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460 The ASCRS Manual of Colon and Rectal Surgery
F. Wound Management
• The incidence of wound sepsis in patients with colon or rectal
injury is high.
• In a prospective study of 100 patients with gunshot wounds
and routine skin closure, the wound infection rate was 11%.
• Primary wound closure in the presence of severe fecal spillage is
a signifi cant risk factor for wound sepsis and fascia dehiscence.
• This high-risk group of patients is best managed by delayed
primary closure of the skin 3–5 days postoperatively.
G. Antibiotic Prophylaxis
• In view of the high incidence of septic complications in patients
with colon injuries, appropriate antibiotic prophylaxis is critical. It
is a standard practice to cover against both aerobes and anaerobes.
• The issue of antibiotic coverage in colon injuries merits further
investigation. The authors’ current choice is ampicillin/sulbactam
prophylaxis in all suspected abdominal hollow viscous injury.
• There is now class I evidence that 24-h prophylaxis is at least as
effective as prolonged prophylaxis for 3–5 days, even in the presence of major risk factors for abdominal sepsis, such as colon injury,
multiple blood transfusions, and high Abdominal Trauma Index.
• With respect to rectal injuries, no study has addressed the type
or length of antibiotic therapy. In the available studies that have
even mentioned antibiotics, length of therapy has been at least
2 days using single or double agents covering both aerobes and
anaerobes. It is the authors’ preference to use ampicillin/sulbactam for prophylaxis in all patients with rectal injuries.
H. Trauma Ostomy Complications
• When deciding about the method of management of a colon or
rectal injury, the surgeon should take into account the problems
related to the creation of a stoma and later on the complications
associated with the subsequent operation for colostomy closure.

22. Colon and Rectal Trauma and Rectal Foreign Bodies 461
• The morbidity of colostomy closure is signifi cant. In a collective review of 809 colostomy closures in trauma patients
during the period 1970–1990, the overall incidence of colonrelated complications was 13.1% (major complications 5.3%;
minor complications 7.8%).
• The timing of colostomy closure does not seem to have an
important role in the incidence of complications.
• The optimal time for colostomy closure should be individualized and time should be allowed for wound healing and nutritional recovery. This might require only a few weeks for some
patients or many months in severely injured patients.
I. Rectal Foreign Bodies
• Rectal foreign bodies represent an uncommon cause of rectal injury, accounting for <5% of cases. More often, patients
present to the hospital with a retained foreign body.
• Most objects can be safely removed in the emergency department; however, a small percentage of patients will require
general anesthesia and operative management with or without
laparotomy.
• The only independent risk factor for operative intervention
was if the foreign body was located in the sigmoid colon (odds
ratio, 2.25; 95% CI, 1.1–4.4; P = 0.04).
• Patients with a history of retained foreign body who present
with peritonitis should be taken directly to the operating
room.
• Without peritonitis, patients should have an attempt at retrieval
at the bedside. If unsuccessful, patients should be taken to the
operating room with an attempt at transanal extraction under
intravenous sedation.
• If transanal extraction is unsuccessful, then a laparotomy
should be performed to maneuver the foreign body into the
rectum for transanal removal. If this is unsuccessful, then a
colotomy may be necessary for foreign body retrieval.

23. Colorectal Cancer: Epidemiology,
Etiology, and Molecular Basis
A. Epidemiology
• Colorectal cancer (CRC) is a disease with a major worldwide
burden. It is the fourth most frequently diagnosed malignancy
in both sexes with almost 1 million people developing CRC
annually. CRC is the third most common cause of cancer death
in the world, responsible for 630,000 deaths annually.
• In the United States, CRC is the third most common cancer in
men and women and the second most common cause of cancer
death overall.
• The worldwide incidence of CRC is increasing.
• Before 1985, the age-adjusted incidence of CRC in the United
States had been increasing; however, since this time, the rates
have declined an average of −1.6% per year (Fig. 23.1 ). This
reduction has been mainly confi ned to the Caucasian race
and is largely limited to a decrease in the incidence of distal
cancers.
• The recent decrease in incidence in the United States may be
attributable to screening, specifi cally screening with fl exible
sigmoidoscopy, although other factors are likely to have infl uenced this trend.
• Currently, the overall probability of an individual developing
CRC in United States over a lifetime is almost 6%.
• From a population perspective, age is the most important risk
factor for CRC. CRC is predominantly a disease of older individuals; 90% of cases are diagnosed over the age of 50. The
risk of CRC continues to increase with age (Fig. 23.2 ).
D.E. Beck et al. (eds.), The ASCRS Manual of Colon and Rectal Surgery, 463
DOI: 10.1007/978-0-387-73440-8_23, © Springer Science + Business Media, LLC 2009

464 The ASCRS Manual of Colon and Rectal Surgery
2
4
6
Rate per 100,000
0
Incidence
0
Mortality
0
0
73
75 77 79 81 83 85 87 89 91 93 95 97
Year of Diagnosis/ Death
Fig. 23.1. CRC incidence and death rates in the United States 1973–1997. (From
Ries et al. Copyright
of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)
©
2000 American Cancer Society. Reprinted by permission
• The incidence per 100,000 people aged 80–84 is more than
seven times the incidence in people aged 50–54.
• In the United States the risk of CRC differs by gender. The incidence of CRC is more than 40% higher in men than women.
• The ratio of colon to rectal cancer differs in the United States
by gender; the ratio of colon to rectal cases for women is 3:1 as
compared with 2:1 for males.
• Race and ethnicity infl uence CRC risk; Ashkenazi Jewish individuals seem to be at a slightly increased risk of CRC. At least
part of this increased incidence may be attributable to a higher
prevalence of the I1307K mutation of the adenomatous polyposis gene, a mutation that confers an increased risk of CRC
development.

23. Colorectal Cancer: Epidemiology, Etiology 465
550
500
450
400
350
300
250
200
Rate per 100,000
150
100
50
0
Male and female
Male
Female
00-04
05-09
10-14
15-19
20-24
25-29
30-34
35-39
40-44
Age at diagnosis
45-49
50-54
55-59
60-64
65-69
70-74
75-79
80-84
85+
Fig. 23.2. Age-specifi c incidence rates in the United States. Age-specifi c incidence both genders – circles . Age-specifi c incidence in males – squares . Age-
specifi c incidence in females – diamonds . [Generated from the Surveillance,
Epidemiology, and End Results (SEER) Program ( http://www.seer.cancer.gov )
*
SEER
Stat Database: Incidence – SEER 9 Regs Public-Use, Nov 2002 Sub
(1973–2000), National Cancer Institute, DCCPS, Surveillance Research Program, Cancer Statistics Branch, released April 2003, based on the November
2002 submission.]
• In the United States, the incidence of CRC is higher in
African-Americans of either gender as compared with Cauca-
sians (Table 23.1 ).
• In African-Americans, the increased rate of cancer is predominantly attributable to a higher rate of proximal cancers.
• The Surveillance Epidemiology and End Results registry (a
National Cancer Institute population-based cancer registry representing 14% of the population in the United States) reports
cancer incidence and stage over time (Table 23.2 ). Between
1992 and 1999 for all patients diagnosed with CRC, 38% of
patients were diagnosed with localized disease, 38% with
regional disease, and 19% with metastatic disease. Five percent of patients were unstaged. As a proportion of total cases,
African-Americans were more likely to present with advanced

466 The ASCRS Manual of Colon and Rectal Surgery
Table 23. 1. Incidence and mortality rates a for CRC by site, race, and ethnicity,
United States 1996–2000.
Asian
American
Caucasian
Incidence Male 64.1 72.4 57.2 37.5 49.8
Female 46.2 56.2 38.8 32.6 32.9
Mortality Male 25.3 34.6 15.8 18.5 18.4
Female 17.5 24.6 11.0 12.1 11.4
African-
American
and Pacifi c
Islander
American
Indian/
Alaska
Native
Hispanic/
Latino
Source : Adapted from Jemal et al.
& Wilkins.
a
Per 100,000 age-adjusted to the 2000 United States standard population.
Table 23. 2. Stage at diagnosis.
Caucasians African-Americans
Localized 38 34
Regional 38 36
Distant 19 24
Unstaged 5 7
11
with permission from Lippincott Williams
disease; 24% of African-Americans have metastatic disease
at presentation. Rates of metastatic disease have fallen over
time, most notably for CRC of the distal colon and rectum in
Caucasians.
• There is substantial geographic variation in the incidence of
CRC, with relatively high rates in North America, Western
Europe, and Australia and relatively low rates in Africa and
Asia (Fig. 23.3 ).
• Mortality from CRC is declining in the United States.
– Improvements in surgical and medical treatments likely
explain some of the change particularly that identifi ed
before 1985. More recently, the reduced mortality rate is
likely secondary to the reduced incidence of CRC.

23. Colorectal Cancer: Epidemiology, Etiology 467
a
Australia (N.S. Wales
Brazil (Porto Alegre
Japan (Osaka 1988/92)
Sweden (1988/92)
Uganda (Kyadondo
USA-SEER Black
USA-SEER White
1988/92)
1990/92)
1991/93)
(1988/92)
(1988/92)
5 10152025303540
0
New cases per 100,000 person-years
b
Australia (N.S. Wales
Brazil (Porto Alegre
Japan (Osaka 1988/92)
Sweden (1988/92)
Uganda (Kyadondo
USA-SEER Black
USA-SEER White
1988/92)
1990/92)
1991/93)
(1988/92)
(1988/92)
0
5 101520253035404550
New cases per 100,000 person-years
Fig. 23.3. ( a ) Age-standardized (to the world population) incidence rates of cancer of the large bowel among females. ( b ) Age-standardized (to the world popu-
lation) incidence rates of cancer of the large bowel among males. (Reprinted
from Lagiou.
15
Copyright © 2002 by Oxford University Press, Inc. Used by per-
mission of Oxford University Press, Inc.)
– African-Americans have the highest mortality rate from
CRC in the United States (Table 23.1 ). The reasons for
the higher mortality rate are likely multifactorial including the higher incidence of CRC, and the differences in
stage distribution.

468 The ASCRS Manual of Colon and Rectal Surgery
B. Etiology
Dietary Constituents and Supplements
• The relationship between diet and CRC risk is at best unclear.
Studies in this area are diffi cult to conduct, because exposures
tend to be multifactorial and change over time with our diet. In
addition, because colorectal carcinogenesis is a multistep process, a number or combination of exposures may be necessary,
and genetic susceptibility is likely to have a role.
• Although it can be stated that an individual with no other risk
factors for CRC who ingests a diet that is high in fi ber, fruits,
and vegetables and low in animal fat and red meat will be on
average at lower risk of CRC than an individual who eats a
diet low in fi ber, fruits, and vegetables and high in animal fat
and red meat, it is diffi cult to determine with certainty which
dietary components or combinations are responsible for the
decreased risk.
Dietary Fat
• Dietary fat, particularly saturated animal fat has been implicated in carcinogenesis in the colon and rectum.
• However, dietary fat consumption is related to a number of other
factors that may infl uence cancer risk, including other dietary
factors such as dietary fi ber and micronutrient consumption, as
well as life-style factors such as exercise and alcohol consumption. Therefore, ecologic comparisons between countries are
subject to a substantial risk of confounding.
• The evidence that red meat consumption is associated with
CRC is in general more compelling than the evidence of an
association with dietary fat. Given the lack of evidence for an
independent association of dietary fat with CRC, it is unlikely
that the animal fat in red meat is responsible for the association
between red meat and CRC.
Red Meat
• There are a number of potential carcinogenic mechanisms
unrelated to fat content that may result in a causal relationship
between red meat ingestion and CRC.

23. Colorectal Cancer: Epidemiology, Etiology 469
– Red meat is high in iron, a prooxidant. Dietary iron may
increase free-radical production in the colon, and these
free radicals may cause chronic mucosal damage or promote other carcinogens.
– In humans, red meat ingestion stimulates production
of N -nitroso compounds in a dose-response manner.
Because many N -nitroso compounds are known carcin-
ogens, this is a potential mechanism for an association
between red meat and CRC.
– Formation of heterocyclic amines and polycyclic aro-
matic hydrocarbons in meat by cooking over an open
fl ame or cooking until well done may be an important
factor because these compounds are carcinogenic in animal models.
• Many epidemiologic studies have been conducted to determine
the effect of ingestion of red meat on CRC risk.
• A daily increase of 100 g of red meat (3.5 ounces) was associated with a 12–17% increased risk of CRC. The risk was substantially higher with the ingestion of processed meat.
• Of note, individuals that consume diets high in red meat generally consume diets low in other dietary factors, such as
antioxidants that may themselves be important in colorectal
carcinogenesis. It is therefore diffi cult to rule out the possibility that the apparent effect of red meat on development of CRC
may be confounded or modifi ed by other dietary or lifestyle
factors.
Fruit and Vegetable Intake
• Fruits and vegetables are a source of antioxidants, including
carotenoids and ascorbate. Other bioactive constituents in
fruits and vegetables that may protect against carcinogenesis
include the indoles and isothiocyanates.
• More recent data, however, have not demonstrated a convincing link between vegetable or fruit intake and a reduced risk of
CRC.
• The Cancer Prevention Study II also demonstrated a nonstatistically signifi cant trend for a higher colon cancer risk in
men with the lowest vegetable consumption and women with
the lowest fruit consumption.

470 The ASCRS Manual of Colon and Rectal Surgery
• Overall, the evidence for an association between fruit and vegetable intake and the risk of CRC is inconsistent. Given this
lack of concordant data, it is unlikely that a large number of
cases of CRC can be attributed directly to a lack of fruit or
vegetables, or that major additional interventions to increase
consumption would lead to a substantial reduction in the incidence of CRC.
Fiber
• The data regarding the association between fi ber and CRC risk
are confl icting.
• Several mechanisms have been proposed for the protective
effects of fi ber: fi ber may increase intestinal transit and
therefore reduce the length of exposure of the colon to carcinogens, and fi ber may dilute or absorb various potential
carcinogens, particularly bile salts. In addition, products
of fi ber degradation and fermentation in the colon (such as
butyrate) may also have a role.
• Overall, there has been little consistent evidence that a high
fi ber intake is associated with a decreased risk of CRC.
• Dietary interventions to increase fi ber intake have proven
unsuccessful in reducing the risk of colorectal neoplasia.
• There is currently no evidence from randomized studies to
suggest that increased dietary fi ber intake will reduce the
incidence or recurrence of adenomatous polyps within a 2- to
4-year period.
Calcium
• Substantial epidemiologic and experimental evidence exists to
support the benefi cial effect of calcium on the prevention of
colorectal neoplasia.
• Calcium has the capacity to bind and precipitate bile acids and
may directly infl uence mucosal cell proliferation.
• More recently, large observational studies have supported a
modest effect of calcium in the prevention of CRC, particularly
calcium supplementation.
• Although the effect of calcium may be modest, given that
CRC is a common disease, the overall impact of optimizing calcium intake from a population standpoint could be
substantial.
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