Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1370_Библиотеки_им_академика_М_И_Перельмана
.pdf
improved outcomes in colon and rectal surgery
determine which method is superior, a recent meta-analysis of
the available literature was used to compare the treatment outcome using EMG vs. pressure biofeedback.(87) EMG biofeedback was primarily used in 18 studies (442 subjects) with a mean
success rate (improved symptoms) of 70%. Pressure biofeedback
training was used in 13 studies (275 subjects) with a mean success
rate of 78%. These results showed a significantly better outcome
in patients with pressure biofeedback protocols. Further analysis compared intraanal to perianal EMG biofeedback and their
results showed no significant difference between the two subgroups (69% vs. 72%, respectively). Overall, these data show success rates ranging from 69 to 78%, regardless of which protocol or
what instrumentation is used; however, without controlled trials,
the optimal protocol for subjects with dyssynergic-type constipation remains unclear.
The role of other factors on the outcome of biofeedback therapy
in patients with pelvic dyssynergy has been studied. In one study,
the only predictor of successful outcome was the number of sessions attended (5 or more) and whether the therapist discharged
the patient (63% success rate) rather than the patient terminating
treatment prematurely (25% success rate).(90) To date, researchers have not been able to identify any physiologic (manometry
and balloon expulsion test), anatomic (rectocele, intussusception,
or abnormal perineal descent), or demographic (age, gender,
duration of symptoms) variables that influence treatment outcome; however, many investigators do suggest that psychopathology may influence biofeedback treatment outcome. Anxiety and
psychological distress are commonly associated with pelvic floor
dyssynergy. One study showed that patients with pelvic floor dyssynergic-type constipation or rectal pain showed a tendency to
use somatization as a defense mechanism to manage psychological distress.(91) This pattern was not seen in a comparison group
of patients with fecal incontinence. Others have suggested that
there may be a psychosomatic basis for chronic idiopathic constipation, including pelvic floor dyssynergy.(92, 93) Studies have
reported up to 65% of constipated subjects were diagnosed with
various psychological disorders (94); however, there is significant
debate whether the psychopathology is a cause or a consequence
of dyssynergic constipation. In a study of patients with slow-transit constipation without pelvic dyssynergy 60% of subjects had a
concurrent affective disorder, with 66% reporting having a previous
affective disorder.(95) Others have shown a high incidence of
sexual or physical abuse in patients suffering from constipation.
Given these results, it is of no surprise that psychological treatment
for subjects with constipation is frequently recommended in addition to biofeedback therapy. Establishment of an effective psychotherapeutic relationship may be critical for success.
Biofeedback therapy has been used for the treatment of slowtransit constipation. A single case series reported the successful
treatment of 4 patients with slow-transit constipation without
pelvic floor dyssynergy using biofeedback therapy (96); however, two of the four patients continued to require laxative use
despite improved symptoms, and there was no objective confirmatory evidence (repeat colonic transit study) to support physiologic improvement. A recent study has compared the benefits
of biofeedback therapy in patients with slow-transit constipation to those with pelvic dyssynergia-type constipation.(97) At
6 months, the dyssynergic group had greater satisfaction (71%
vs. 8%), and more frequently reported ≥ 3 bowel movements
per week (76% vs. 8%) than the slow-transit group following a
5 weekly biofeedback sessions. These data indicate that pelvic
floor biofeedback benefits patients with pelvic floor dyssynergia, but not patients with slow transit constipation. Biofeedback
therapy has been suggested as the initial therapy for patients with
outlet obstruction associated with pelvic floor dyssynergy. This
concept is supported by a recent randomized, controlled trial
of patients with pelvic floor dyssynergy where biofeedback was
shown to be more effective than laxative therapy with PEG.(98)
Further well designed prospective randomized controlled trials
are necessary to establish biofeedback therapy as the primary
treatment for patients with this condition.
Failure of biofeedback therapy poses a significant treatment
problem as most patients do not improve with surgical intervention. Division of the puborectalis muscle in the posterior midline
has been reported in patients with intractable pelvic dyssynergy.
However, results are disappointing with very few patients obtaining any benefit from the procedure.(99) These data suggest that
this procedure has no role in the treatment of patients with this
condition. Botulinum toxin injection has been proposed as an
alternative therapeutic modality for these patients with refractory pelvic floor dyssynergy. Injection of the toxin is directed into
the puborectalis muscle and external anal sphincter. Symptom
improvement was reported in up to 75% of patients with benefit
lasting from 1 to 3 months. Fecal incontinence was reported in
25% of patients, and was transient lasting only 1 to 3 months
after injection.(100–101) Others have reported similar beneficial
effects of botulinum toxin injection for dyssynergic-type constipation.(102) However, because the effects of the toxin wear
off within 3 months of administration, repeated injections are
necessary to maintain symptomatic improvement. Furthermore,
given the expense of this drug, this treatment modality should be
reserved for those patients with severe symptomatic pelvic dyssynergia that has failed all other therapies.
SURGERY OPTIONS
Surgical intervention for functional constipation is limited to
patients with documented severe slow-transit constipation that
is refractory to medical management. Patient selection is critical for success. Minimal evaluation requires colon transit studies
to document slow-transit constipation, and pelvic floor physiology testing to rule out pelvic floor dysfunction. Operative procedures performed for the treatment of slow-transit constipation
include segmental colectomy, subtotal colectomy with ileosigmoid anastamosis, and total abdominal colectomy with ileorectal anastamosis. Each procedure has its champions; however, the
overwhelming body of literature indicates superiority of total
abdominal colectomy with ileorectal anastamosis.
Total abdominal colectomy with ileorectal anastamosis is the
treatment of choice for patients with slow-transit constipation.
The anastamosis is usually performed in the proximal rectum
at or near the sacral promontory. At this level, the anastamosis
is easier to perform, eliminates the risks associated with rectal
mobilization, and bowel diameter does not limit the size of the
anastomotic lumen.(103)
operative and nonoperative therapy for chronic constipation
Timing of surgery is best decided by the patient, as this surgery is an irreversible step in the treatment of constipation. Most
patients are accepting of surgical intervention when all conservative measures have failed to result in an acceptable quality of life.
In addition to standard operative risk for colectomy, patients
should be counseled that abdominal pain and bloating may
persist postoperatively even after normalization of bowel frequency. This is significant as a recent report showed that persistent abdominal pain had the strongest correlation with quality of
life scores following colectomy in these patients.(104) Standard
bowel preparations may not be sufficient as many patients with
slow-transit constipation have one bowel-movement per week
and are already taking PEG products to assist with bowel function. A clear liquid diet for 48 hours along with multiple enemas
and laxatives may be necessary to adequately evacuate the colon
and rectum of stool. Perioperative antibiotics are given according to current standards (intravenous) and physician preference
(oral) as described in Chapter 2.
Overall success of total abdominal colectomy with ileorectal anastamosis for slow-transit constipation is approximately 90%, and
reported rates of symptomatic improvement ranges from 50% to
100%.(104, 105) This variability may be the direct result of how success after surgery is defined.(104) Many studies use patient satisfaction
as criteria for success; however, patient derived subjective assessment
is an inaccurate measurement of surgical outcome and likely varies
between patients and studies. In a review of the literature evaluating
subtotal colectomy for slow-transit constipation, Knowles et al. found
that only half of the 31 studies that documented success or satisfaction
reported the method of data acquisition.(19) Furthermore, in these
studies success rate was based on patient judgment in 14, on function
in 6, and on a combination of both in 5. Criteria used to assess success or satisfaction was not reported in 6 studies. Patient satisfaction
and gastrointestinal functional outcomes (i.e. bowel-movement frequency) do not correlate with quality of life.(104, 106) A recent report
showed a significant increase in bowel-movement frequency after
subtotal colectomy; however, the persistence of abdominal pain and
the development of postoperative incontinence or diarrhea adversely
affected quality of life scores.(104) The authors concluded that bowel
movement frequency alone does not provide an accurate assessment
of patient’s outcome. This has led investigators to suggest the use of
standardized outcome measures such as questionnaire-based protocols that assess quality of life.(106) These instruments should be used
along with postoperative complications, functional outcome measures
as well as gastrointestinal function to provide more uniform outcomes
measurement of operative success in these patients.
Acute and long-term complications are significant and include
prolonged postoperative ileus, recurrent bowel obstruction,
abdominal pain and bloating, diarrhea, incontinence, and recurrent constipation, and are addressed in detail below. These factors all affect quality of life scores with incontinence having the
greatest negative impact.(104) In fact, postoperative quality of
life assessment after total abdominal colectomy and ileorectal
anastamosis showed significantly decreased scores compared to
those of the general population (107); however, 93% of patients
that met selection criteria for total abdominal colectomy with ileorectal anastamosis for slow-transit constipation would undergo
colectomy again given the chance.(104)
Early reports found that if the whole intraabdominal colon
was not removed, symptoms often recurred.(108) In fact, results
of segmental colectomy have been disappointing with small
series reporting up to 100% failure rate.(19) Reports of subtotal
colectomy with ileosigmoid anastamosis resulted in an increased
incidence of constipation and conversion to total colectomy
was necessary in 50% of cases.(109) Other authors support this
concept and cite increased incidence of constipation recurrence
and persistence resulting in the need to reoperate to remove the
remaining colon.(107, 110) Removal of the colon with preservation of the cecum and ileocecal valve has been described; however, long-term results were poor as maintenance of the cecal
reservoir resulted in dilatation and recurrence of constipation
symptoms.(111) Modifications of colonic transit studies using
multiple ingestible markers and scintigraphic defecography have
been used to determine segmental colonic inertia.(112) Although
the validity of these techniques to determine segmental motility
dysfunction has been questioned (113), these tests have been used
in recent studies to identify and successfully treat patients with
segmental colonic inertia.(105, 114) In one study, 28 patients
were treated with segmental resection with a median follow-up of
50 months.(114) Early failure with persistent or recurrent constipation occurred in 3 (11%) patients and required further surgery.
Patient satisfaction was reported in 23 (82%) patients; however,
outcome was reported as excellent in 10 patients, good in 7, fair
in 7, poor in 4. If successful outcomes were assigned to the excellent and good category, the success rate would fall to 61%. Again,
variability in method to define success may play a factor in these
results. Another study evaluated 15 patients with slow-transit
constipation classifying them into total colonic slow-transit (8
patients) and left slow-transit (7 patients). (105) Total abdominal
colectomy or left colectomy was performed according to this classification and resulted in improvement in symptoms (increased
daily evacuations) in 8 (100%) and 6 (86%) patients, respectively.
The authors report that patients with left colonic slow-transit all
had prolonged latency times and were treated with percutaneous
nerve evaluation. None received permanent implantation of the
device, but it does raise the question as to whether colon transit
studies were affected in these patients. The weighted finding of
prolonged latency times in patients with left colonic slow-transit
is interesting as sacral nerve stimulation has been successful for
the treatment of slow-transit and dyssynergic-type constipation.
(115) Although segmental colectomy seems promising for the
treatment of segmental colonic inertia, controlled data are lacking and further studies are needed to verify and support its use.
In a small subset of patients with slow-transit constipation ileostomy may be necessary due to poor operative risk or in elderly
patients with impaired continence.
COMMON COMPLICATIONS
Morbidity of colectomy in patients with slow-transit constipation
includes several factors. First, the direct risks of colon resection are
related to the anastamosis (leak, stricture), infections (wound and
intraabdominal abscess), bleeding, and anesthesia. Mortality related
to colectomy in this group has been <1%.(103) Long-term complications resulting from colectomy in patients with slow-transit constipation are significant, and have been shown to negatively impact
improved outcomes in colon and rectal surgery
outcomes with decreased quality of life.(104) Common complications in this group of patients include recurrent bowel obstruction,
abdominal pain, diarrhea, incontinence, and recurrent constipation, and warrant further discussion. Recurrence of constipation is
addressed in detail in the section to follow.
In patients undergoing total abdominal colectomy with ileorectal anastamosis, the most frequently occurring complication
is small bowel obstruction. The reported incidence ranges from
8 to 38% with surgical intervention required in up to 75%.(104,
110, 116) The etiology of obstruction is commonly attributed to
adhesions formed from the extensive colectomy; however, others
have reported findings of small bowel pseudo-obstruction due
to proposed neuropathic disorder of the myenteric plexus affecting overall bowel motility.(104, 117, 118) A retrospective review
examined the incidence of postoperative complications following subtotal colectomy with ileorectal anastamosis in 48 patients
with colonic inertia, 30 with Crohn’s disease, and 22 with either
Familial Adenomatous Polyposis, or other neoplasia.(119) Small
bowel obstruction occurred in 10 to 18% of each group, with
no significant difference between groups. Others have reported
intestinal obstruction rates of 35% following total abdominal
colectomy for slow-transit constipation. In this study, 33% of
patients had evidence of a delay in small bowel transit time suggesting this disorder is not limited to the colon, but also affects
the small bowel. Recent reviews have speculated that routine use
of antiadhesive agents such as Seprafilm® may reduce the incidence of adhesion induced small bowel obstruction.(103)
Postoperative persistence of abdominal pain and alteration in
bowel function are significant issues that adversely affect quality
of live. A recent retrospective review on quality of life after subtotal colectomy for slow-transit constipation showed that abdominal pain was persistent in 41% of patients, diarrhea in 52%, and
incontinence in 45%.(104) Collectively, these factors had the
strongest correlation with quality of life survey, and the development of incontinence had the most negative impact on the
score. As mentioned above, the high rate of persistent abdominal
pain after surgery warrants detailed counseling of the patients
regarding expectations and outcomes. Patients must be aware
that normalization of bowel frequency may not relieve them of
their pain. Diarrhea following total abdominal colectomy with
ileorectal anastamosis is not uncommon with reported incidence
ranging from 0 to 46%.(104) This is not surprising as the colon
is effective at water absorption and is responsible for desiccating
the stool. Over time intestinal adaptation occurs and normalizes
consistency and frequency of the stool, with more than 90% of
patients having either solid or semisolid stools by 6 months.(120)
During the intestinal adaptation period, diarrhea is treated with
fiber, motility agents (loperamide, diphenoxylate and atropine
sulfate), and binders (cholestyramine) to reduce bowel frequency.
The incidence of postoperative incontinence has been reported
in 0% to 52% of patients with a mean of 14%.(104) Intractable
diarrhea, especially in the setting of fecal incontinence, may
require conversion to a permanent ileostomy.
RECURRENCE
It is clear that colectomy for refractory constipation has demonstrated successful outcomes for total abdominal colectomy with
ileorectal anastamosis in 89 to 100% after appropriate preoperative workup, including colon transit study, defecography, and
anorectal physiology tests.(19) Therefore, the greatest assurance
to success in the operative treatment of constipation starts with
appropriate patient selection.
Recurrence or persistence of constipation following colectomy has
been reported to occur in up to 33% of patients.(104) Patients with
combined slow-transit constipation with pelvic floor dyssynergy are
less likely to result in successful outcomes after surgery. Outcomes
in patients undergoing surgery for slow-transit constipation with or
without pelvic floor dyssynergy have been compared.(121) The presence of pelvic floor dysfunction significantly decreased success rates
from 78% to 56%. It has been shown that slow-transit constipation
with associated pelvic floor dyssynergia can be treated initially with
biofeedback therapy followed by surgery with similar improvement
in outcomes such as median stool number per day, spontaneous
stools, laxative use, and quality of life.(107)
Patients with slow-transit constipation are believed to have a global neuropathic disorder of the myenteric plexus that affects colonic
motility.(117) It has been proposed that this neuropathic disorder
may extend proximal into the small bowel, or even the entire gastrointestinal tract resulting in a global gastrointestinal motility disorder (panenteric inertia). Failure to identify these patients may be
a reason for early recurrence of constipation or even the high incidence of postoperative bowel obstruction. Preoperative evaluation
of whole gastrointestinal transit should be performed in all patients
undergoing surgery for slow-transit constipation. Successful identification of these patients should raise question as to whether they
will benefit from colectomy. If this entity is identified after surgery,
conversion to an ileostomy may be required.
Finally, recurrence of constipation may be a direct result of
incomplete colonic resection. Segmental colectomy, ileosigmoid
anastamosis, and preservation of the cecum and ileocecal valve
with cecorectal anastamosis are all associated with a higher incidence of constipation recurrence or persistence. Surgical failure
in these patients frequently requires reoperation for conversion
to ileorectal anastamosis.
In patients with recurrent constipation after colectomy, workup
is directed at the issues addressed above. First, anatomic evaluation of the remaining rectum should be performed. Flexible
signoidoscopy is adequate and can be performed in the office after two
Fleets enemas. Special attention is made to the anastamosis as stricture formation will result in constipation. In the absence of organic
disease, pelvic floor physiology testing is repeated to determine
the presence of pelvic floor dyssynergia. Presence of this condition
requires biofeedback therapy to improve symptoms and outcome.
Upper gastrointestinal small bowel follow trough and other tests of
whole gut transit will determine whether panenteric inertia is present.
In these patients, persistent constipation and pseudo-obstruction
are difficult to manage and may require end ileostomy. A careful
review of the original operative report will provide evidence as to
whether adequate colectomy was performed. Complimentary tests
such as colon transit studies (radiopaque markers or scintigraphy)
and gastrografin enema (avoid barium if constipation is significant)
will help determine if there is residual dysmotile colon remaining.
Persistent constipation with evidence of residual colon may require
completion colectomy with ileorectal anastamosis.
operative and nonoperative therapy for chronic constipation
SUMMARY
Constipation is a common and complex polysymptomatic clinical disorder that has multiple etiologies. Successful treatment
requires careful workup and patient selection. A careful history
and physical exam are the first step. Many medical conditions
and medications can cause constipation, and correction of these
disorders can improve symptoms. Anatomic evaluation of the
colon to rule out neoplasia, stricture, and other organic disease
is required. When these secondary causes of constipation are
excluded, a functional chronic constipation exists. Functional
constipation consists of three overlapping subtypes including
slow-transit constipation, dyssynergic defecation, and mixed disorders. Initial therapy for all patients includes dietary and lifestyle
modification with and without laxatives. Persistent constipation
that is refractory to medical management requires further testing.
The tests obtained will vary depending on the patients history,
surgeons experience, and testing availability. Colonic motility is
determined by colon transit studies such as radiopaque markers
or scitigraphic defecography. Pelvic floor function and physiology
is determined by anal manometry, balloon expulsion test, defecography, and electromyography. Isolated slow-transit constipation is successfully treated with total abdominal colectomy with
ileorectostomy. Lesser operations result in poor outcome with a
high incidence of reoperation. Before surgery global gastrointestinal motility should be assessed as the presence of panenteric
inertia can negatively impact outcomes. Pelvic floor dyssynergia
is treated with biofeedback therapy to improve pelvic muscle
coordination for defecation. Surgical therapy has poor results
and should be discouraged. The combination of slow-transit
constipation and pelvic floor dyssynergia are more complex.
Optimal outcomes require successful treatment of pelvic floor
dysfunction with biofeedback therapy before surgery.
REFERENCES
1. Johanson JF, Sonnenberg A, Koch TR. Clinical epidemiology of chronic constipation. J Clin Gastroenterol 1989; 11:
525–36.
2. Higgins PD, Johanson JF. Epidemiology of constipation in
North America: a systematic review. Am J Gastroenterol
2004; 99: 750–9.
3. Davies GJ, Crowder M, Reid B et al. Bowel function measurements of individuals with different eating patterns. Gut
1986; 27: 164–8.
4. Rendtorff RC, Kashgarian M. Stool patterns of healthy adult
males. Dis Colon Rectum 1967; 10: 222–8.
5. Chang L, Toner BB, Fukudo S et al. Gender, age, society, culture, and the patient’s perspective in the functional gastrointestinal disorders. Gastroenterology. 2006; 130: 1435–46.
6. Rao SS, Tuteja AK, Vellema T et al. Dyssynergic defecation:
demographics, symptoms, stool patterns, and quality of life.
J Clin Gastroenterol 2004; 38: 680–5.
7. Pietrusko RG. Use and abuse of laxatives. Am J Hosp Pharm
1977; 34: 291–300.
8. Agnew J. Man’s purgative passion. Am J Psychother 1985;
39: 236–46.
9. Longstreth GF, Thompson WG, Chey WD et al. Functional
bowel disorders. Gastroenterol 2006; 130: 1480–91
10. Bassotti G, Roberto GD, Sediari L, Morelli A. Toward a definition of colonic inertia. World J Gastroenterol 2004; 10:
2465–7.
11. Rao SSC. Dyssynergic defecation. Gastroenterol Clin North
Am 2001; 30: 97–114.
12. Preston DM, Lennard-Jones JE. Anismus in chronic constipation. Dig Dis Sci 1985; 30: 413–8.
13. Whitehead WE, Devroede G, Habib FI et al. Functional disorders of the anorectum. Gastroenterology International
1992; 5: 92–108.
14. Pepin C, Ladabaum U. The yield of lower endoscopy in
patients with constipation: survey of a university hospital,
a public county hospital, and a Veterans Administration
medical center. Gastrointest Endosc. 2002; 56: 325–32.
15. Koch A, Voderholzer WA, Klauser AG et al. Symptoms in
chronic constipation. Dis Colon Rectum 1997; 40: 902–6.
16. Glia A, Lindberg G, Nilsson LH, Mihocsa L, Akerlund JE.
Clinical value of symptom assessment in patients with constipation. Dis Colon Rectum 1999; 42: 1401–8.
17. Degen LP, Phillips SF. Variability of gastrointestinal transit
in healthy women and men. Gut 1996; 39: 299–305.
18. Stivland T, Camilleri M, Vassallo M et al. Scintigraphic measurement of regional gut transit in idiopathic constipation.
Gastroenterology 1991; 101: 107–15.
19. Knowles CH, Scott M, Lunniss PJ. Outcome of colectomy
for slow transit constipation. Ann Surg 1999; 230: 627–38.
20. Wexner SD, Daniel N, Jagelman DG. Colectomy for constipation: physiologic investigation is the key to success. Dis
Colon Rectum 1991; 34: 851–6.
21. Hinton JM, Lennard-Jones JE, Young AC. A new method for
studying gut transit times using radiopaque markers. Gut
1969; 10: 842–7.
22. Metcalf AM, Phillips SF, Zinsmeister AR et al. Simplified
assessment of segmental colonic transit. Gastroenterology
1987; 92: 40–7.
23. Chaussade S, Khyari A, Roche H et al. Determination of total
and segmental colonic transit time in constipated patients.
Results in 91 patients with a new simplified method. Dig
Dis Sci 1989; 34: 1168–72.
24. Nam YS, Pikarsky AJ, Wexner SD et al. Reproducibility of
colonic transit study in patients with chronic constipation.
Dis Colon Rectum 2001; 44: 86–92.
25. Burton DD, Camilleri M, Mullan BP, Forstrom LA, Hung JC.
Colonic transit scintigraphy labeled activated charcoal compared with ion exchange pellets. J Nucl Med 1997; 38: 1807–10.
26. Camilleri M, Zinsmeister AR. Towards a relatively inexpensive, noninvasive, accurate test for colonic motility disorders. Gastroenterology 1992; 103: 36–42.
27. Bharucha AE, Phillips SF. Slow transit constipation.
Gastroenterol Clin North Am 2001; 30: 77–95.
28. Ghosh S, Papachrysostomou M, Batool M, Eastwood MA.
Long-term results of subtotal colectomy and evidence of noncolonic involvement in patients with idiopathic slow-transit
constipation. Scand J Gastroenterol 1996; 31: 1083–91.
29. Rao SS, Welcher KD, Leistikow JS. Obstructive defecation: a
failure of rectoanal coordination. Am J Gastroenterol 1998;
93: 1042–50.
improved outcomes in colon and rectal surgery
30. Rao SS, Ozturk R, Laine L. Clinical utility of diagnostic tests for constipation in adults: a systematic review.
J Gastroenterol 2005; 100: 1605–15.
31. Sun WM, Rao SS. Manometric assessment of anorectal
function. Gastroenterol Clin North Am 2001; 30: 15–32.
32. Rantis PC, Vernava AM 3rd, Daniel GL, Longo WE. Chronic
constipation:is the workup worth the cost? Dis Colon
Rectum 1997; 40: 280–6.
33. Iwai N, Yanagihara J, Tokiwa K et al. Reliability of anorectal manometry in the diagnosis of Hirschsprung’s disease.
Z Kinderchir 1988; 43: 405–7.
34. Le Blanc I, Michot F, Duparc F et al. Anorectal manometry
and ileo-anal anastomosis: pre- and postoperative manometric comparison. Ann Chir 1994; 48: 183–7.
35. Rao SS, Welcher KD, Leistikow JS. Obstructive Defecation:
A failure of rectoanal coordination. Am J Gastroenterol
1998; 93: 1042–50.
36. Fleshman JW, Dreznik Z, Cohen E, Fry RD, Kodner IJ.
Baloon expulsion test facilitates diagnosis of pelvic floor
outlet obstruction due to nonrelaxing puborectalis muscle.
Dis Colon Rectum 1992; 35: 1019–25.
37. Rao SS, Hatfield R, Soffer Em et al. Manometric tests of
anorectal function in healthy adults. Am J Gastroenterol
1999; 94: 773–83.
38. Beck DE. Simplified balloon expulsion test. Dis Colon
Rectum 1992; 35: 597–8.
39. Minguez M, Herreros B, Sanchez V et al. Predictive value
of the balloon expulsion test for excluding the diagnosis of
pelvic floor dyssynergia in constipation. Gastroenterology
2004; 126: 57–62.
40. Vrees MD, Weiss EG. The evaluation of constipation. Clin
Colon Rectal Surg 2005; 18: 65–75.
41. Karlbom U, Edebol Eeg-Olofsson K, Graf W, Nilsson S,
Påhlman L. Paradoxical puborectalis contraction is associated with impaired rectal evacuation. Int J Colorectal Dis
1998; 13: 141–7.
42. Jorge JM, Ger GC, Gonzalez L, Wexner SD. Patient position
during cinedefecography. Influence on perineal descent and
other measurements. Dis Colon Rectum 1994; 37: 927–31.
43. Jones PN, Lubowski DZ, Swash M, Henry MM. Is paradoxical contraction of puborectalis muscle of functional importance? Dis Colon Rectum 1987; 30: 667–70.
44. Agachan F, Pfeifer J, Wexner SD. Defecography and proctography. Results of 744 patients. Dis Colon Rectum 1996; 39:
899–905.
45. Whitehead WE, Wald A, Diamant NE et al. Functional
disorders of the anus and rectum. Gut 1999: 45(Suppl 2):
II55–II59.
46. Weidner AC, Low VH. Imaging studies of the pelvic floor.
Obstet Gynecol Clin North Am 1998; 25: 825–48.
47. Podnar S. Electrodiagnosis of the anorectum: a review of
techniques and clinical applications. Tech Coloproctol 2003;
7: 71–6.
48. Yeh CY, Pikarsky A, Wexner SD et al. Electromyographic
findings of paradoxical puborectalis contraction correlate
poorly with cinedefecography. Tech Coloproctol 2003; 7:
77–81.
49. Siegel JD, Di Palma JA. Medical treatment of constipation.
Clin Colon Rectal Surg 2005; 18: 76–80.
50. Heaton KW, Wood N, Cripps HA et al. The call to stool and
its relationship to constipation: a community study. Eur J
Gast Hepatol 1994; 6: 145–9.
51. Meshkinpour H, Selod S, Movahedi H et al. Effects of regular exercise in management of chronic idiopathic constipation. Dig Dis Sci 1998; 43: 2379–83.
52. Young RJ, Beerman LE, Vanderhoff JA. Increasing oral fluids in chronic constipation in children. Gastroenterology
Nurs 1998; 21: 156–61.
53. Whitehead WE, Drinkwater D, Cheskin IJ et al. Constipation
in the elderly living at home: definition, prevalence, and
relationship to life style and health status. J Am Geriatr Soc
1989; 37: 423–9.
54. Burkitt DP, Walker AP, Painter NS. Effect of dietary fiber on
stools and the transit-times, and its role in the causation of
disease. Lancet 1972; 2: 1408–12.
55. Tucker DM, Sandstead HH, Logan GM. Dietary fiber
and personality factors as determinants of stool output.
Gastroenterology 1981; 81: 879–83.
56. Vanderholzer WA, Schatke W, Muhldorfer BE et al. Clinic
response to dietary fiber treatment of chronic constipation.
Am J Gastroenterol 1997; 92: 95–8.
57. Anti M, Pignataro G, Armuzzi A et al. Water supplementation enhances the effect of high-fiber diet on stool frequency and laxative consumption in adult patients with
functional constipation. Hepatogastroenterology 1998;
45: 727–32.
58. Schiller LR. Review article: the therapy of constipation.
Aliment Pharmacol Ther 2001; 15: 749–63.
59. Tramonte SM, Brand MB, Mulrow CD et al. The treatment
of chronic constipation in adults. A systematic review. J Gen
Intern Med 1997; 12: 15–24.
60. Madoff RD, Fleshman JW. AGA technical review on the diagnosis and care of patients with anal fissure. Gastroenterology
2003; 124: 235–45.
61. Locke GR III, Pemberton JH, Phillips SF. AGA position
statement: guidelines on constipation 2000; 119: 1761–78.
62. Lembo A, Camilleri M. Current concepts:chronic constipation. N Engl J Med 2003; 349: 1360–7.
63. Di Palma JA. Current treatment options for chronic constipation. Rev Gastroenterol Disord 2004; 4: S34–S42.
64. Bass P, Dennis S. The laxative effects of lactulose in normal and constipated patients. J Clin Gastroenterol 1981;
3(suppl): 23–8.
65. Lederle F, Busch D, Mattox K et al. Cost-effective treatment of
constipation in the elderly: a randomized double-blind comparison of sorbitol and lactulose. Am J Med. 1990; 89: 597–601.
66. Schiller LR. Osmotic effects of polyethylene glycol.
Gastroenterology 1988; 94: 933–41.
67. Toledo TK, Di Palma JA. Review article: colon cleansing preparation for gastrointestinal procedures. Aliment
Pharmacol Ther 2001; 15: 605–11.
68. Di Palma JA, Smith JR, Cleveland MB. Overnight efficacy of
polyethylene glycol laxative. Am J Gastroenterol 2002; 97:
1776–9.
operative and nonoperative therapy for chronic constipation
69. Di Palma JA, DeRidder PH, Orlando RC, Koltz BE, Cleveland
MB. A randomized, placebo-controlled multicenter study
of the safety and efficacy of a new polyethylene glycol laxative. Am J Gastroenterol 2000; 95: 446–50.
70. Corazziari E, Badiali D, Bazzocchi G et al. Long term efficacy, safety, and tolerability of low daily doses of isosmotic
polyethylene glycol electrolyte balanced solution (PMF-
100) in the treatment of functional constipation. Gut 2000;
46: 522–6.
71. Passmore AP, Davies KW, Flanagan PG et al. A comparison
of Agiolax and lactulose in elderly patients with chronic
constipation. Pharmacology 1993; 47(Suppl 1): 249–52.
72. Oster JR, Materson BJ, Rogers AI. Laxative abuse syndrome.
Am J Gastroenterol 1980; 74: 451–8.
73. Urso FP, Urso MJ, Lee CH. The cathartic colon: pathological
findings and radiologic/pathologic correlation. Radiology
1975; 116: 557–9.
74. Smith B. Pathologic changes in the colon produced by
anthraquinone purgatives. Dis Colon Rectum 1973; 16:
455–8.
75. Kiernan JA, Heinicke EA. Sennosides do not kill myenteric
neurons in the colon of the rat or mouse. Neuroscience
1989; 30: 837–42.
76. Nusko G, Schneider B, Schneider I et al. Anthranoid laxative
use is not a risk factor for colorectal neoplasia: results of a
prospective case controlled study. Gut 2000; 46: 651–5.
77. Capoletti J, Malinowska DH, Tewari KP et al. SPI-0211 activates T84 cell chloride transport and recombinant human
CIC-2 chloride currents. Am J Physiol Cell Physiol 2004;
297: C1173–83.
78. Camilleri M, Bharucha AE, Ueno R et al. Effect of a selective
chloride channel activator, lubiprostone, on gastrointestinal
transit, gastric sensory, and motor functions in healthy volunteers. Am J Physiol Gastrointes Liver Physiol 2006; 290:
G942–7.
79. Johanson JF, Wald A, Tougas G et al. Effect of tegaserod
in chronic constipation: a randomized, double-blind,
controlled trial. Clin Gastroenterol Hepatol 2004; 2:
796–805.
80. Verne GN, Eaker EY, Davis RH, Sninsky CA. Colchicine is
an effective treatment for patients with chronic constipation: an open-label trial. Dig Dis Sci 1997; 42: 1959–63.
81. Soffer E, Metcalf A, Launspach J. Misoprostol is effective
treatment for patients with slow transit constipation. Dig
Dis Sci 1994; 39: 929–33.
82. Prather CM, Camilleri M, Zinsmeister AR et al. Tegaserod
accelerates orocecal transit in patients with constipationpredominant irritable bowel syndrome. Gastroenterology
2000; 118: 463–8.
83. Kamm MA, Muller-Lissner S, Talley NJ et al. Tegaserod
for the treatment of chronic constipation: a randomized,
double-blind, placebo-controlled multinational study. Am
J Gastroenterol 2005; 100: 362–72.
84. Gonenne J, Camilleri M Ferber I, Burton D et al. Effect of
alvimopan and codeine on gastrointestinal transit: a randomized controlled study.Clin Gastroenterol Hepatol 2005;
3: 784–91.
85. Paulson DM, Kenedy DT, Donvick RA et al. Alvimopan: an
oral, peripherally acting µ-opioid receptor antagonist for the
treatment of opioid-induced bowel dysfunction- a 21 day
treatment-randomized clinical trail. J Pain 2005; 6: 184–92.
86. Camilleri M. Alvimopan, a selective peripherally acting µ-opioid
antagonist. Neurogastroenterol Motil 2005; 17: 157–65.
87. Heymen S, Jones KR, Scarlett Y, Whitehead WE. Biofeedback
treatment of constipation: a critical review. Dis Colon
Rectum 2003; 46: 1208–17.
88. Enck P. Biofeedback training in disordered defecation: a
critical review. Dig Dis Sci 1993; 38: 1953–60.
89. Rao SS, Enck P, Loening-Baucke V. Biofeedback therapy for
defecation disorders. Dig Dis Sci 1997; 15(Suppl 1): 78–92.
90. Gilliland R, Heymen S, Altomare DF et al. Outcome and
predictors of success of biofeedback for constipation. Br J
Surg 1997; 84; 1123–6.
91. Heymen S, Wexner SD, Gulledge AD. MMPI assessment of
patients with functional bowel disorders. Dis Colon Rectum
1993; 36: 593–6.
92. Devroede G, Girard G, Bouchoucha M et al. Idiopathic
constipation by colonic dysfunction. Relationship with
personality and anxiety. Dig Dis Sci 1989; 34: 1428–33.
93. Kumar D, Bartolo DC, Devroede G et al. Symposium on
constipation. Int J Colorectal Dis 1992; 7: 47–67.
94. Nehra V, Bruce B, Rath-Harvey DM, Pemberton JH,
Camilleri M. Psychological disorders in patients with evacuation disorders and constipation in a tertiary practice. Am
J Gastroenterol 2000; 95: 1755–8.
95. Dykes S, Smilgin-Humphreys S, Bass C. Chrinic idiopathic
constipation: a psychological enquiry. Eur J Gastroenterol
Hepatol 2001; 1: 29–44.
96. Brown SR, Donati D, Seow-Choen F, Ho YH. Biofeedback
avoids surgery in patients with slow-transit constipation:
report of four cases. Dis Colon Rectum 2001; 44: 737–9.
97. Chiarioni G, Salandini L, Whitehead WE. Biofeedback benefits only patients with outlet dysfunction, not patients with
isolated slow transit constipation. Gastroenterology 2005;
129: 86–97.
98. Chiarioni G, Whitehead WE, Pezza V, Morelli A, Bassotti G.
Biofeedback is superior to laxatives for normal transit constipation due to pelvic floor dyssynergia. Gastroenterology
2006; 130: 657–64.
99. Barnes PRH, Hawley PR, Preston DM, Lennard-Jones JE.
Experience with posterior division of the puborectalis muscle in the management of chronic constipation. Br J Surg
1985; 72: 475–7.
100. Joo JS, Agachan F, Wolff B, Nogueras JJ, Wexner SD. Initial
North American experience with botulinum toxin type A
for the treatment of anismus. Dis Colon Rectum 1996; 39:
520–4.
101. Hallan RI, Williams NS, Melling J et al. Treatment of anismus in intractable constipation with botulinum. Lancet
1988; 2: 714–7.
102. Maria G, Brisinda G, Bentivoglio AR, Cassetta E, Albanese
A. Botulinum toxin in the treatment of outlet obstruction
constipation caused by puborectalis syndrome. Dis Colon
Rectum 2000; 43: 376–80.
improved outcomes in colon and rectal surgery
103. Beck DE. Surgical management of constipation. Clin Colon
Rectal Surg 2005; 18: 81–4.
104. FitzHarris GP, Garcia-Aguilar J, Parker SC et al. Quality of
life after subtotal colectomy for slow-transit constipation:
both quality and quantity count. Dis Colon Rectum 2003;
46: 433–40.
105. Ripetti V, Caputo D, Greco S, Alloni R Copolla R. Is total
colectomy the right choice in intractable slow-transit constipation? Surgery 2006; 140: 435–40.
106. Lim JF, Ho YH. Total colectomy with ileorectal anastamosis leads to appreciable loss in quality of life irrespective of
primary diagnosis. Tech Coloproctol 2001; 5: 79–83.
107. Nyam DC, Pemberton JH, Ilstrup DM, Rath DM. Longterm results of surgery for chronic constipation. Dis Colon
Rectum 1997; 40: 273–9.
108. Lane WA. The results of the operative treatment of chronic
constipation. Br Med J 1908; 1: 126–30.
109. Kamm MA. Role of surgical treatment in patients with
severe constipation. Ann Med 1990; 22: 435–42.
110. Vasilevsky C, Nemer FD, Balcos EG, Christenson CE,
Goldberg SM. Is subtotal colectomy a valuable option in the
management of chronic constipation? Dis Colon Rectum
1988; 31: 679–81.
111. Fasth S, Hedlund H, Svaninger T, Oresland T,
Hulten L. Functional results after subtotal colectomy
and cecorectal anastamosis. Acta Chir Scand 1983; 149:
623–7.
112. Arhan P, Devroede G, Jehannin B et al. Segmental colonic
transit time. Dis Colon Rectum 1981; 24: 625–9.
113. Ehrenpreis ED, Jorge JMN, Schiano TD et al. Why colonic
marker studies don’t measure transit time. Gastroenterology
1997; 110A: 728.
114. Lundin E, Karlbom U, Pahlman L, Graf W. Outcome of segmental colonic resection for slow-transit constipation. Br J
Surg 2002; 89: 1270–4.
115. Kenefick NJ, Nicholls RJ, Cohen RG, Kamm MA. Permanent
sacral nerve stimulation for treatment of idiopathic constipation. Br J Surg 2002; 89: 882–8.
116. Ternent CA, Bastawrous AL, Morin NA et al. Practice
parameters for the evaluation and management of constipation. Dis Colon Rectum 2007; 50: 2013–22.
117. Krishnamurthy S, Shuffler MD, Rohrmann CA, Pope CE
II. Severe idiopathic constipation is associated with a distinctive abnormality of the colonic myenteric plexus.
Gastroenterology 1985; 88: 26–34.
118. Mollen RM, Kuijpers HC, Claassen AT. Colectomy for slowtransit constipation: preoperative evaluation is important
but not a guarantee for a successful outcome. Dis Colon
Rectum 2001; 44: 577–80.
119. Nakamura T, Pikarsky AJ, Potenti FM et al. Are complications of subtotal colectomy with ileorectal anastamosis
related to the original disease? Am Surg 2001; 67: 417–20.
120. Pikarsky AJ, Singh JJ, Weiss EGm Nogueras JJ, Wexner SD.
Long-term followup of patients undergoing colectomy for
colonic inertia. Dis Colon Rectum 2001; 44: 179–83.
121. Redmond JM, Smith GW, Barofsky I et al. Physiological tests to
predict long-term outcome of total abdominal colectomy for
intractable constipation. Am J Gastroenterol 1995; 90: 748–53.
4
Colorectal trauma
S David Cho, Sharon L Wright, and Martin A Schreiber
CHALLENGING CASE
A 23-year-old man sustained a through and through gun shot
wound to the left lower abdomen. The patient was mildly hypotensive on arrival to the emergency room, but responded to administration of 2 L of normal saline. The abdominal exam reveals
the bullet holes and moderate tenderness. The rectal exam was
normal. Chest and abdominal radiographs were normal except
for markers at the gunshot wounds, electrolytes and hemoglobin
levels were normal. After administration of a second generation
cephalosporin and a type and cross for blood, the patient was
taken to the operating room for an abdominal exploration. The
only injury found was a lateral injury to the mid sigmoid colon.
There was minimal stool contamination of the lower abdomen.
CASE MANAGEMENT
The colonic wound edges were debrided and the colon was
repaired primarily with a two layer suture closure. The abdomen
was copiously irrigated. The laparotomy wound was closed and
the patient received one dose of antibiotics postoperatively.
INTRODUCTION
The management of traumatic colon injury has been the subject of much debate and has evolved considerably over the past
century. During World War I, primary repair was practiced for
all colon injuries, with a resultant mortality in excess of 60%.
(1, 2) Civilian series reported similar results, with LoCicero and
colleagues reporting a 67% mortality rate from 1927–1942.(3)
The mortality rate dropped to approximately 30% during World
War II (2) at a time when several changes in management were
introduced. Most notably, Ogilvie (4) described exteriorization
of colon injuries, leading to the practice of mandatory colostomy,
which reduced mortality to about 45%.(4) Mortality dropped
further during the Korean and Vietnam conflicts, to about 10%
(1), which many attributed to the standardization of colostomy. The thinking at that time was that diversion of the fecal
stream and avoiding an anastomosis would greatly reduce infectious complications.(5) The specter of infection was particularly
ominous during a time when antibiotics had just been introduced. Many combat surgeons did not have significant training
in managing colon injuries, high-velocity wounds, or operating
under conditions of resource constraint and combat triage, during which follow-up of an anastomosis would be difficult.(4, 6)
These concepts became incorporated into civilian settings as well
and became the standard for at least 30 years. Other innovations
during this period included the introduction of antibiotics, and
improvements in transport, surgical devices, critical care, and
resuscitation (2, 5, 7, 8) that may well have been responsible for
the improvements in survival. Despite these factors, colostomy
remained the standard of care for the first three-quarters of the
twentieth century.
This practice was first successfully challenged by the landmark
work of Stone and Fabian (9) in 1979, when they published the
results of their randomized trial of primary repair without diversion versus colostomy in 268 patients with colon injuries. They
noted a similar wound infection rate, and a significantly lower
peritoneal infection rate with primary repair (15% vs. 29%).
Their overall complication rate was 1% for primary repair and
10% for colostomy. Further, they noted an increase in hospital
length of stay of approximately 6 days in the colostomy group.
Although the study excluded more severely injured patients, it
was the first to provide evidence that colostomy was not mandatory in all cases. Based on this work, a growing body of evidence
contributed to a shift toward primary repair of traumatic colon
injury during the 1980s and 1990s.
Currently, primary repair, defined as a single-staged operation
establishing bowel continuity (either by direct suture repair or
resection and anastomosis) without proximal diversion, is being
increasingly used for most colon injuries in civilian settings.(10,
11) The military conflict in Iraq and Afghanistan has both reinvigorated the debate between primary repair and diversion, and
has brought new perspectives to this issue. Clearly, optimal treatment depends not on the uniform application of one technique
or the other, but depends on sound judgment and an understanding of the current evidence.
EPIDEMIOLOGY
Colon injury occurs in 30% of abdominal gunshot wounds
and 5% of stab wounds, and is the second most common
intraabdominal organ injury in civilian penetrating trauma.
(12) Penetrating mechanisms cause 85–95% of colon injuries
in civilian practice.(6, 13–16) In contrast, in a recent review
of colon injuries sustained by American soldiers in Operation
Iraqi Freedom over a 2-year period, 71% of injuries were caused
by improvised explosive devices (IED) and 24% were caused by
gunshot wounds. Blunt injury is rare, with colon involvement
in 0.2% of trauma admissions but 20–30% of blunt hollow
viscus injuries.(17) Motor vehicle crashes and traffic accidents
account for the majority of blunt colorectal injuries.(18, 19)
Approximately 80–90% of colon injuries in civilian settings are
nondestructive.(20)
While mortality has dropped in recent decades to <3% (21,
22), morbidity has remained high. Colon related complications
have been consistently reported in 15–30% of cases since 1979.
(9, 14, 23–27)
PREOPERATIVE ASSESSMENT
The initial assessment of any trauma patient always begins with
the ABCs (airway, breathing, and circulation) and adherence to
Advanced Trauma Life Support (ATLS) principles including the
primary and secondary surveys, rapid treatment of immediately
improved outcomes in colon and rectal surgery
Figure 35.1a Seat-belt sign. The patient was involved in a roll-over motor vehicle
crash.
life-threatening injuries, establishment of appropriate intravenous access, and administration of fluids or blood products when
appropriate.
In cases of severe injury accompanied by marked physiologic
derangement, most notably the ‘lethal triad’ (acidosis, hypothermia, and coagulopathy) (28) of trauma, the principles of
damage control surgery are applicable. These include rapid triage, abbreviated laparotomy, and return to the intensive care unit
(ICU) for rewarming and correction of acidosis and coagulopathy. Intraoperatively the abdomen is packed, massive hemorrhage
is controlled, and injured bowel is stapled off and left in discontinuity if necessary. In 12 to 24 hours the patient is brought back to
the operating room at least once for reexploration and definitive
repair.(29)
Diagnosis
The diagnosis of bowel injury is notoriously difficult. Colon injuries are primarily diagnosed intraoperatively.(30) However, diagnostic techniques warrant a brief discussion.
PHYSICAL EXAM
Peritoneal signs in the abdominal trauma victim are most often
caused by hollow viscus injury. However, physical exam may be difficult to perform in the multisystem trauma patient. Intoxication,
traumatic head injury, or distracting injuries may obviate a reliable physical exam.
The “seat belt sign” has been described as a physical exam finding that predicts bowel injury. The classic finding is ecchymosis of
the anterior abdominal wall secondary to the compressive force
of the lap belt (Figure 35.1a). It is associated with a more than
doubled (2.9%) relative risk of bowel injury.(31) Flexion distraction injuries of the thoracolumbar spine, termed “Chance fractures”, also should raise suspicion for blunt bowel injury.(32)
Diagnostic peritoneal lavage
Diagnostic peritoneal lavage (DPL) is a rapid and inexpensive
test to evaluate the intraperitoneal contents and it remains a
diagnostic option in patients with suspected abdominal injury.
Via an open or closed technique, the abdominal cavity is lavaged
with 1 L of isotonic solution, then aspirated and tested for evidence of intraabdominal injury. In blunt trauma, DPL is considered positive if 10 mL of blood is aspirated before instillation
of lavage fluid. Microscopic criteria for a positive DPL in blunt
trauma include more than 100,000 red blood cells (RBCs)/mm3
or 500 white blood cells/ mm3. The criteria for a positive DPL
in penetrating trauma are much less standardized and vary from
more than 1,000 RBCs/mm3 to gross aspiration of >10 cc of
blood. In both blunt and penetrating trauma, presence of bile,
amylase, bacteria, or particulate matter should indicate visceral
injury and need for laparotomy. The accuracy of DPL is 92% to
98%, as reported by the Eastern Association for the Surgery of
Trauma guidelines.(33)
Otomo et al. (34) posited new criteria specifically designed to
diagnose intestinal injuries using DPL. Due to the fact that hemoperitoneum is not necessarily an indication for operation, they
considered the DPL positive when there was a relative increase in
the WBC count compared to the RBC indicating peritoneal irritation. They prospectively evaluated 250 patients with blunt abdominal trauma. In addition to other criteria, when the RBC count in
the lavage fluid was greater than 10 × 104/mm3), then the DPL
was considered positive when the WBC count exceeded the RBC
count/150. They report that these criteria have a diagnostic sensitivity of 96.6% and specificity of 99.4% for intestinal injury.
Advantages of DPL include rapidity, higher sensitivity, lower
cost, and immediate performance and interpretation. Unlike
computed tomography, performance of DPL does not require
transfer to a noncritical area. The major disadvantages are a 1%
to 3% risk of iatrogenic intraperitoneal injury and the high sensitivity of the test, which may lead to nontherapeutic laparotomies.(33) The utility of DPL has significantly decreased in the
era of nonoperative management of solid organ injuries and it
is primarily used in unstable trauma patients with an unknown
source of hemorrhage. However, DPL may diagnose hollow viscus injuries that are missed by other modalities. There are relative
contraindications to the performance of a DPL which include
pregnancy, obesity, and prior celiotomy. Lastly, DPL is primarily
of value if the abdominal injury is intraperitoneal. If the injury is
confined to the extraperitoneal colon and rectum, DPL may not
identify these injuries.
Ultrasound
Focused abdominal sonography for trauma (FAST) is now a commonly used modality in the initial diagnostic management of
abdominal trauma. FAST has been used as a screening modality
for patients with blunt trauma to determine which stable patients
should undergo further diagnostic imaging with CT scanning. It
has also been used in hemodynamically unstable patients to rapidly determine presence of intraperitoneal fluid and the need for
immediate surgery analogous to the use of gross blood on DPL.
In FAST, the ultrasound probe is used to serially evaluate the
pericardium, Morison’s pouch (hepatorenal space), splenorenal
recess, and the pouch of Douglas (retrovesical portion of the
intraperitoneal cavity) for free fluid. A small amount of physiologic fluid is occasionally seen in the pelvis, but anything more
colorectal trauma
Figure 35.1b CT scan of a patient with colon injury who demonstrated a “seatbelt” sign. Note the presence of free fluid (arrow) consistent with blood in the
abdominal cavity. Of note, this patient did not have a solid organ injury raising
suspicion of a hollow viscus injury.
should be considered abnormal and should prompt either operative exploration or further investigation.
FAST has a sensitivity of 42% to 63%, a specificity of 98% to
100%, a positive predictive value of 67% to 100%, negative predictive value of 93% to 98%, and an accuracy of 92% to 98%.
(33–40) Its advantages include rapidity, easy repeatability, its
noninvasive nature, the absence of radiation exposure, and low
cost. Disadvantages to FAST are interobserver variability and
the fact that hollow viscus injuries may not be associated with
an adequate volume of free intraabdominal fluid to be diagnosed
by FAST.
intact sensorium without evidence of raised intracranial pressure, and absence of contraindications for pneumoperitoneum,
Ahmed et al. found that exploratory laparoscopy is safe and accurate in the diagnosis of penetrating abdominal injuries, and identified those injuries that necessitated open repair.(44) In their
study, they report avoiding nontherapeutic exploratory laparotomy in 75% of their patients. The authors describe laparoscopy
as having the advantage of identifying injuries to the peritoneum,
diaphragm, mesentery and omentum.
Mitsuhide et al. (45), prospectively evaluated the use of diagnostic laparoscopy in conjunction with CT scan in patients with
blunt abdominal injury. Diagnostic laparoscopy was performed
in hemodynamically stable patients who had either local peritoneal signs and indirect CT signs (bowel thickening or isolated
intraperitoneal fluid), an increase in abdominal pain or tenderness, or intraperitoneal fluid increased on serial CT scan. A total
of 25 laparotomies were performed in 399 patients, 14 based on
physical exam or CT findings and another 11 after laparoscopy.
In total, 17 laparoscopic examinations were completed and 10
injuries were repaired. Thus, in these 399 patients, laparoscopy
detected 1 mesenteric laceration and 7 bowel injuries that were
not diagnosed on CT scan. There were no nontherapeutic laparotomies, and 7 laparotomies were avoided. They concluded that
laparoscopy can prevent nontherapeutic laparotomy and delayed
diagnosis in patients with suspected blunt bowel injury.
Risks of laparoscopy in trauma patients include tension pneumothorax upon CO2 insufflation, which can be decreased by
limiting initial insufflation pressures to 8 mmHg.(45) Other risks
include hypotension following insufflation secondary to intravascular volume depletion, and gas embolism in patients with
intraabdominal solid viscus injury.
Computed tomography
Computed tomography (CT) scanning of the abdomen and pelvis is the procedure of choice for the evaluation of the hemodynamically stable blunt trauma patient.(33) It is recommended in
patients with equivocal physical exam findings, multiple injuries,
and neurologic injury.
Abdominal CT has a sensitivity of 64% to 88%, specificity of
97% to 99%, and an accuracy of 82% to 99% for the diagnosis of hollow viscus injury.(41, 42) Disadvantages include high
cost, radiation exposure, and the need to transport patients to the
radiology suite.
Signs of bowel trauma seen on CT include mesenteric stranding, free intraperitoneal fluid in the absence of solid organ injury,
extraluminal air or contrast material, and bowel wall thickening.
(43) Figure 35.1b demonstrates these findings. Improvements
in CT technology have led to increasing sensitivity of CT in the
detection of the more subtle signs of injury to the bowel.
Laparoscopy
Laparoscopy has been evaluated in the diagnosis of intraabdominal injury in a selected group of trauma patients as a method to
evaluate penetrating injuries. Potential advantages include avoiding nontherapeutic laparotomy and diagnosing and treating blunt
bowel injuries that are otherwise missed by imaging techniques.
In patients with penetrating abdominal trauma, stable vital signs,
Injury scales
In the effort to standardize assessment of traumatic injuries and
potentially predict outcomes, a number of scoring systems have
been published. While these scales do not attempt to replace
sound judgment, experience and individualization of treatment,
they are useful as a common means of assessment and communication amongst surgeons caring for patients with these injuries. The three most commonly used in association with colonic
injury are briefly discussed here.
Flint and colleagues (16) described three grades of colonic injury
(Table 35.1), derived from a series of 137 patients. Interestingly,
this report appears to have been at least in part generated by the
discussion begun by Stone and Fabian (9) just 2 years earlier. The
aim of their study was to determine if selection of candidates for
primary repair could be based on the severity of colon injury.
They noted an increase in mortality from 4% to 25% between
injury grades 1 and 3, and no complications for grade 1 versus a
31% complication rate for grade 3 injury. Although no statistics
were reported, the authors concluded that primary repair was safe
for injury grade 1, while colostomy was the procedure of choice
for grades 2 and 3.
Moore and co-workers proposed a Penetrating Abdominal
Trauma Index (PATI) in 1981.(46) These authors cited a need for
an injury severity index that specifically addressed intraabdominal injury, one that focused on morbidity rather than mortality,
Соседние файлы в папке Библиотека им академика М.И. Перельмана