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SMALL INTESTINE 361
stool together with an improvement of symptoms such as a diminution of abdominal distension, crampy pain, and vomiting indicate
resolution of the obstruction. With partial small bowel obstruction,
large volumes of watery stool can occur in the context of vomiting
and distention. A Richter hernia whereby only a part of the circumference of the small bowel may be entrapped is a special situation
in which the risk of strangulation persists despite the presence of
ongoing bowel function. As discussed earlier in this chapter, radiographic studies may be able to dierentiate complete and partial
obstruction. In situations where CT scans are noncontributory, a
Gastrogran follow-through can be both therapeutic and diagnostic, in that failure of contrast material administered orally or by the
nasogastric tube to reach the colon by 24 hours may serve as an
indication for surgical exploration.
Nonadhesive Obstruction
Hernias
Hernias are the second most common cause of intestinal obstruction
aer adhesions. A careful examination of the inguinal and femoral
canals, as well as any abdominal or ank incisions and stoma sites, is
mandatory in any patient presenting with abdominal pain or obstruction and may reveal a tender or nonreducible swelling. Obese patients
may have no bulge, but palpation should reveal a tender lump. Parastomal hernias also can be subtle, although pain and a cough impulse
are usually present if the impacted bowel is obstructed. An obturator
hernia is a rare entity, and when incarcerated, it presents with intestinal obstruction associated with pain along the inner aspect of the
thigh (the Howship-Romberg sign). When small bowel obstruction
develops as a result of a hernia, urgent exploration is oen required
to avoid the risk of strangulation. Findings of erythema and edema
of the skin overlying the incarcerated hernia, along with tenderness,
such warning signs are not present and tenderness is not present over
the hernia, gentle manual pressure over the hernia together with the
administration of an anxiolytic agent and elevation of the foot end of
the bed for inguinal and femoral hernias has been described as being
eective in reducing an incarceration. If this approach is successful,
elective repair may be performed in the near future. “Reduction en
masse” in which a strangulated segment may be reduced into the
peritoneal cavity together with the hernial ring is a rare complication
that produces the paradox of continued obstruction aer apparent
reduction of the hernia.
Crohn Disease
Stricture of the small bowel as a result of inammation or brosis
from Crohn disease may precipitate small bowel obstruction. In some
instances an inammatory phlegmon or internal or enterocutaneous
stula also may accompany the obstruction. Small bowel may also
be drawn into areas of intra-abdominal inammation as a result of
abscesses from any cause, such as diverticulitis or tumor (desmoplastic reaction) and become obstructed. In these circumstances, the
management of obstruction is usually dictated by the primary condition. Surgery occasionally may be indicated for the obstruction itself,
in which case the primary disease needs to be addressed as discussed
in the relevant chapters relating to these conditions.
Intussusception
Intussusception is a rare cause of small bowel obstruction in adults.
In most cases the lead point for the intussusception is an intraluminal neoplasm that is passed distally in the bowel by peristalsis. As
the proximal segment (the intussusceptum) is drawn further into the
distal bowel (the intussuscipiens), the mesentery is compressed and
ischemia of the intussusceptum may result. Intermittent episodes of
obstruction accompanied by the passage of bloody stool mixed with
mucus (“red currant jelly”) is pathognomonic. e diagnosis may be
made by imaging or colonoscopy, but in many cases it presents as an
unexpected nding at laparotomy. Because of the dierence in cause
of the intussusception in adults when compared with the pediatric
population, attempts at reduction of the intussusception, either by
hydrostatic techniques or at surgery, are not advised.
Gallstone Ileus
Gallstone ileus is another very rare cause of small bowel obstruction. Patients are usually elderly women. e condition is caused by a
large gallstone eroding from the gallbladder directly into an adjacent
segment of the small or large intestine (the duodenum, jejunum, or
hepatic exure of the colon) that has become adherent to the gallbladder as a result of inammation. e stone then passes distally into the
intestinal tract until it becomes impacted. e site of impaction is
usually in the narrowest portion of the small intestine, typically in the
terminal ileum. A plain radiograph of the abdomen may reveal the
classic ndings of small bowel obstruction, a radiopaque gallstone
outside the right upper quadrant, and pneumobilia. is combination, Rigler’s triad, is present in fewer than 10% of cases, because most
gallstones are radiolucent.
Bariatric Patient
Small bowel obstruction occurs in approximately 3.5% of patients
with a history of laparoscopic Roux-en-Y gastric bypass. ese
patients appear to be at a higher risk of developing an internal hernia
compared with patients aer open bypass surgery because iatrogenic
mesenteric defects remain patent as a result of less intensive adhesion formation aer laparoscopy. A frequent site of herniation is the
“Petersen space” between the Roux limb mesentery and the transverse mesocolon in patients who have undergone an antecolic Rouxen-Y bypass. Although immediate closure of mesenteric defects is
advocated by bariatric surgeons to decrease the risk of internal herniation, such closure can be dicult to achieve in morbidly obese
patients. Even so, any patient who has had a gastric bypass should be
considered at risk. Herniation with strangulation may occur late aer
the bypass once the patients have lost weight and are predisposed to
herniation by the thinner mesentery surrounding the (sometimes
partly closed) defects. Patients who have undergone gastric bypass
may present with vague complaints, an unremarkable physical
examination, and laboratory values. A low index of suspicion for this
potentially life-threatening complication is essential, and an early CT
scan is recommended. In patients with a strong suspicion for internal hernia and volvulus, surgery may be recommended even in cases
with negative imaging studies because false negative reports may be
misleading.
Surgical Technique
Malignancy
Small bowel obstruction as a result of malignant disease usually
results from metastases or involvement of the small intestine by
advanced cancer in a nearby organ. Primary small bowel cancers,
usually adenocarcinomas or gastrointestinal stromal cell tumors, are
less common causes of obstruction. Diagnosis is oen made by imaging, although sometimes the cancer is apparent only at laparotomy.
Adhesive Obstruction
Whereas most patients can be placed supine, the Lloyd-Davies position allows ease of access to the pelvis and the performance of colonoscopy. When patients have previously undergone pelvic surgery
or radiation, or when the level of obstruction is not clear, the latter
position is preferable. Aer adequate resuscitation, a midline incision that encompasses any previous scar (if also midline) is used
Small Bowel oBStruction362
for laparotomy. e risk for inadvertent enterotomy is high during
abdominal entry because the bowel loops are distended and likely
to be adherent to the abdominal wall. Patients with a thinned-out
abdominal wall or a frank incisional hernia pose a special problem
because there is a particular risk of damage to the distended intestine. We use a scalpel for entry into the peritoneal cavity. Liing up
on the abdominal wall on either side allows controlled division of
the skin and subcutaneous tissues, the fascia, and the peritoneum
and entry into any windows of peritoneal cavity that are relatively
free of adhesions. When no such windows exist, our preference is
to precisely incise the peritoneum. Once the surface of the intestine
is encountered, dissection is then developed in a lateral direction to
“clear the lateral space” because this then permits the identication
of the fused peritoneum to intra-abdominal contents, upon which
further peritoneal entry is facilitated. An alternative strategy is to
enter the peritoneal cavity above or below the previous incisional
scar prior to the dissection being developed along the entire length
of the incision.
In some cases, a single constricting band may be encountered,
which is divided to relieve the obstruction. In other cases, many
adhesions are encountered, with the peritoneal cavity sometimes
totally obliterated by scar tissue. Great care is necessary during lysis
to minimize inadvertent damage to the small bowel or other structures and allow identication of the site of obstruction. e incision is
gradually extended by continually separating underlying small bowel
from the undersurface of the midline scar so that the entire length
of incision is ultimately opened. e incision is extended when indicated. Adhesiolysis then extends outward on either side of the midline to develop the lateral space. If bowel distention is severe, needle
decompression occasionally may be used to gain additional working
space. Typically, this involves the placement of a purse-string suture
on the antimesenteric portion of a distended segment of small bowel
for control through which a wide-bore needle is introduced tangentially into the lumen. Suction tubing attached to the end of the
needle facilitates decompression of air, as well as liquid stool. In some
instances, interrupted seromuscular sutures may be placed or the
previously placed purse-string suture may be tied to facilitate closure
of the needle puncture site. Attention is then turned to the remainder
of the abdomen. Oen the most dicult adhesions may be encountered in the pelvis or pelvic side walls. Gentle traction is applied to
small bowel while the dissection is pursued along the lateral aspects
of the pelvis, with the dissection then directed distally to deliver the
bowel from the pelvis. e posterior aspect of the small bowel and the
attached mesentery is then dissected away from the retroperitoneum
from down to up. Once mobilization has been completed, interloop
adhesions are lysed. Injection of saline solution in the planes between
adjacent segments of small bowel and between the small bowel and
the abdominal wall, other structures, and retroperitoneum may facilitate dissection of dense adhesions. e need for complete adhesiolysis aer the point of obstruction is freed depends upon the cause of
the obstruction, the likelihood of associated disease, and the intensity
of the adhesions and the presence of a proximal enterotomy. When
adhesions are particularly dense, adhesiolysis can be limited as long
as the point of transition is demonstrated, the cause of the transition
is obvious, and the obstructing element can be addressed or resection
can be completed relatively easily.
Aer adhesiolysis, the bowel is inspected for any coexisting disease and for enterotomies or serosal tears created during the course
of mobilization. e classic technique of “milking” the intestinal contents back into the stomach to be aspirated by a nasogastric tube has
recently been evaluated in a randomized controlled trial but was not
found to aect outcome in any meaningful way and therefore should
be abandoned. When the intestine is grossly distended and edematous, there is a risk of extensive serosal denudation as a result of
stripping of the serosa. When the small bowel needs to be emptied to
facilitate abdominal closure or anastomosis, we prefer using a “handover-hand” emptying technique. In this technique, the small bowel is
compressed in the palm of one hand between the at of the ngers
and the thenar eminence followed sequentially by the other hand. We
have found that this technique is associated with a much lower risk
for inadvertent small bowel injury.
Bowel viability usually can be assessed using the triad of color,
peristalsis, and mesenteric pulsations. If viability is questionable, the
ischemic segment should be wrapped in warm, wet packs, 100% oxygen should be administered, and viability should be reassessed aer
10 to 15 minutes. If some doubt still exists, use of the Doppler ow
probe or systemic injection of uorescein dye followed by inspection
of the bowel under a Wood’s lamp may aid decision making. If viability is doubtful for a short segment of small bowel, resection of the
segment is the best strategy. However, if an extensive segment is of
questionable viability, then a second-look operation may be required
the following day, which will allow resuscitation of the patient and an
opportunity for borderline viable small bowel to demarcate and thus
potentially limit the extent of small bowel resection.
Hernias
Incarcerated inguinal hernias are explored through an oblique inguinal incision, although, on occasion, a midline laparotomy or vertical incision overlying the hernia and extending upwards toward the
abdomen or downward toward the thigh may be a better option, particularly for strangulated femoral hernias. With a local incision, the
constricting ring should be released aer the hernia sac is opened,
and the bowel can be inspected for viability. If the hernia contents
reduce spontaneously before an adequate assessment of their viability
could be performed, a laparotomy may be required. If the contents of
the hernia are viable, the bowel is returned to the peritoneal cavity,
the sac is excised, and standard hernia repair is performed. Necrotic
bowel can usually be resected through an inguinal approach, and aer
healthy small bowel is delivered through the defect, an anastomosis
is performed. Repair of an inguinal hernia that contains strangulated
bowel is best performed using a layered repair with permanent monolament suture. Mesh repair of an incarcerated inguinal (or other)
hernia was long believed to be hazardous because of the risk of infection with subsequent need for mesh removal. Recent reports, however, have challenged this dogma, and polypropylene mesh repair has
been advocated as being eective and safe even for patients requiring
resection of strangulated bowel. Although consensus has not been
reached on the issue, some authors support prolonged postoperative
antibiotic prophylaxis when mesh repair of an incarcerated hernia
is performed. Incarcerated femoral hernias can be approached using
a low inguinal incision, a preperitoneal approach, or a low midline
incision. Conversion to a lower midline incision may be necessary if
necrotic bowel is present.
Crohn Disease and Other Inflammatory Conditions
When obstruction is a result of inammatory conditions such as
Crohn disease, diverticulitis, desmoid disease, and other intraabdominal disease, management of the obstruction is part of management of the disease and is discussed in the corresponding chapters.
Malignancy
In cases of obstruction resulting from an advanced systemic malignancy, palliation of obstruction can be achieved and is expected to
improve quality of life. In general, resection may oer better palliation than bypass, but the ndings at the time of surgery determine
the best approach. In cases that include a localized obstruction that
cannot be easily resected, bypass is the best strategy. When extensive
carcinomatosis is present, including cases with a frozen abdomen,
creation of a loop stoma in the bowel proximal to the obstruction may
be the only meaningful option and provides palliation of obstructive symptoms. In some cases, a combination of resection, bypass, or
ostomy may allow relief of obstruction and restitution of oral intake
so that patients can be discharged home. If no small bowel can be
SMALL INTESTINE 363
mobilized, then a gastrostomy tube is placed for decompression. If
this situation is recognized preoperatively, placement of a percutaneous gastrostomy tube together with hyperalimentation is a reasonable alternative that allows discharge of the patient from the hospital
to home surroundings. Involvement of a palliative care specialist in
these cases is important because narcotic pain medication, antiemetic
agents, anticholinergic drugs, and somatostatin analogs will be the
mainstays of treatment.
Intussusception
When intussusception is identied preoperatively or during surgery
as a cause of obstruction, resection of the lead point and any associated strangulated tissue is the best approach.
Gallstone Ileus
e obstructing gallstone usually can be milked proximally into
healthy bowel, where an enterotomy is made for stone extraction. If
the stone is tightly impacted, then resection of the segment is indicated. Because multiple stones may occur in 5% of cases, the entire
small bowel should be carefully palpated to identify the presence of
other stones. In most cases, the gallbladder and the bilioenteric stula is le alone at the primary surgery, with a cholecystectomy performed electively at a later date, if required.
The Bariatric Patient
Gastric bypass patients with an internal hernia or volvulus may present with vague symptoms and an unremarkable physical examination and laboratory values. A low index of suspicion is required for
this potentially life-threatening complication, with early CT scanning
and surgery even with negative imaging studies. In such instances,
laparoscopy to rule out or diagnose internal hernia, reduce the herniated segment, and close any mesenteric defects is preferred. If strangulation has occurred or anatomy predisposes to further recurrence,
resection of the involved segment or revision of the anastomosis may
be required.
Laparoscopic versus Open Lysis of Adhesions
Laparoscopic lysis of adhesions for small bowel obstruction was rst
described in 1991 by Batsug and colleagues. Studies have shown that
in select cases, laparoscopic adhesiolysis is safe and may oer better
outcomes in terms of earlier return of bowel function, shorter length
of hospital stay, and improved cosmetic results compared with the
open technique. Despite these benets compared with laparotomy,
Mancini etal, using National Inpatient Sample data, found that in
2002 only 11.4% of all patients with adhesive small bowel obstruction in the United States were treated laparoscopically. Some persons
have raised concerns about the safety of laparoscopy in the setting
of dilated small bowel because of a perceived higher risk of inadvertent and missed enterotomies. An important factor in patient selection relates to the ability to gain safe access into the peritoneal cavity
rather than the absolute number of previous operations. Factors
that were associated with successful laparoscopic lysis of adhesions
included operations limited to one or two areas of the abdomen (i.e.,
the pelvis), proximal obstruction, length of time since last laparotomy
greater than 1 year, ability to insuate more than 1 L of CO
, and
2
absence of overt peritonitis or gross abdominal distension. Although
studies have shown that laparoscopy is safe under such circumstances
when performed by surgeons experienced in minimally invasive techniques, a low threshold to convert to an open technique is warranted.
Early Postoperative Bowel Obstruction
Early postoperative small bowel obstruction poses a unique challenge and requires specic attention. e major diculty with this
condition lies in its overlap with ileus. Even when a mechanical
obstruction has been shown, management usually diers from that
of obstruction remote from surgery because most postoperative
obstructions resolve spontaneously. In addition, attempts at repeat
laparotomy in the early postoperative period may be hazardous and
can result in disastrous complications. Typically, an intense inammatory response usually begins within the abdomen 7 to 10 days
postoperatively and persists for at least 6 weeks. Surgery during this
period is dangerous when dense hypervascular adhesions obliterate the peritoneal cavity. e risk of enterotomy and subsequent
stulization is high. In addition, injury to the small bowel mesentery, as well as extensive deserosalization of the bowel, may lead
to extensive resections. Because of these risks, as well as the low
risk for the development of strangulation, patients with postoperative obstruction should be managed conservatively with nasogastric
suction and intravenous uids. If resolution does not occur within
5 to 7 days, the patient is started on hyperalimentation and a percutaneous gastrostomy tube is placed for longer term decompression.
Patients who have persistent obstruction are discharged from the
hospital with parenteral nutrition, with the gastrotomy tube used
as a vent to relieve obstruction. In most such patients the condition
spontaneously resolves, although this process may be gradual. Such
patients initially tolerate oral liquids, with the gastrostomy tube
le clamped until such time as nausea or fullness dictates release
of the clamp so as to vent the gastrointestinal tract. Progressively
reduced frequency of the need for venting of the gastrostomy tube
is noted as the gastrointestinal tract resumes function. Such patients
are then transitioned to solid foods, and once reliable oral intake
can be ensured, the gastrostomy tube is removed and parenteral
nutrition is discontinued. In cases where obstruction is persistent,
laparotomy may be performed in 3 to 6 months. Immediate surgery
is indicated for peritonitis or signs of sepsis. ere is a place for
very early exploration within the rst 7 to 10 days postoperatively if
obstruction is recognized promptly, because adhesions encountered
during this period are not usually severe.
Prevention of Adhesions
Adhesions can occur aer any laparotomy and are likely a result of
injury to the serosal surfaces that lead to an inammatory response
and scarring. In general, reduction of iatrogenic peritoneal damage, inhibition of the inammatory response, prevention of brin
formation and promotion of brinolysis, prevention of collagen
formation and deposition, and nally, the use of mechanical barriers are mechanisms that have been used to prevent the development of adhesions. Potentially, any of these aims may be achieved
by use of clean surgical technique, systemic medications, or topi
cal agents applied directly to the site of the operation. Although
various investigators have evaluated these agents, few clinical trials have been performed, and even fewer of these strategies have
found their way into clinical practice. Regardless, careful, clean
operative technique with gentle handling of tissues and avoidance of leaving devascularized tissue, use of powder-free gloves to
avoid the deposition of talc, and copious lavage of the peritoneal
cavity at the conclusion of the operation are simple measures that
should be universal. Local chemoprophylactic agents to reduce or
eliminate adhesions through a barrier mechanism have been developed. Although a large multicenter study by Fazio and associates
that evaluated the role of a bioresorbable membrane of modied
sodium hyaluronate and carboxymethylcellulose (Sepralm, Sano,
Paris, France) demonstrated that the overall bowel obstruction rate
was unchanged, the incidence of adhesive small-bowel obstruction requiring reoperation was signicantly reduced (relative risk
of 47%). However, other reports have raised concerns about an
increased rate of intra-abdominal abscess formation and anastomotic leakage when Sepralm was wrapped around a fresh anastomosis. A recent Cochrane review concluded that although the
-
Small Bowel oBStruction364
incidence of intestinal obstruction or the need for surgery is in fact
not improved by Sepralm, its use is safe and Sepralm may be
applied at the surgeon’s discretion.
Systemic agents such as heparin, corticosteroids, and nonsteroidal antiinammatory drugs (NSAIDs) have all been shown to
decrease brin deposition and thus reduce adhesion formation
in experimental models. NSAIDs work by inhibiting the early
inammatory response. Heparin inhibits the coagulation cascade
through factor Xa and antithrombin formation. Corticosteroids
exert a multitude of antiinammatory and immune-modulating
eects, but their eectiveness in preventing adhesion formation
has not been proven in experimental models. Similarly, the prevention of brin formation with therapeutic anticoagulation has
not been shown to exert a signicant eect on adhesion formation
in animal models, and concerns regarding its clinical value given
an increased risk of postoperative hemorrhage remain justied.
Novel medications that succeed in reducing the early inammatory
response and counteract the formation and deposition of brin
products without aecting wound healing and causing postoperative bleeding are needed.
Finally, a number of studies have reported a lower incidence of
adhesion-related small bowel obstruction aer laparoscopic compared with open colorectal resection. A 25% reduction in postoperative adhesions in patients undergoing laparoscopic as opposed to
open gastrointestinal surgery, as well as a signicant attenuation of
the severity of the adhesions encountered, has been shown. In fact,
a recent large British study on 187,000 patients admitted to National
Health Services hospitals could demonstrate signicantly lower rates
of readmission and reintervention rates for adhesion-related small
bowel obstruction aer laparoscopic compared with open colorectal surgery. Although the use of a pneumoperitoneum itself has been
shown to exert some proadhesive eects by inducing peritoneal
hypoxia, leading to an increased release of vascular endothelial
growth factor, it appears as if the benecial aspects of laparoscopy
in reducing adhesion formation outweigh these opposing mechanisms in the clinical setting. Smaller incisions, less tissue trauma and
bleeding, a reduced inammatory response, and an earlier recovery
of bowel function with the minimally invasive approach are likely
responsible for this advantage.
SUMMARY
Small bowel obstruction is a common medical and surgical problem
with multiple causes. Postoperative adhesions account for the majority of these cases, but clinicians need to be aware of other causes such
as incarcerated hernias, volvulus, or intussusception, which may
mandate early operation. CT scanning has become the diagnostic
modality of choice, yet plain radiographs, contrast studies, MRI, and
sonography may be helpful in some circumstances. Intestinal ischemia with impending bowel wall necrosis needs to be excluded based
on clinical, radiographic, and laboratory ndings during the initial
and sequential clinical assessments. Patients likely to have intestinal
ischemia require immediate resuscitation and surgical exploration.
Nonoperative management is recommended in patients with adhesion-related small bowel obstruction when the risk of bowel ischemia
is deemed to be low, because most of these patients will regain function without repeat laparotomy within 1 to 2 days. Beyond this time
frame, however, surgical exploration should not be deferred unless
specic factors such as early postoperative obstruction or advanced
malignancy are present (Fig. 71-1). Careful, repetitive clinical assessment by experienced clinicians is critical in such patients to allow
for timely intervention before unrecognized bowel ischemia leads to
clinical deterioration, organ failure, and death.
Clinical suspicion of acute small bowel obstruction
H and P, laboratory and imaging studies
“High risk” “Low risk” “Special circumstances”
• Pneumoperitoneum
• Clinical, laboratory or radiographic
suspicion of bowel ischemia
• Clinical or radiographic evidence
of strangulation/closed loop obstruction
• Sepsis
Urgent (same day) laparotomy Laparotomy indicated upon worsening pain,
• Clinical signs of small bowel obstruction
without suspicion of ischemia, strangulation,
or sepsis
• Most cases of adhesion-related small bowel
obstruction
increasing signs of ischemia or after failed
resolution within 48 hours
Laparoscopy feasible if adequate experience,
fewer and smaller prior operations, mild
abdominal distension and max (recent)
radiographic diameter of small bowel < 4cm
• Early postop period (4 weeks)
• Advanced malignant disease
with suspicion/evidence of
peritoneal carcinomatosis
• Minimal abdominal distension
• Minimal pain/tenderness
Watch and wait for 5 days max
• Venting PEG tube placement or
• Laparotomy with LOA, internal
bypass or proximal ostomy
FIGURE 71-1 Adhesion-related small bowel obstruction: treatment algorithm.
SMALL INTESTINE 365
S u g g e S t e d R e a d i n g
Attard JP, MacLean AR. Adhesive small bowel obstruction: epidemiology, bi-
ology and prevention. Can J Surg. 2007;50(4):291–300.
Beck DE, Opelka FG, Bailey HR, et al. Incidence of small bowel obstruction
and adhesiolysis aer open colorectal and general surgery. Dis Colon Rec-
tum. 1999;42:241–248.
Burns EM, Currie A, Bottle A, etal. Minimal access colorectal surgery is as-
sociated with fewer adhesion-related admissions than open surgery. Br J
Surg. 2013;100(1):152–159.
Chen XL, Ji F, Lin Q, etal. A prospective randomized trial of transnasal il-
eus tube vs nasogastric tube for adhesive small bowel obstruction. World J
Gastroenterol. 2012;18(16):1968–1974.
Dietz D. Small bowel obstruction. Current erapy in Colon and Rectal Sur-
gery. 2nd ed. Philadelphia: Mosby; 2004. [chapter 74].
Farid M, Fikry A, El Nakeeb A, et al. Clinical impacts of oral Gastro-
gran follow-through in adhesive small bowel obstruction. J Surg Res.
2010;162(2):170–176.
Fazio VW, Cohen Z, Fleshman JW, etal. Reduction in adhesive small bowel
obstruction by Sepralm adhesion barrier aer intestinal resection. Dis
Colon Rectum. 2006;49(1):1–11.
Fevang BT, Fevang J, Stangeland L, etal. Complications and death aer surgi-
cal treatment of small bowel obstruction. A 35-year institutional experience. Ann Surg. 2000;231(4):529–537.
Jenkins JT, Taylor AJ, Behrns KE. Secondary causes of intestinal obstruction:
rigorous preoperative evaluation is required. Am Surg. 2000;66:662–666.
Kossi J, Salminen P, Rantala A, etal. Population-based study of the surgical
workload and economic impact of bowel obstruction caused by postoperative adhesions. Br J Surg. 2003;90:1441–1444.
Maglinte DD, Howard TJ, Lillemoe KD, etal. Small-bowel obstruction: state-
of-the-art imaging and its role in clinical management. Clin Gastroenterol
Hepatol. 2008;6(2):130–139.
Zerey M, Sechrist CW, Kercher KW, etal. e laparoscopic management of
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M M
S B
S
Mary Jo Alberino, Dileep Atluri, and Ezra Steiger
INTRODUCTION
Short bowel syndrome (SBS) is a form of intestinal failure that most
oen results from surgical resection related to Crohn disease, mesenteric infarction, radiation enteritis, or surgery for recurrent bowel
obstructions. It is characterized by the inability to absorb protein/
energy requirements or to maintain uid, electrolyte, or micronutrient balance when consuming a normal diet. Aer surgical resection,
the remaining small intestine undergoes structural and functional
adaptation over 1 to 2 years that gradually improves absorption. Successful medical management of SBS is dependent on a combination
of diet, medications, oral or tube enteral supplements, parenteral
nutrition (PN), and intestinotrophic hormones (Fig. 72-1).
ANATOMY OF SHORT BOWEL
SYNDROME
A thorough evaluation of the patient’s remaining gastrointestinal
tract is the basis for making therapeutic recommendations. Operative
reports should have antimesenteric measurements of residual bowel,
its location, and any gross pathologic changes. In addition, the extent
and location of bypassed segments should be noted as an aid to potential reconstruction in the future. An upper gastrointestinal barium
radiograph with small bowel follow-through or computed tomography (CT) scan enterography provide an estimate of the length of the
remaining small bowel. ree anatomic congurations of SBS that
have management and outcomes implications have been described.
Type 1 is an end jejunostomy with most of the small intestine and all
of the colon either resected or out of continuity. A minimum of 100 cm
of intestine is needed to avoid permanent PN. Type 2 is a remnant
small bowel anastomosed to part of the colon. In this conguration,
at least 60 cm of residual small intestine is required to avoid permanent PN. Type 3 anatomy is a jejunoileal colonic anastomosis with
the entire colon intact, in which case at least 30 cm of small intestinal
length is required to avoid permanent PN. Table 72-1 summarizes the
anatomic factors favoring enteral autonomy and anatomic congurations that make permanent PN dependence likely. Plasma citrulline levels lower than 20 μmol/L in adults and 15 μmol/L in pediatric
patients also have been associated with permanent dependence on
PN. Citrulline is produced mainly by small intestinal enterocytes,
and its level correlates with residual small intestine length and functional enterocyte mass.
DIETARY MANAGEMENT OF SHORT BOWEL SYNDROME
Patients should follow strict dietary guidelines established by a dietitian with expertise in the management of SBS. ese guidelines
366
include eating frequent meals and the avoidance of simple carbohydrates (foods with sugar) in favor of complex carbohydrates (e.g.,
pasta). See Table 72-2 for diet guidelines based on the patient’s anat-
omy. Patients should be encouraged to avoid drinking hyperosmolar
beverages such as fruit juices and hypo-osmolar beverages like water,
which increase gastrointestinal uid output in persons with SBS. Sipping of an isotonic oral rehydration solution (ORS) throughout the
day should be encouraged to maximize intestinal uid reabsorption.
ORS is a glucose–electrolyte solution that promotes water reabsorption by way of the sodium–glucose cotransport mechanism and is
used to treat cholera-associated diarrhea. ORS recipes are shown
in Table 72-3. Aer large resections, oral multivitamins should be
given twice daily and fat-soluble vitamins (A, D, E, and K) and trace
element levels should be monitored. Table 72-4 shows deciency
manifestations and repletion doses for common vitamins and trace
elements. Magnesium and potassium deciencies are also very common and require careful monitoring with oral or intermittent intravenous (IV) repletion.
PHARMACOLOGIC TREATMENT OF SHORT BOWEL SYNDROME
e pathophysiologic mechanisms and treatment opportunities for
SBS are shown in Table 72-5. e major medications used to treat
SBS include antidiarrheal agents, antisecretory and bile acid-binding
agents, and pancreatic enzymes (see Table 72-6). Combinations of
antidiarrheal agents in increasing dosages are oen helpful if single
agents are ineective and should be tried before adding opiates to the
regimen. Histamine receptor antagonists and proton pump inhibitors are eective in reducing gastric acid hypersecretion that occurs
in the rst 6 to 12 months aer massive small bowel resection, and
they reduce uid and electrolyte losses. Octreotide can be administered intravenously, subcutaneously, or intramuscularly to reduce
secretions from the entire gastrointestinal tract but can interfere with
adaptation and increase the incidence of biliary lithiasis and cholestasis. Patients with fat malabsorption, clinically characterized by bulky,
greasy, foul-smelling stools that oat, may be helped by pancreatic
enzymes. Bile salt–binding agents are used in patients with residual
colon in continuity when unabsorbed bile salts enter the colon and
stimulate large uid outputs.
PARENTERAL AND ENTERAL NUTRITION
PN should be started in the postoperative period in patients having less than 100 cm of small bowel to an enterostomy, or less than
60 cm of small bowel anastomosed to a segment of colon, or less
than 30 cm of small intestine with an intact ileocecal valve and
SBS no colon SBS with colon
>100 cm SB <100 cm SB <30 cm SB + colon >30cm SB + colonUltra SBS, <50 cm SB
SMALL INTSESTINE 367
Start PN Start PN
Diet modifications: high starch, high salt,
high fat, low simple sugar food choices and
ORS intake
Medications: antidiarrheals, antisecretory,
antibiotics/probiotics as needed
PN/IVF: Wean as tolerated
Yes No
Achieved enteral autonomy Satisfies criteria for usage of intestinotrophic
Long-term PN
Fluid restriction:
<2000 mL/day
Diet modifications: high starch, high salt,
low fat, low simple sugar, low oxalate
food choices and ORS intake
Medications: antidiarrheals, antisecretory, bile
acid binders, antibiotics/probiotics as needed
PN/IVF: Wean as tolerated
Weaned off PN?
hormones?
YesNo
Trial of intestinotrophic hormones
Surgical considerations for bowel
lengthening procedure or referral for
intestinal transplantation
FIGURE 72-1 Algorithm for medical management of short bowel syndrome. IVF, Intravenous fluid; ORS, oral rehydration solution; PN, parenteral
Achieved enternal autonomy
YesNo
nutrition; SB, short bowel; SBS, short bowel syndrome.
TABLE 72-1: Anatomic Factors Affecting Enteral Autonomy
Factors Favoring Enteral Autonomy Factors Associated with Parenteral Nutrition Dependence
Length of remaining bowel
>30 cm of small bowel with colon
>100 cm of small bowel alone
Jejunum resection
Preserved ileocecal valve
Presence of colon
Absence of mucosal disease
Normal hepatic and pancreatic function
Jejunoileal anastomosis and remaining small bowel length <35 cm
Jejunocolic anastomosis and remaining small bowel length <60 cm
Large ileal resection
Patients with end jejunostomy and remaining small bowel length
<115 cm
Medical ManageMent of Short Bowel SyndroMe368
TABLE 72-2: Diet Guidelines Based on Anatomy
Physiology of Macronutrient Absorption Diet with Colon Diet without Colon
CHO will reduce osmotic load and delay
intestinal transit
Complex CHO (50%-60%) Complex CHO (40%-50%)
Simple sugars have a greater osmolality
Low simple sugar Low simple sugar
resulting in increased intestinal losses
Protein is generally well tolerated Protein (20%-30%) Protein (20%-30%)
High fat intake may worsen malabsorption in
Low fat (20%-30%) Moderate fat (30%-40% or more)
patients with a colon by inducing choleraic
diarrhea, whereas fat intake can be used as
a source of additional calories for weight
gain in patients without a colon
To maximize absorption, patients should be
Small frequent meals Small frequent meals
encouraged to eat small frequent meals or
snacks throughout the day and to limit the
amount of uid consumed with food
CHO, Complex carbohydrates.
TABLE 72-3: Oral Rehydration Solution Recipes
Homemade ORS Gatorade ORS Gatorade G2 ORS
1 L water
2/3 tsp salt
2 Tbsp sugar
Sugar-free avoring to taste
ORS, Oral rehydration solution.
2 cups Gatorade
2 cups water
½ tsp salt
4 cups Gatorade G2
½ tsp salt
TABLE 72-4: Vitamin and Mineral Supplementation in Short Bowel Syndrome
Vitamin Clinical Manifestations Repletion Dose
Vitamin A Night blindness, dry skin, decreased saliva,
diarrhea, headache, vomiting, hair loss,
liver damage
Vitamin B6 Dermatitis, glossitis, anemia, seizures, pe-
ripheral neuropathy
Vitamin B12 Macrocytic anemia, fatigue, paresthesia of
hands or feet, dementia, glossitis
Vitamin D 25-hydroxy Rickets, osteomalacia, reduced serum cal-
cium, muscle twitching
Vitamin E RBC hemolysis, edema, skin lesions, anemia,
neurologic symptoms
Copper General weakness, skin sores, bone disease,
vomiting, diarrhea, anemia, peripheral
neuropathy
Zinc sulfate Diarrhea, anorexia, prolonged wound heal-
ing, skin disorders, muscle pain
Selenium Nausea, vomiting, abdominal pain, hair and
nail changes, nerve damage, fatigue
IM, Intramuscular; I U, international unit; RBC, red blood cell.
5000-50,000 IU/day
50-150 mg/day
1000 mcg IM 1-4×/month
1000-50,000 IU/day
150-450 IU/day
4-6 mg/day
50-150 mg elemental/day
200 mcg/day
SMALL INTSESTINE 369
TABLE 72-5: Pathophysiological Mechanisms of Malabsorption and Treatment Targets
Pathophysiologic Mechanisms of Malabsorption Treatment
Gastric Acid Hypersecretion
Acidic pH inactivates pancreatic enzymes
Increased gastric uid and electrolyte loss
H
blockers
2
Proton pump inhibitors
Loss of Intestinal Absorptive Surface Area
Rapid Intestinal Transit
Due to disruption of neuroendocrine feedback mechanisms
Ileal resection leads to decreased “brake” hormones (peptide YY, GLP-1, neurotensin) that
normally delay gastric emptying and intestinal transit
Reduced intestinal absorptive time
Bacterial Overgrowth
Intestinal obstruction, dilated bowel segments, and loss of ileocecal valve contribute to bacte-
rial overgrowth
Bile Salt Diarrhea
If a sucient quantity of bile salts come in contact with colonic mucosa in the absence of
adequate absorption at the terminal ileum, secretory diarrhea may result
Bile Salt Wasting
May happen if >100 cm of distal ileum is removed or diseased as intestinal losses exceed the
synthetic capacity of liver; this in turn leads to fat malabsorption and steatorrhea
GLP-1, Glucagon-like peptide 1.
Hyperphagia/tube feeds
Trophic hormones
Antidiarrheal medications
Pancreatic enzymes
Oral rehydration solution
Surgical reconstruction
Antidiarrheal medications
Antisecretory agents
Pancreatic enzymes
Antibiotics
Probiotics
Prebiotics
Surgical reconstruction
Bile acid–binding agents
Low-fat diet
Pancreatic enzymes
colon. Oral uid intake is usually limited to 1500 to 2000 mL per
day to control gastrointestinal tract uid output. Increasing oral
uid intake produces even more gastrointestinal uid output, so the
patient’s thirst should be satised by increasing IV uid intake. Volume requirements should include replacement of enteric losses and
provision for insensible losses and adequate urine output. Caloric
requirements are usually 25 to 35 kcal per kilogram per day, and
protein is supplied at 1.5 to 2.0 g per kilogram per day. Long-term
PN management includes careful monitoring of uid, electrolyte,
mineral, trace element, and vitamin status, as well as assessing
central venous access lines for possible infection. Enteral nutrition via a gastrostomy or jejunostomy tube can be used in patients
who have an adequate length of small intestine. In patients who just
need intermittent uid and electrolyte replacement, nocturnal ORS
infused through a gastrostomy or jejunostomy tube may obviate the
need for central venous access.
HORMONAL TREATMENT FOR SHORT BOWEL SYNDROME
Recombinant human growth hormone in combination with glutamine has been shown to improve intestinal growth, function, and
adaptation in animal studies, but results in human studies have
been mixed. Benets in humans were shown in terms of decreased
PN dependency, increased weight and lean body mass, and better energy and nitrogen absorption, but it was unclear how much
sodium and uid retention and dietary modication contributed
to the weight gain. In addition, the benecial eects are not oen
sustained aer discontinuing treatment, and safety of long-term
treatment has not been studied. Glucagon-like peptide 2 is produced by intestinal enteroendocrine cells and stimulates crypt cell
growth while reducing enterocyte apoptosis. In clinical studies it has
decreased the amount of PN support needed by patients with SBS
and may help some patients achieve enteral autonomy. Infrequent
adverse eects include nausea, stoma enlargement, and abdominal
pain. Glucagon-like peptide 2 and growth hormone have the potential to enhance adaptation in patients dependent on long-term PN
or home IV uids, but both are expensive. Figure 72-2 shows the
suggested protocol for considering the use of these intestinotrophic
hormones.
COMPLICATIONS ASSOCIATED WITH SHORT BOWEL SYNDROME
Patients with a short intestine in continuity with the colon are at risk
for the development of oxalate nephrolithiasis. Normally, oxalate is
bound to calcium in the intestine and is passed on through the colon
without being absorbed. When fat is malabsorbed in patients with
SBS, the fat preferentially binds to calcium, leaving oxalate free to be
absorbed by the colon and excreted in the urine. Adequate hydration,
a low-fat/low-oxalate diet, and calcium supplementation should be
instituted in these patients.
Small intestine bacterial overgrowth occurs when colonic bacteria colonize the small intestine. Clinically it is characterized by
atulence, abdominal distention, explosive bowel movements, foamy
or frothy stool, weight loss, and abdominal pain. Small bowel aspirate/culture is the gold standard for conrming the diagnosis but is
rarely performed. Hydrogen breath testing yields conicting results
Medical ManageMent of Short Bowel SyndroMe370
TABLE 72-6: Medications for Short Bowel Syndrome
Medication Starting Dose Maximum Dose
Antidiarrheal Agents*
Loperamide 2 mg, 4×/day 16 mg/day
Diphenyl oxalate hydrophone 2.5 mg, 4×/day 20 mg/day
Codeine 15 mg, 4×/day 240 mg/day
Tincture of opium 0.5 mL 4×/day 6 mL/day
Antisecretory
Famotidine
Ranitidine
PPIs 20 mg 40 mg
Octreotide
Clonidine 0.025 mg by mouth 2×/day 0.2 mg by mouth 2×/day
Pancreatic Enzymes
Creon
–6 (6000 lipase units)
–12 (12,000 lipase units)
–24 (24,000 lipase units)
†
†
†
‡
20 mg 40 mg
20 mg 40 mg
PN: 300 g/day
SQ: 100 g 3×/day
IM (long acting): 10 mg/month
PN: 1200 g/day
SQ: 1200 g/day
IM (long acting): 40 mg/month
1 tab with meals and/or snacks <10,000 units per kg/day
500-2500 units/kg/meal
<4000 units per gram of fat ingested/day
Bile Acid–Binding Resins
Cholestyramine 2-4 g before meals, 3×/day Maximum dose not established
Colestipol hydrochloride Granular form: 5 g, 1-4×/day
Maximum dose not established
Tab form: 1 g, 1-4×/day
*All antidiarrheal agents should be given by mouth 30-60 minutes before meals and at bedtime (4×/day).
†
Compatible with parenteral nutrition.
‡
Pancreatic enzymes are oen dosed as 500-2500 lipase units per kilogram body weight.
IM, Intramuscular; PN, parenteral nutrition; PPI, proton-pump inhibitor; SQ, subcutaneous.
in patients with rapid intestinal transit, and therefore the condition
is usually treated empirically with restriction of dietary simple sugar,
the use of probiotics, and 7 to 14 days of nonabsorbable oral antibiotics (see Box 72-1). Repeat courses of therapy may be required using
dierent antibiotics 7 to 14 days each month to help patients with
chronic small intestine bacterial overgrowth.
D-lactic acidosis can occur when colonic bacteria ferment simple
PN predispose to its occurrence. Steatosis and cholestasis appear
initially and can progress to brosis, cirrhosis, and eventually liver
failure. Early detection of steatosis and brosis is dicult without a
liver biopsy. PN-dependent patients with intestinal failure–associated
liver disease should be evaluated for a liver biopsy and review of other
causes of the elevated liver tests, including hepatitis, drugs, and PN
uid composition.
sugars in the colon, producing D-lactate, an isomer of lactic acid.
Clinically the patient presents with neurologic symptoms including altered mental status, slurred speech, memory impairment, and
abnormal motor coordination. Diagnosis should be suspected in the
presence of symptoms and an unmeasured anion gap if the laboratory is unable to measure D-lactic acid levels. Treatment includes
dietary restriction of simple sugars, bicarbonate replacement, and
oral antibiotics. Ringers lactate solution and probiotics containing
lactobacillus bacteria should be avoided because they may promote
an increase in D-lactic acid levels.
Intestinal failure–associated liver disease has been dened as the
persistent elevation of liver tests 1.5 times above the upper limit of
normal. It is thought that both the presence of SBS and the use of
CONCLUSION
Patients with SBS require aggressive medical management to maximize their intestinal absorption and minimize complications of
SBS. Medical treatment relies on diet, ORS, antidiarrheal agents,
antisecretory drugs, and vitamin and mineral supplements and in
some instances intestinotrophic hormonal therapy. An expert team
of intestinal rehabilitation physicians and dietitians working in a
comprehensive intestinal rehabilitation center aords patients with
SBS the best opportunity to adapt and return to a more normal
lifestyle.