Download OBSTRUCTION

OBSTRUCTION
The description of patients presenting with small bowel obstruction dates back to the
third or fourth century, when Praxagoras created an
enterocutaneous fistula to relieve a bowel obstruction. Despite this success with operative
therapy, the nonoperative management of these patients with
attempted reduction of hernias, laxatives, ingestion of heavy metals (e.g., lead or
mercury), and leeches to remove toxic agents from the blood was the
rule until the late 1800s, when antisepsis and aseptic surgical techniques made operative
intervention safer and more acceptable. A better understanding
of the pathophysiology of bowel obstruction and the use of isotonic fluid resuscitation,
intestinal tube decompression, and antibiotics have greatly
reduced the mortality rate for patients with mechanical bowel obstruction.[30] [31]
However, patients with a bowel obstruction still represent
Figure 46-11 The mucosal barrier of the gut. Antigens contact specialized microfold (M)
cells overlying Peyer’s patches, which then process and present the antigen to the
immune
system. When B lymphocytes are stimulated by antigenic material, the cells develop into
antibody-forming cells that secrete various types of immunoglobulins (Igs), the most
important of which is IgA. (Adapted from Duerr RH, Shanahan F: Food allergy. In
Targan SR, Shanahan F [eds]: Immunology and Immunopathology of the Liver and
Gastrointestinal Tract. New York, Igaku-Shoin, 1990, p 510.)
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Figure 46-12 Common causes of small bowel obstruction in industrialized countries.
some of the most difficult and vexing problems that surgeons face with regard to the
correct diagnosis, the optimal timing of therapy, and the
appropriate treatment. Ultimate clinical decisions regarding the management of these
patients dictates a thorough history and work-up and a heightened
awareness of potential complications.
Etiology
The causes of a small bowel obstruction can be divided into three categories: (1)
obstruction arising from extraluminal causes such as adhesions,
hernias, carcinomas, and abscesses; (2) obstruction intrinsic to the bowel wall (e.g.,
primary tumors); and (3) intraluminal obturator obstruction (e.g.,
gallstones, enteroliths, foreign bodies, and bezoars) ( Box 46–1 ). The cause of small
bowel obstruction has changed dramatically during the past
century.[32] At the turn of the 20th century, hernias accounted for more than half of
mechanical intestinal obstructions. With the routine elective repair of
hernias, this cause has dropped to the third most common cause of small bowel
obstruction in industrialized countries. Adhesions secondary to previous
surgery are by far the most common cause of small bowel obstruction ( Fig. 46–12 ).
Adhesions, particularly after pelvic operations (e.g., gynecologic procedures,
appendectomy, and colorectal resection), are responsible for more than
60% of all causes of bowel obstruction in the United States.[33] [34] This preponderance
of lower abdominal procedures to produce adhesions that result in
obstruction is thought to be due to the fact that the bowel is more mobile in the pelvis and
more tethered in the upper abdomen.
Malignant tumors account for approximately 20% of the cases of small bowel obstruction.
The majority of these tumors are metastatic lesions that
obstruct the intestine secondary to peritoneal implants that have spread from an
intra-abdominal primary tumor such as ovarian, pancreatic, gastric, or
colonic. Less often, malignant cells from distant sites, such as breast, lung, and melanoma,
may metastasize hematogenously and account for peritoneal
implants and result in an obstruction. Large intra-abdominal tumors may also cause small
bowel obstruction through extrinsic compression of the bowel
lumen. Primary colonic cancers (particularly those arising from
Box 46-1. Causes of Mechanical Small Intestinal Obstruction in
Adults *
Lesions Extrinsic to the Intestinal Wall
Adhesions (usually postoperative)
Hernia
External (e.g., inguinal, femoral, umbilical, or ventral
hernias)
Internal (e.g., congenital defects such as paraduodenal,
foramen of Winslow, and diaphragmatic hernias or
postoperative secondary to mesenteric defects)
Neoplastic
Carcinomatosis
Extraintestinal neoplasms
Intra-abdominal abscess
Lesions Intrinsic to the Intestinal Wall
Congenital
Malrotation
Duplications/cysts
Inflammatory
Crohn’s disease
Infections
Tuberculosis
Actinomycosis
Diverticulitis
Neoplastic
Primary neoplasms
Metastatic neoplasms
Traumatic
Hematoma
Ischemic stricture
Miscellaneous
Intussusception
Endometriosis
Radiation enteropathy/stricture
Intraluminal/Obturator Obstruction
Gallstone
the cecum and ascending colon) may present as a small bowel obstruction. Primary small
bowel tumors can cause obstruction but are exceedingly rare.
Hernias are the third leading cause of intestinal obstruction and account for
approximately 10% of all cases. Most commonly, these represent ventral or
inguinal hernias. Internal hernias, usually related to prior abdominal surgery, can also
result in small bowel obstruction. Less common hernias can also
produce obstruction, such as femoral, obturator, lumbar, and sciatic hernias.
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Crohn’s disease is the fourth leading cause of small bowel obstruction and accounts for
approximately 5% of all cases. Obstruction can result from acute
inflammation and edema, which may resolve with conservative management. In patients
with long-standing Crohn’s disease, strictures can develop that
may require resection and reanastomosis or strictureplasty.
An important cause of small bowel obstruction that is not routinely considered is
obstruction associated with an intra-abdominal abscess, commonly
from a ruptured appendix, diverticulum, or dehiscence of an intestinal anastomosis. The
obstruction may occur as a result of a local ileus in the small
bowel adjacent to the abscess. In addition, the small bowel can form a portion of the wall
of the abscess cavity and become obstructed by kinking of the
bowel at this point.
Miscellaneous causes of bowel obstruction account for 2% to 3% of all cases but should
be considered in the differential diagnosis. These include
intussusception of the bowel, which in the adult is usually secondary to a pathologic lead
point such as a polyp or tumor; gallstones, which can enter the
intestinal lumen by a cholecystenteric fistula and cause obstruction; enteroliths
originating from jejunal diverticula; foreign bodies; and phytobezoars.
Pathophysiology
Early in the course of an obstruction, intestinal motility and contractile activity increase
in an effort to propel luminal contents past the obstructing
point. The increase in peristalsis that occurs early in the course of bowel obstruction is
present both above and below the point of obstruction, thus
accounting for the finding of diarrhea that may accompany partial or even complete small
bowel obstruction in the early period. Later in the course of
obstruction, the intestine becomes fatigued and dilates, with contractions becoming less
frequent and less intense.
As the bowel dilates, water and electrolytes accumulate both intraluminally and in the
bowel wall itself. This massive third-space fluid loss accounts for
the dehydration and hypovolemia. The metabolic effects of fluid loss depend on the site
and duration of the obstruction. With a proximal obstruction,
dehydration may be accompanied by hypochloremia, hypokalemia, and metabolic
alkalosis associated with increased vomiting. Distal obstruction of the
small bowel may result in large quantities of intestinal fluid into the bowel; however,
abnormalities in serum electrolytes are usually less dramatic.
Oliguria, azotemia, and hemoconcentration can accompany the dehydration. Hypotension
and shock can ensue. Other consequences of bowel
obstruction include increased intra-abdominal pressure, decreased venous return, and
elevation of the diaphragm, compromising ventilation. These
factors can serve to further potentiate the effects of hypovolemia.
As the intraluminal pressure increases in the bowel, a decrease in mucosal blood flow can
occur. These alterations are particularly noted in patients with
a closed-loop obstruction in which greater intraluminal pressures are attained. A
closed-loop obstruction, produced commonly by a twist of the bowel,
can progress to arterial occlusion and ischemia if left untreated and may potentially lead
to bowel perforation and peritonitis.
In the absence of intestinal obstruction, the jejunum and proximal ileum of the human are
virtually sterile. With obstruction, however, the flora of the
small intestine changes dramatically, in both the type of organism (most commonly
Escherichia coli, Streptococcus faecalis, and Klebsiella) and the
quantity, with organisms reaching concentrations of 109 to 1010 /mL. Studies have
shown an increase in the number of indigenous bacteria translocating
to mesenteric lymph nodes and even systemic organs.[35] However, the overall
importance of this bacterial translocation on the clinical course has not
been entirely defined.
Clinical Manifestations and Diagnosis
A thorough history and physical examination are critical to establishing the diagnosis and
treatment of the patient with an intestinal obstruction. In the
majority of patients, a meticulous history and physical examination complemented by
plain abdominal radiographs are all required to establish the
diagnosis and to devise a treatment plan. More sophisticated radiographic studies may be
necessary in certain patients in whom the diagnosis and cause
are uncertain. However, a computed tomographic (CT) scan of the abdomen should not
be the starting point in the work-up of a patient with intestinal
obstruction.
History
The cardinal symptoms of intestinal obstruction include colicky abdominal pain, nausea,
vomiting, abdominal distention, and a failure to pass flatus and
feces (i.e., obstipation). These symptoms may vary with the site and duration of
obstruction. The typical crampy abdominal pain associated with
intestinal obstruction occurs in paroxysms at 4- to 5-minute intervals and occurs less
frequently with distal obstruction. Nausea and vomiting are more
common with a higher obstruction and may be the only symptoms in patients with gastric
outlet or high intestinal obstruction. An obstruction located
distally is associated with less emesis, and the initial and most prominent symptom is the
cramping abdominal pain. Abdominal distention occurs as the
obstruction progresses, and the proximal intestine becomes increasingly dilated.
Obstipation is a later development, and it must be reiterated that
patients, particularly in the early stages of bowel obstruction, may relate a history of
diarrhea that is secondary to increased peristalsis. Therefore, the
important point to remember is that a complete bowel obstruction cannot be ruled out
based on a history of loose bowel movements. The character of
the vomitus is also important to obtain in the history. As the obstruction becomes more
complete with bacterial overgrowth, the vomitus becomes more
feculent, indicating a late and established intestinal obstruction.
Enterolith
Bezoar
* Foreign bodyAdapted from Tito WA, Sarr MG: Intestinal obstruction. In Zuidema GD
(ed): Surgery of the Alimentary Tract. Philadelphia, WB Saunders, 1996, pp 375–416.
1337
Physical Examination
The patient with intestinal obstruction may present with tachycardia and hypotension,
demonstrating the severe dehydration that is present. Fever
suggests the possibility of strangulation. Abdominal examination demonstrates a
distended abdomen, with the amount of distention somewhat
dependent on the level of obstruction. Previous surgical scars should be noted. Early in
the course of bowel obstruction, peristaltic waves can be
observed, particularly in thin patients, and auscultation of the abdomen may demonstrate
hyperactive bowel sounds with audible rushes associated with
vigorous peristalsis (i.e., borborygmi). Late in the obstructive course, minimal or no
bowel sounds are noted. Mild abdominal tenderness may be present
with or without a palpable mass; however, localized tenderness, rebound, and guarding
suggest peritonitis and the likelihood of strangulation. A careful
examination must be performed to rule out incarcerated hernias in the groin, the femoral
triangle, and the obturator foramen. A rectal examination
should be performed to assess for intraluminal masses and to examine the stool for occult
blood, which may be an indication of malignancy,
intussusception, or infarction.
Radiologic and Laboratory Examinations
The diagnosis of intestinal obstruction is often immediately evident after a thorough
history and physical examination. Therefore, plain radiographs
usually confirm the clinical suspicion and define more accurately the site of obstruction.
The accuracy of diagnosis of the small intestinal obstruction on
plain abdominal radiographs is estimated to be approximately 60%, with an equivocal or
a nonspecific diagnosis obtained in the remainder of cases.
Characteristic findings on supine radiographs are dilated loops of small intestine without
evidence of colonic distention. Upright radiographs
demonstrate multiple air-fluid levels, which often layer in a stepwise pattern ( Fig.
46–13 ). Plain abdominal films may also demonstrate the cause of the
obstruction (e.g., foreign bodies or gallstones) ( Fig. 46–14 ). In uncertain cases or when
one is unable to differentiate partial from complete obstruction,
further diagnostic evaluations may be required.
In the more complex patient in whom the diagnosis is not readily apparent, CT has
proved to be beneficial ( Fig. 46–15 ). [36] A CT is particularly
sensitive for diagnosing complete or high-grade obstruction of the small bowel and for
determining the location and cause of obstruction. The CT
examination is less sensitive, however, in patients with partial small bowel
obstruction.[37] [38] In addition, CT is helpful if an extrinsic cause of bowel
obstruction (e.g., abdominal tumors, inflammatory disease, or abscess) is suggested ( Fig.
46–16 ). CT has also been described as useful in determining
bowel strangulation. Unfortunately, CT findings associated with strangulation are those
of irreversible ischemia and necrosis.
Figure 46-13 Plain abdominal radiographs of a patient with a complete small bowel
obstruction. A, Supine film shows dilated loops of small bowel in an orderly arrangement,
without
evidence of colonic gas. B, Upright film shows multiple, short, air-fluid levels arranged
in a stepwise pattern. (Courtesy of Melvyn H. Schreiber, M.D., The University of Texas
Medical Branch.)
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Figure 46-14 Plain abdominal film shows complete bowel obstruction caused by a large
radiopaque gallstone (arrow) obstructing the distal ileum.
Figure 46-15 CT scan through the mid abdomen shows dilated small bowel loops filled
with fluid and decompressed ascending and descending colon. These are typical CT
findings
in small bowel obstruction. (Courtesy of Eric Walser, M.D., The University of Texas
Medical Branch.)
Barium studies have been a useful adjunct in certain patients with a presumed obstruction.
In particular, enteroclysis, which involves the oral insertion
of a tube into the duodenum to instill air and barium directly into the small intestine and
to follow the movement fluoroscopically,
Figure 46-16 CT scan of the abdomen of a patient with a mechanical bowel obstruction
secondary to an abscess in the right lower quadrant (arrow). Multiple dilated and
fluid-filled
loops of small bowel are noted. (Courtesy of Melvyn H. Schreiber, M.D., The University
of Texas Medical Branch.)
has been helpful in the assessment of obstruction.[36] [39] Enteroclysis has been
advocated as the definitive study in patients in whom the diagnosis of lowgrade,
intermittent small bowel obstruction is clinically uncertain. In addition, barium studies
can precisely demonstrate the level of the obstruction as
well as the cause of the obstruction in certain instances ( Fig. 46–17 ). The main
disadvantages of enteroclysis are the need for nasoenteric intubation,
the slow transit of contrast material in patients with a fluid-filled hypotonic small bowel,
and the enhanced expertise required by the radiologist to
perform this procedure.
Ultrasound has been reported to be useful in pregnant patients where radiation exposure
is a concern. Magnetic resonance imaging (MRI) has been
described in patients with obstruction; however, it appears to be no better diagnostically
than CT.
To summarize, plain abdominal radiographs are usually diagnostic of bowel obstruction
in more than 60% of the cases, but further evaluation (possibly
by CT or barium radiography) may be necessary in 20% to 30% of cases. CT
examination is particularly useful in patients with a history of abdominal
malignancy, in postsurgical patients, and in patients who have no history of abdominal
surgery and present with symptoms of bowel obstruction.
Barium studies are recommended in patients with a history of recurring obstruction or
low-grade mechanical obstruction to precisely define the
obstructed segment and degree of obstruction.
Laboratory examinations are not helpful in the actual diagnosis of patients with small
bowel obstruction but are extremely important in assessing the
degree of dehydration. Patients with a bowel obstruction should routinely have laboratory
measurements of serum sodium, chloride, potassium,
bicarbonate, and creatinine. The serial determination of serum electrolytes should be
performed to assess the adequacy of fluid resuscitation.
Dehydration may result in hemoconcentration, as noted by an elevated
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Figure 46-17 Barium study demonstrates jejunojejunal intussusception. (Courtesy of
Melvyn H. Schreiber, M.D., The University of Texas Medical Branch.)
hematocrit. This value should be monitored because fluid resuscitation results in a
decrease in the hematocrit and some patients (e.g., those with
intestinal malignancies) may require blood transfusions before surgery. In addition, the
white blood cell count should be assessed. Leukocytosis may be
found in patients with strangulation; however, an elevated white blood cell count does not
necessarily denote strangulation. Conversely, the absence of
leukocytosis does not eliminate strangulation as a possibility.
Simple Versus Strangulating Obstruction
The majority of patients with small bowel obstruction are classified as having simple
obstructions that involve mechanical blockage of the flow of
luminal contents without compromised viability of the intestinal wall. In contrast,
strangulation obstruction, which usually involves a closed-loop
obstruction in which the vascular supply to a segment of intestine is compromised, can
lead to intestinal infarction. Strangulation obstruction is
associated with an increased morbidity and mortality risk, and therefore recognition of
early strangulation is important in differentiating from simple
intestinal obstruction. “Classic” signs of strangulation have been described and include
tachycardia, fever, leukocytosis, and a constant, noncramping
abdominal pain. However, a number of studies have convincingly shown that no clinical
parameters or laboratory measurements can accurately detect
or exclude the presence of strangulation in all cases.[40]
CT examination is useful only in detecting the late stages of irreversible ischemia.
Various serum determinations, including lactate dehydrogenase,
amylase, alkaline phosphatase, and ammonia levels, have been assessed with no real
benefit. Initial reports have described some limited success in
discriminating strangulation by measuring serum D-lactate, creatine phosphokinase
isoenzyme (particularly the BB isoenzyme), or intestinal fatty acid
binding protein; however, these are only investigational and cannot be widely applied to
patients with obstruction. Finally, noninvasive determinations
of mesenteric ischemia were described by Richards and associates[41] using a
superconducting quantum interference device (SQUID) magnetometer to
noninvasively detect mesenteric ischemia. Intestinal ischemia is associated with changes
in the basic electric rhythm of the small intestine. Clinical
assessment of this technique is under way.
To reiterate, it is important to remember that bowel ischemia and strangulation cannot be
reliably diagnosed or excluded preoperatively in all cases by
any known clinical parameter, combination of parameters, or current laboratory and
radiographic examinations.
Treatment
Fluid Resuscitation and Antibiotics
Patients with intestinal obstruction are usually dehydrated and depleted of sodium,
chloride, and potassium, requiring aggressive intravenous
replacement with an isotonic saline solution such as lactated Ringer’s. Urine output
should be monitored by the placement of a Foley catheter. After the
patient has formed adequate urine, potassium chloride should be added to the infusion if
needed. Serial electrolyte measurements, as well as hematocrit
and white blood cell count, are performed to assess the adequacy of fluid repletion.
Because of large fluid requirements, patients, particularly the
elderly, may require central venous assessment and, in some cases, the placement of a
Swan-Ganz catheter. Broad-spectrum antibiotics are given
prophylactically by some surgeons based on the reported findings of bacterial
translocation occurring even in simple mechanical obstructions. In
addition, antibiotics are administered as a prophylaxis for possible resection or
inadvertent enterotomy at surgery.
Tube Decompression
In addition to intravenous fluid resuscitation, another important adjunct to the supportive
care of patients with intestinal obstruction is nasogastric
suction. Nasogastric suction with a Levin tube empties the stomach, reducing the hazard
of pulmonary aspiration of vomitus and minimizing further
intestinal distention from preoperatively swallowed air. The use of long intestinal tubes
(e.g., Cantor or Baker tubes) has been advocated by some
groups. However, prospective randomized trials demonstrated
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no significant differences with regard to the decompression achieved, the success of
nonoperative treatment, or the morbidity rate after surgical
intervention compared with the use of nasogastric tubes.[42] Furthermore, the use of
these long tubes has been associated with a significantly longer
hospital stay, duration of postoperative ileus, and postoperative complications in some
series. Therefore, it appears that long intestinal tubes offer no
benefit in the preoperative setting over nasogastric tubes.
Patients with a partial intestinal obstruction may be treated conservatively with
resuscitation and tube decompression alone. Resolution of symptoms
and discharge without the need for surgery have been reported in 60% to 85% of patients
with a partial obstruction.[32] Enteroclysis can assist in
determining the degree of obstruction, with higher-grade partial obstructions requiring
earlier operative intervention. Although an initial trial of
nonoperative management of most patients with partial small bowel obstruction is
warranted, it should be emphasized that clinical deterioration of the
patient or increasing small bowel distention on abdominal radiographs during tube
decompression warrants prompt operative intervention. The decision
to continue to treat a patient nonoperatively with a presumed bowel obstruction is based
on clinical judgment and requires constant vigilance to ensure
that the clinical course has not changed.
Operative Management
In general, the patient with a complete small bowel obstruction requires operative
intervention. A nonoperative approach to selected patients with
complete small intestinal obstruction has been proposed by some, who argue that
prolonged intubation is safe in these patients provided that no fever,
tachycardia, tenderness, or leukocytosis is noted. Nevertheless, one must realize that
nonoperative management of these patients is undertaken at a
calculated risk of overlooking an underlying strangulation obstruction and delaying the
treatment of intestinal strangulation until after the injury
becomes irreversible. Retrospective studies report that a 12- to 24-hour delay of surgery
in these patients is safe but that the incidence of strangulation
and other complications increases significantly after this time period.[43]
The nature of the problem dictates the approach to management of the obstructed patient.
Patients with intestinal obstruction secondary to an adhesive
band may be treated with lysis of adhesions. Great care should be used in the gentle
handling of the bowel to reduce serosal trauma and avoid
unnecessary dissection and inadvertent enterotomies. Incarcerated hernias can be
managed by manual reduction of the herniated segment of bowel and
closure of the defect.
The treatment of patients with an obstruction and a history of malignant tumors can be
particularly challenging. In the terminal patient with widespread
metastasis, nonoperative management, if successful, is usually the best course; however,
only a small percentage of cases of complete obstruction can
be successfully managed nonoperatively. In this case, a simple bypass of the obstructing
lesion, by whatever means, may offer the best option rather
than a long and complicated operation that may entail bowel resection.
Patients with an obstruction secondary to Crohn’s disease will often resolve with
conservative management if the obstruction is acute. If a chronic
fibrotic stricture is the cause of the obstruction, then a bowel resection or strictureplasty
may be required.
Patients with an intra-abdominal abscess can present in a manner indistinguishable from
those with mechanical bowel obstruction. CT is particularly
useful in diagnosing the cause of the obstruction in these patients; drainage of the abscess
percutaneously may be sufficient to relieve the obstruction.
Radiation enteropathy, as a complication of radiation therapy for pelvic malignancies,
may cause bowel obstruction. Most cases can be treated
nonoperatively with tube decompression and possibly corticosteroids, particularly during
the acute setting. In the chronic setting, nonoperative
management is rarely effective and will require laparotomy with possible resection of the
irradiated bowel or bypass of the affected area.
At the time of exploration, it can sometimes be difficult to evaluate bowel viability after
the release of a strangulation. If intestinal viability is
questionable, the bowel segment should be completely released and placed in a warm,
saline-moistened sponge for 15 to 20 minutes and then
reexamined. If normal color has returned and peristalsis is evident, it is safe to retain the
bowel. A prospective controlled trial comparing clinical
judgment with the use of a Doppler probe or the administration of fluorescein for the
intraoperative discrimination of viability found that the Doppler
flow probe added little to the conventional clinical judgment of the surgeon.[44] In
difficult borderline cases, fluorescein fluorescence may supplement
clinical judgment. Another approach to the assessment of bowel viability is the “second
look” laparotomy 18 to 24 hours after the initial procedure. This
decision should be made at the time of the initial operation. A second-look laparotomy is
clearly indicated in a patient whose condition deteriorates after
the initial operation.
Some groups have evaluated the efficacy of laparoscopic management of acute small
bowel obstruction.[45] [46] The laparoscopic treatment of small bowel
obstruction appears to be effective and leads to a shorter hospital stay in a highly selected
group of patients. Patients fitting the criteria for consideration
of laparoscopic management include those with (1) mild abdominal distention allowing
adequate visualization, (2) a proximal obstruction, (3) a partial
obstruction, and (4) an anticipated single-band obstruction. Currently, patients who have
advanced, complete, or distal small bowel obstructions are not
candidates for laparoscopic treatment. Unfortunately, the majority of patients with
obstruction are in this group. Similarly, patients with matted
adhesions or carcinomatosis or those who remain distended after nasogastric intubation
should be managed with conventional laparotomy. Therefore,
the future role of laparoscopic procedures in the treatment of these patients remains to be
defined.
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Management of Specific Problems
Recurrent Intestinal Obstruction
All surgeons can readily (and most often painfully) remember the complicated patient
with multiple previous abdominal operations and a “frozen”
abdomen who presents with yet another bowel obstruction. An initial nonoperative trial is
usually desirable and often safe. In those patients who do not
respond conservatively, reoperation is required. This can often be a long and arduous
procedure with great care taken to prevent enterotomies. In these
difficult patients, various surgical procedures and pharmacologic agents have been tried
in an effort to prevent recurrent adhesions and obstruction.
External plication procedures have been described in which the small intestine or its
mesentery is sutured in large, gently curving loops.[47] [48] Common
complications have included the development of fistulas, gross leakage, peritonitis, and
death. For this reason, and because of the low overall success
rate, these procedures have largely been abandoned. Several series have reported
moderate success with internal fixation or stenting procedures using a
long intestinal tube inserted via the nose, a gastrostomy, or even a jejunostomy and left in
place for 2 weeks or longer.[49] [50] Complications associated
with these tubes include prolonged drainage of bowel contents from the tube insertion
site, intussusception, and difficult removal of the tube, which may
require surgical reexploration.
Pharmacologic agents, including corticosteroids and other anti-inflammatory agents,
cytotoxic drugs, and antihistamines, have been used with limited
success. The use of anticoagulants, such as heparin, dextran solutions, dicumarol, and
sodium citrate, has modified the extent of adhesion formation, but
their side effects far outweigh their efficacy. Intraperitoneal instillation of various
proteinases (e.g., trypsin, papain, and pepsin), which cause enzymatic
digestion of the extracellular protein matrix, has been unsuccessful. Hyaluronidase has
been of questionable value, and conflicting results have been
obtained with fibrinolytic agents such as streptokinase, urokinase, and fibrinolytic snake
venoms. In a prospective, multicenter trial, Becker and
colleagues[51] reported that the use of a hyaluronate-based, bioresorbable membrane
reduced the incidence and severity of postoperative adhesion
formation. Another study by Vrijland and associates found that placement of this
membrane reduced the severity, but not the incidence, of postoperative
adhesion in patients undergoing a Hartmann procedure.[52] This could represent a
significant advance if the long-term incidence of obstruction is likewise
shown to be reduced.
To date, the most effective means of limiting the number of adhesions is a good surgical
technique, which includes the gentle handling of the bowel to
reduce serosal trauma, avoidance of unnecessary dissection, exclusion of foreign material
from the peritoneal cavity (the use of absorbable suture
material when possible, the avoidance of excessive use of gauze sponges, and the
removal of starch from gloves), adequate irrigation and removal of
infectious and ischemic debris, and preservation and use of the omentum around the site
of surgery or in the denuded pelvis.[53]
Acute Postoperative Obstruction
Small bowel obstruction that occurs in the immediate postoperative period presents a
challenge in both the diagnosis and treatment. Diagnosis is often
difficult because the primary symptoms of abdominal pain and nausea or emesis may be
attributed to a postoperative ileus. Electrolyte deficiencies,
particularly hypokalemia, can be a cause of ileus and should be corrected. Plain
abdominal films are usually not helpful in distinguishing an ileus from
obstruction. CT may be useful in this regard and, in particular, enteroclysis studies may
be quite helpful in determining if an obstruction exists and, if
so, then the level of the obstruction. Conservative management should be attempted for a
partial obstruction. Complete obstruction requires reoperation
and correction of the underlying problem.
Ileus
An ileus is defined as intestinal distention and the slowing or absence of passage of
luminal contents without a demonstrable mechanical obstruction.
An ileus can result from a number of causes, including drug induced, metabolic,
neurogenic, and infectious ( Box 46–2 ).
Pharmacologic agents that can produce an ileus include anticholinergic drugs, autonomic
blockers, antihistamines, and various psychotropic agents,
such as haloperidol and tricyclic antidepressants. One of the more common causes of
drug-induced ileus in the operative patient is the use of opiates,
such as morphine or meperidine. Metabolic causes of ileus are common and include
hypokalemia, hyponatremia, and hypomagnesemia. Other
metabolic causes include uremia, diabetic coma, and hypoparathyroidism. Neurogenic
causes of an ileus include postoperative ileus, which occurs after
abdominal operations. Spinal injury, retroperitoneal irritation, and
1342
orthopedic procedures on the spine or pelvis can result in an ileus. Finally, a number of
infectious causes can result in an ileus; common infectious
causes include pneumonia, peritonitis, and generalized sepsis from a nonabdominal
source.
Patients often present in a manner similar to those with a mechanical small bowel
obstruction. Abdominal distention, usually without the colicky
abdominal pain, is the typical and most notable finding. Nausea and vomiting may occur
but may also be absent. Patients with an ileus may continue to
pass flatus and diarrhea, and this may help distinguish these patients from those with a
mechanical small bowel obstruction.
Radiologic studies may help to distinguish ileus from small bowel obstruction. Plain
abdominal radiographs may reveal distended small bowel as well
as large bowel loops. In cases that are difficult to differentiate from obstruction, barium
studies may be beneficial.
The treatment of an ileus is entirely supportive with nasogastric decompression and
intravenous fluids. The most effective treatment to correct the
underlying condition may be aggressive treatment of the sepsis, correction of any
metabolic or electrolyte abnormalities, and discontinuation of
medications that may produce an ileus. Pharmacologic agents have been used but for the
most part have been ineffective. Drugs that block sympathetic
Box 46-2. Causes of Ileus †
Post laparotomy
Metabolic and electrolyte derangements (e.g., hypokalemia,
hyponatremia, hypomagnesemia, uremia, diabetic coma)
Drugs (e.g., opiates, psychotropic agents, anticholinergic agents)
Intra-abdominal inflammation
Retroperitoneal hemorrhage or inflammation
Intestinal ischemia
Systemic sepsis
† Adapted from Turnage RH, Bergen PC: Intestinal obstruction and ileus. In Feldman
M, Scharschmidt FG, Sleisenger MH (eds): Gastrointestinal and Liver Disease.
Pathophysiology/Diagnosis/Management. Philadelphia, WB Saunders, 1998, pp 1799–
1810.
input (e.g., guanethidine) or stimulate parasympathetic activity (e.g., bethanechol or
neostigmine) have been tried. In addition, hormonal manipulation,
using cholecystokinin or motilin, has been evaluated, but the results have been
inconsistent. Intravenous erythromycin has been ineffective, and
cisapride, although apparently beneficial in stimulating gastric motility, does not appear
to alter intestinal ileus.
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