevation of luminal pressures convert intermittent cramps to

constant and worsening pain. When luminal pressure exceeds mural venous pressure and then capillary

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perfusion pressures, inflammatory cells are recruited from surrounding peritoneal structures. This

sequence of events leads to intense inflammation, release of exudate in the area of the appendix and the

first localization of pain from the umbilicus to the area of peritoneum lying nearest the inflamed

appendix. Peritoneal findings (localized tenderness, involuntary guarding, rebound, or referred

tenderness) and fevers appear. Subsequently, 20 to 24 hours into the illness, the blood supply of the

appendix is compromised. Gangrene and perforation follow and, if not contained by surrounding

structures, free perforation leads to a rigid abdomen. Toxins from necrotic tissue and bacterial

overgrowth are released into the systemic circulation and shock ensures. Torsion of a loop of small

intestine around an adhesive band or inside a hernia leads to a similar pattern of events. As discussed

below, torsions of the large bowel are usually accompanied by massive distention of the loop by air and

feces, but the compromise of intestinal wall perfusion and evolution into peritonitis, systemic toxicity,

and shock are similar.

Open-Loop Obstructions. Complications in open-loop obstructions do not necessarily evolve as rapidly

as in closed-loop obstructions. Not uncommonly, an open-loop obstruction located in the proximal

jejunum can be decompressed by the patient’s ability to vomit. Proximal obstruction is characterized by

vomiting and loss of gastric, pancreatic, and biliary secretions, with resulting electrolyte disturbances.

These disturbances include dehydration, metabolic alkalosis, hypochloremia, hypokalemia, and usually

hyponatremia. In contrast, obstructions of the distal ileum may lead only to a slowly progressing

distention of the small intestine, with accommodation by intestinal myoelectrical function and minor

alterations in fluid and electrolyte balances. Open-loop obstructions located in the midgut are often

complicated by events similar to those seen in closed-loop obstructions or combinations of events seen

in high and low obstructions (Table 49-2). Patients with distal jejunal obstruction tend to present with a

combination of complications resulting from loss of intestinal contents from vomiting, as well as

distention and compromise of intestinal wall perfusion.

2 In simple or uncomplicated obstruction, the intestinal lumen is partially or completely occluded

without compromise of intestinal blood flow. Simple obstructions may be complete, meaning that the

lumen is totally occluded, or incomplete, meaning that the lumen is narrowed but permitting distal

passage of some fluid and air. In strangulation obstruction, blood flow to the obstructed segment is

compromised and tissue necrosis and gangrene are imminent.

Clinical Presentation and Differential Diagnosis

3 The four key symptoms associated with acute mechanical bowel obstruction include abdominal pain,

vomiting, distention, and obstipation. When bowel obstruction is the most likely diagnosis, “abdominal

pain out of proportion to physical findings” represents a surgical emergency. Colon obstruction is

usually accompanied by varying levels of pain with massive abdominal distention and obstipation. As

noted earlier, the signs and symptoms of acute but simple small intestinal obstructions are related to the

level of the obstruction and the closed- or open-loop nature of the obstruction. Other abdominal

conditions, such as appendicitis, diverticulitis, perforated peptic ulcer, cholecystitis, or

choledocholithiasis can usually be distinguished from SBO, by clinical examination and basic laboratory

data. It should be emphasized that bowel obstruction can complicate any of these abdominal conditions.

The presence of another abdominal process does not exclude the complication of SBO.