Dwayne said:"Teri" <[email hidden]> wrote in message
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Quoted message said:"Dwayne" <[email hidden]> wrote in message
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Quoted message said:I use mine (stainless steel) all the time to make tomato sauce - a coupla
Quoted message said:people in my family have diverticulitis,
That is what my wife has, but I didnt know how to spell it.
Dwayne
Actually the fable that eating seeds, et cetera can cause diverticulitis
is BS. As you can see, as per Uptodate (copyright,) there is only an
association with low fiber. There are no good quality scientific studies
which suppor the old wive'e tales.
UpToDate performs a continuous review of over 330 journals and other
resources. Updates are added as important new information is published.
The literature review for version 12.3 is current through August 2004;
this topic was last changed on June 26, 2003. The next version of
UpToDate (13.1) will be released in February 2005.
INTRODUCTION — Diverticular disease of the colon is common. This topic
review will focus on the epidemiology and pathophysiology of the
disorder. It is useful to begin with a series of definitions of the
terms that are commonly used:
A diverticulum is a sac-like protrusion of the colonic wall.
Diverticulosis merely describes the presence of diverticula.
Diverticulitis refers to inflammation of diverticula.
Diverticular disease is a term encompassing diverticulosis and
diverticulitis. Symptomatic diverticular disease includes hemorrhage,
inflammation (diverticulitis), or complications of diverticulitis such
as abscess, fistula, obstruction, or free perforation.
EPIDEMIOLOGY — Diverticular disease was uncommonly encountered at the
beginning of the twentieth century. As an example, the first report of
surgical resection for complicated diverticulitis was by Mayo in 1907
[1]. The prevalence has increased from 5 to 10 percent 80 years ago [2]
to 35 to 50 percent in an autopsy series published in 1969 [3]; there
are no recent population-based studies. The prevalence of diverticular
disease is age-dependent, increasing from less than 5 percent at age 40,
to 30 percent by age 60, to 65 percent by age 85 [4,5].
A male preponderance was noted in early series, but more recent studies
have suggested either equal distribution or a female preponderance [4].
This may be explained by a gender distribution which varies with age; in
one series, men were more often affected under age 50, there was a
slight female preponderance between the ages of 50 and 70, and a marked
female preponderance over age 70 [6]. An excess number of males has also
been noted for acute diverticulitis in patients under than 40 years of
age [7,8].
There are geographic variations both in the prevalence and pattern of
diverticulosis.
"Westernized" nations have prevalence rates of 5 to 45 percent,
depending upon the method of diagnosis and age of the population [3,9].
Diverticular disease in these countries is predominantly left-sided,
with right-sided diverticulitis being present in only 1.5 percent of
cases [10].
The findings are markedly different in Africa and Asia [2,11] where
the prevalence is less than 0.2 percent, and diverticulosis is usually
right-sided.
Japan, after adopting a more Western lifestyle, has experienced an
increase in the prevalence of right-sided diverticulosis. In one report
of 615 patients with colonic diverticular disease, right-sided
diverticula were present in approximately 70 percent of all patients and
were responsible for approximately 75 percent of cases of diverticulitis
[12]. A review of 13,947 barium enema examinations performed over a
15-year period in Japan revealed a steady increase in the incidence of
diverticulosis of the right colon [13]. Left-sided diverticula did not
increase in frequency over time. The increase in the incidence of
right-sided diverticula in Japan is similar to the increase in the
incidence of left-sided diverticula in westernized countries. A
right-sided predominance has also been noted in Singapore, where 70
percent of cases occur in patients less than 40 years old [14], and in
Hong Kong [15,16].
ETIOLOGY — The increase in incidence in the developed nations suggests
that environmental and lifestyle factors play an important role in the
pathogenesis of diverticular disease.
Dietary fiber intake — Several studies have suggested that low dietary
fiber predisposes to the development of diverticular disease [5,17,18]
although this hypothesis has not been confirmed in all studies
[11,19-23]. One report that evaluated a cohort of over 47,000 men
provided strong evidence for the role of dietary fiber [18]. After
adjustment for age, energy-adjusted total fat intake, and physical
activity, total dietary fiber intake was noted to be inversely
associated with the risk of symptomatic diverticular disease. The
relative risk was 0.58 for men in the highest quintile compared to those
in the lowest quintile for fiber intake. The observation that
diverticular disease is less common in vegetarians than nonvegetarians
is also compatible with a role for dietary fiber, since vegetables and
fruits are important sources of fiber (show table 1) [24].
If it is beneficial, dietary fiber may act by producing a large bulky
stool, resulting in a wider-bore colon that is less likely to permit
efficient segmentation and therefore less likely to develop diverticula
(see "Pathophysiology of diverticula formation" below) [5]. In addition,
increasing dietary fiber is often employed as first-line therapy for
treatment of constipation. However, there is no clear correlation
between constipation and diverticular disease, probably stemming from
the retrospective nature of most studies and the difficulties in
defining constipation in a large series of patients.
Other dietary factors — Other dietary factors that might contribute to
the pathogenesis of diverticular disease have been examined. There is no
substantially increased risk associated with smoking, caffeine, or
alcohol [25]. On the other hand, an association has been noted between
obesity in men under 40 years and acute diverticulitis. This finding is
compatible with observations that the risk of symptomatic diverticular
disease is particularly increased (relative risk 2.35 to 3.32) by a diet
characterized by a high intake of total fat or red meat and a low intake
of dietary fiber [18].
Physical activity — Lack of vigorous exercise also may be a risk factor
for diverticular disease. In a prospective study of almost 48,000
American men aged 40 to 75 who were free of known colonic disease, the
risk of developing symptomatic diverticular disease was inversely
related to overall physical activity (0.63 for highest versus lowest
extremes) after adjustment for age and dietary fat and fiber [26]. Most
of the decrease in risk with exercise was associated with vigorous
activity such as jogging and running. An interaction was noted between
physical activity and dietary fiber; men in the lowest quintile for both
had a relative risk of 2.56 compared to men in the highest quintile for
both. How physical activity might prevent diverticular disease is not known.
Possible relation with colon cancer — There may also be a relation
between diverticulosis and colon cancer. One series of 7000 patients
found an excess number of colon and rectal cancers in the first two
years after the diagnosis of diverticular disease but not with more
prolonged follow-up [27]. There was, however, a long-term excess of
left-sided colon cancers, suggesting a possible relation between these
tumors and diverticular disease.
LOCATION — A typical colonic diverticulum is a "false" or pulsion
diverticulum, ie, it does not contain all layers of the wall as a true
(congenital) diverticulum does; instead, mucosa and submucosa herniate
through the muscle layer, covered only by serosa (show histology 1).
Diverticula develop at four well-defined points around the circumference
of the colon, sites at which the vasa recta penetrate the circular
muscle layer. These vessels enter the wall on each side of the
mesenteric taenia and on the mesenteric border of the two antimesenteric
taeniae (show figure 1).
Diverticula are distributed unevenly in the colon. Ninety-five percent
of patients have sigmoid diverticula, while 35 percent also have more
proximal disease. Among the latter group, 7 percent have diverticula
throughout the colon, and 4 percent have diverticula limited to a
segment proximal to the sigmoid [28]. The location of diverticular
disease requiring surgery is similar, with 95 percent of all operative
cases involving the sigmoid [6].
PATHOPHYSIOLOGY OF DIVERTICULA FORMATION — The points at which
diverticula develop, ie, where vasa recta penetrate the bowel wall, are
considered to be areas of weakness [29]. Most patients with sigmoid
diverticula exhibit myochosis, which consists of thickening of the
circular muscle layer, shortening of the taeniae, and luminal narrowing.
There is no hypertrophy or hyperplasia of the bowel wall, but increased
elastin deposition is found in the taeniae [30]. There are also
structural changes in collagen that are similar to, but greater in
magnitude than, those that occur as a result of aging [31].
These changes may decrease resistance of the wall to intraluminal
pressure. Structural changes in the wall may also be responsible for the
appearance of diverticula at an early age in connective tissue disorders
such as Ehlers-Danlos and Marfan's syndromes and in autosomal dominant
polycystic kidney disease [32]. (See "Extrarenal manifestations of
polycystic kidney disease"😉.
The law of Laplace explains the development of diverticula. The law
states that pressure P is proportional to wall tension T, and inversely
proportional to bowel radius R:
P = kT ÷ R
where k is a conversion factor. Since the sigmoid colon is the segment
of the colon with the smallest diameter, it will tend to be the site of
the highest pressure. This is not true under normal circumstances
because pressure should be the same throughout the colon. However,
segmentation of the colon (a motility process in which segmental
muscular contractions separate the lumen into chambers) is exaggerated
in diverticulosis, occluding both ends of the chamber during muscular
contraction [33]. This increases intraluminal pressure and may
predispose to herniation of mucosa. The neural basis for the abnormal
motility observed in patients with diverticulosis remains unclear. One
report found that a central event appeared to be upregulation of smooth
muscle M3 receptors [34].
Thus, abnormal colonic motility may predispose to the development of
diverticula. It has been suggested that dietary fiber, by producing a
large bulky stool, results in a wider-bore colon that is less likely to
permit efficient segmentation and therefore less likely to develop
diverticula [5].
Pathophysiology of diverticulitis — Diverticulitis, ie, inflammation of
diverticula, produces variable clinical manifestations, ranging from
subclinical inflammation to generalized peritonitis. The underlying
cause is micro- or macroscopic perforation of a diverticulum. It was
previously believed that obstruction of diverticula, eg, by fecoliths,
increased diverticular pressure and caused perforation; such obstruction
is now thought to be rare (show endoscopy 1 and show histology 1) [11].
The primary process is thought to be erosion of the diverticular wall by
increased intraluminal pressure or inspissated food particles.
Inflammation and focal necrosis ensue, resulting in perforation.
The inflammation is frequently mild, and a small perforation is walled
off by pericolic fat and mesentery. This may lead to a localized abscess
or, if adjacent organs are involved, a fistula or obstruction. In
comparison, poor containment results in free perforation and peritonitis.
Pathophysiology of diverticular bleeding — As a diverticulum herniates,
the penetrating vessel responsible for the wall weakness at that point
becomes draped over the dome of the diverticulum, separated from the
bowel lumen only by mucosa (show endoscopy 2) [29]. Over time, the vasa
recta is exposed to injury along its luminal aspect, leading to
eccentric intimal thickening and thinning of the media. These changes
may result in segmental weakness of the artery, predisposing to rupture
into the lumen. Diverticular bleeding typically occurs in the absence of
diverticulitis [29]. (See "Colonic diverticular bleeding"😉.
The anatomic relationship between diverticula and vasa recta is similar
in both the right and left colon; however, right-sided diverticula have
wider necks and domes. This could expose the vasa recta to injury over a
greater length, which could explain the higher incidence of right-sided
hemorrhage [29].
SUMMARY — Diverticula occur at points of weakness in the bowel wall
where blood vessels penetrate. The development of diverticula is
probably multifactorial, involving both increases in intraluminal
pressure and abnormalities in the bowel wall. Raised intraluminal
pressure may be caused by abnormalities in motility that predispose to
segmentation, and is likely to be exacerbated by a low fiber diet.
Histologic changes in the muscle and collagen of the bowel wall decrease
the tensile strength of the wall; these changes are similar to, but more
pronounced than, the changes that occur with age. Trauma to diverticula
may produce either inflammation, which results in perforation, or
changes in the vasa recta in the diverticular wall, which predisposes to
weakness and rupture of the vessel.
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--
"Dum Spiro, Spero."
As long as I breath, I hope.
Cicero (Ancient Rome)
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Quoted message said:<((((º>`·.¸¸.·´¯`·.¸.·´¯`·.¸. ><((((º> ·´¯`·. , .·´¯`·.. ><((((º>
Let there be fish!!!
