distension of the intestine above, fixes the gut in this state of
torsion and effectually prevents it from untwisting. A semi-rotation of
the paretic and distended bowel about the mesenteric axis is sufficient
to interfere with the supply and return of blood and provoke enteritis.
Indeed, the rotation is rarely sufficiently great to produce complete
obstruction, and the symptoms are frequently rather those of
inflammation than of internal strangulation. For weeks before the final
attack the patient usually has symptoms of intestinal disorder, such as
flatulence, constipation, and spells of colic, due no doubt to the
changes provoked by the elongated mesentery and bent or curved
intestine. When torsion takes place the attack is sudden and the
symptoms violent and urgent. Vomiting, meteorism, insuperable
constipation, and frequently tenesmus, are soon followed by collapse
and speedy death. The patient may die in twenty-four hours; he rarely
lives beyond the fourth day. In some cases excessive tenesmus and
bloody stools are seen in the early stages of torsion of the bowel. The
condition may be mistaken for intussusception, but can usually be
distinguished by the premonitory symptoms of twisting and by the more
rapid course, the sudden meteorism, and quick collapse of the latter.
Still another way by which displacement of intestine may occasion
obstruction to the passage of its contents is when a portion of the
intestine has a long and narrow mesentery, and around this mesentery,
which is like a pedicle, another portion of the bowel is thrown,
encircling and compressing it. The accompanying figure, taken from
_Ziemssen's Cyclopædia_, gives a good idea of this condition (Fig. 23).
It represents a {842} loop of the small intestine placed around the
mesenteric pedicle of the sigmoid flexure. Leichtenstern calls this
"intertwining or knotting of two intestinal loops."
[Illustration: FIG. 23. Anterior view of the strangulated intestine and
stricture. _a_, gastric extremity; _b_, rectal extremity.]
[Illustration: FIG. 24. Posterior view of the strangulated intestine
and stricture. _a_, gastric extremity; _b_, rectal extremity.]
In consequence of inflammation of the peritoneum and effusion of lymph,
peritoneal surfaces are joined together, and before the lymph is fully
organized these surfaces are separated by the constant movements of the
organs and the change in the relationship of the parts, and strings and
bands of various shapes and sizes are formed in which a portion of the
intestine may become entangled and constricted. Sometimes the bowel
accidentally becomes engaged in a loop or noose of false membrane, or
becomes bound down under a band of fibrin; or, the peritoneal surfaces
of some of the organs having been joined together or to the wall of the
abdomen or pelvis, a loop of bowel may escape into a slit or opening
and become incarcerated; or a fold of bowel may fall into a fissure in
the omentum or mesentery or broad ligament of the uterus or suspensory
ligament of the liver, and become constricted; or the appendix
vermiformis may be twisted around the intestine in such a way as to
cause ligation of the tube, or, by becoming attached to some
neighboring part, it may form a loop through which the intestine may
pass and become obstructed. In the same way the bowel may be
constricted by a diverticulum. (This is well shown in Figs. 23, 24, and
25.) Bands entangling the bowel and causing strangulation may be
attached to the fimbriated process of the Fallopian tube or the ovary
or uterus. Indeed, it is impossible to describe in a limited space the
almost infinite ways in which these bands and strings may engage and
incarcerate the intestinal tube (Figs. 24, 25).
{843} [Illustration: FIG. 25. An appearance of the natural relations of
the diverticulum to the intestine. _a_, gastric extremity; _b_, rectal
extremity.]
Internal strangulated hernia may result from the bowel falling into a
pouch of the peritoneum and becoming ligated by the orifice of the
pouch, or passing into the foramen of Winslow, of which there are three
cases of strangulation recorded; or a retro-peritoneal hernia may be
formed; or, more common still, a hernia of the intestine through the
diaphragm.
In diaphragmatic hernia an opening is more frequently found in the
posterior part of this muscle. Two hundred and fifty-two cases of this
form of internal hernia have been collected by Leichtenstern, in which
the diagnosis was made in only five cases. He found the oesophageal
opening, a spot just behind the sternum, and a gap between the lumbar
and costal parts of the muscle, the weakest points in the diaphragm.
Diaphragmatic and other forms of internal hernia may exist and not
produce symptoms of strangulation either at the time of formation or
subsequently, just as we so commonly see in cases of external hernia.
When the bowel is constricted, however, and its circulation interfered
with, symptoms of internal strangulation come on, and are exactly like
the symptoms of external strangulated hernia. The attack is sudden, the
symptoms acute and urgent, and the course and termination very rapid.
Unless the constriction is relieved death may take place in twenty-four
hours; life is rarely protracted beyond three or four days.
The patient has first eructations, soon succeeded by nausea and
vomiting. The matter vomited consists of the contents of the stomach,
then of gastric fluid, bile, and the contents of the intestines. When
the last is ejected the vomiting is called fecal or stercoraceous. The
patient complains of a sense of constriction about the abdomen, griping
pains about the umbilicus, flatulence, tenesmus, and insuperable
constipation. One or two free stools from the large intestine below the
site of strangulation may be passed, but this should not deceive the
practitioner. As a rule, peritonitis soon follows strangulation. The
belly becomes tympanitic and tender, the pulse small and wiry, and the
face anxious. When gangrene supervenes the pain subsides, the pulse
becomes weak and intermittent, the surface cold and clammy, and the
patient soon dies in a state of collapse. Slight delirium may precede
death, or the mind remain unimpaired to the end. Very often, when
gangrene sets in and pain disappears, the patient has a grateful sense
of relief and is hopeful of recovery.
{844} Intussusception, Invagination.
One of the most frequent and important causes of intestinal obstruction
is intussusception or invagination of the bowel; by which term is meant
the protrusion or slipping of one portion of bowel into a portion
immediately adjoining.
This condition is sometimes found after death in persons old or young,
but particularly the latter, in whom during life there were no symptoms
of intestinal obstruction or intestinal trouble of any kind. The
displaced intestine in these subjects is easily reduced, is unattended
by any signs of inflammation, and is evidently the result of spasmodic
contraction of the transverse muscular fibres of the bowel at one part,
with distension and relaxation at another part, by which, just before
death, one piece of the bowel is pushed into an adjacent piece. Not
unfrequently two or more invaginations are seen in the same subject.
Flint[4] counted as many as fifteen in a child who died of typhoid
fever. This invagination of the death-struggle almost invariably
involves the small intestine, and may be the protrusion of a piece of
the bowel above into a piece immediately below, or the reverse, a
portion of bowel below being pushed into a portion above. It has been
suggested that this slight and temporary intussusception may occur
during life and give rise to temporary symptoms of intestinal
obstruction, which disappear when reduction of the displacement
spontaneously takes place.
[Footnote 4: _Practice of Medicine_.]
[Illustration: FIG. 26.]
[Illustration: FIG. 27.]
It will be seen by the diagrams that three successive portions of
intestine enter into the formation of an intussusception--an entering,
returning, and receiving portion. Two mucous surfaces and two serous
surfaces are thus brought into apposition. The mesentery attached to
the included lengths of bowel--viz. the entering and returning
lengths--is necessarily pulled down with the bowel in its descent, and
is also embraced by the receiving portion of the intestinal tube. The
traction excited by this portion of mesentery, thus wedged in between
the middle and inner layers of the bowel, materially alters what would
otherwise be the relationship of the parts. Fig. 26 shows simple
invagination of the ileum like the finger of a glove, in consequence of
the traction exerted. The entering or invaginated portion does not
always lie in the axis of the enveloping tube, but is more or less
curved, until very often its lower orifice is in contact with the wall
of the outer layer. The concavity of this curve looks {845} toward the
mesenteric edge of the invaginated portion of bowel, and the convexity
toward the opposite side of the receiving portion. The convex side of
the middle cylinder is often thrown into transverse folds or
convolutions. Intussusception, which gives rise to symptoms
characteristic of intestinal obstruction during life, is invariably
from above downward. It is doubtful whether there is on record a single
well-authenticated case of inflammatory invagination where the lower
segment of bowel protruded into the upper.
Reference to the diagrams will show that the lumen of the bowel is
diminished, and that more or less intestinal obstruction must follow
invagination. This obstruction is increased by the inflammation which
necessarily follows this condition. The large and numerous
blood-vessels of that portion of the mesentery involved in the
invagination are compressed and stretched; arterial supply, and
especially venous return, are interfered with; congestion quickly
follows, with copious inflammatory exudation; the layers of intestine
become swollen, and blood, sometimes in abundance, is poured out from
the mucous membrane. Peritonitis, limited sometimes to the invaginated
part, more often spreading to the peritoneum covering neighboring
structures, soon begins, and the contiguous serous surfaces are
agglutinated and the intussusception rendered irreducible. Lymph and
other inflammatory products are poured out freely; the coats of the
intestine become distended and thicker, and the inner and middle layers
of the invagination are separated by the deposit; the invaginated part
becomes more and more curved toward the mesenteric border of the outer
layer; and occlusion of the bowel, begun by the invagination, is made
more or less complete by the changes wrought by inflammation (Fig. 27).
That intestinal obstruction is not always complete in intussusception
is shown by the fact that fecal matter, often in considerable quantity,
is passed through the bent and narrowed tube, the intestine retaining,
at least for a time, its contractile power. The changes produced by
inflammation are chiefly seen in the inner and middle layers of
intestine, the receiving or outer layer of the invagination often
escaping any serious damage. These changes vary with the character and
duration of the inflammation. Sometimes they are limited to an
agglutination of the opposed serous membranes, an effusion of blood and
serum from the mucous surfaces, and an enormous distension and swelling
of all the invaginated parts; or the inflammation may end in
mortification of the middle or both the inner and middle cylinders, the
dead part coming away in shreds or in large fragments, or, if the
patient lives long enough, the entire invaginated tube being discharged
through the anus. If the inflammation involves the invaginated parts
unequally, strips and shreds of the bowel are detached by ulceration
and sloughing, and may escape in the discharge from the bowels in
pieces so small as to be unnoticed; but if the intussuscepted part dies
en masse, a circular line of demarcation is formed by ulceration, and
the dead segment is detached and drops into the cavity of the bowel
below, and escapes through the rectum. It is often so complete that the
inner and middle cylinders can be recognized, and the part of the
intestinal tube to which the expelled bowel belonged can be determined.
In favorable cases the blood-vessels of the healthy bowel above and
below the dead segment pour out a circular mass of coagulable lymph,
which, becoming organized, closes the breach and {846} completes the
intestinal tube. To accomplish this it is necessary that the ends of
the two portions of bowel should be accurately coaptated: if they are
not, some opening may be left through which the contents of the gut may
escape into the peritoneal cavity, producing fatal peritonitis; or the
new formation may be imperfectly organized, and burst during some
peristaltic movement of the bowel or from the pressure of gas
accumulating in the gut; or the supply of lymph may be so redundant as
to obstruct the calibre of the bowel, or end in cicatricial
contraction, stricture, and obstruction. Aitken[5] records four
instances where the curved end of the invaginated portion of bowel by
prolonged pressure caused ulceration and perforation of the coats of
the enclosing bowel, the invaginated portion passing through the side
of the enclosing segment and projecting into the cavity of the
peritoneum.
[Footnote 5: _Science and Practice of Medicine_.]
Gangrene and ulceration, however, do not always follow intussusception.
The mesenteric injuries may be sufficient to produce congestion and
exudation, and the patient survive the invagination for weeks, and
death eventually occur without sloughing or ulceration; or spontaneous
reduction of the invagination may take place and recovery of the
patient follow. The last termination must be rare, and impossible when
firm adhesion between the serous surfaces has taken place; but that it
does exceptionally occur is proved by cases where the diagnosis of
intussusception was undoubted, the invagination being felt in the
rectum or seen prolapsed through the anus. The most common termination,
if the patient survives, is mortification of the invaginated part and
separation in mass or by shreds or fragments.
Intussusception may occur in any portion of the intestinal canal, but
some points are more liable to it than others. 56 per cent. of the
cases collected by Brinton were ileo-cæcal; in 32 per cent. the small
intestine alone was involved; 28 iliac and 4 jejunal; in 12 per cent.
the colon, including its sigmoid flexure, was the part implicated.
When the rectum is involved, it usually forms the outer layer of the
invagination, the middle and inner layers being formed by the bowel
which has passed from above into it; when prolapse of the rectum itself
occurs, the mucous membrane is generally alone involved, but along with
this the muscular coat may also descend and a true invagination of the
rectum be found.
The most common variety of intussusception is the ileo-cæcal. It is in
this form that we find the greatest length of bowel involved. This
invagination begins generally at the ileo-cæcal valve, the lips of
which at first turn toward, and descend into, the cavity of the cæcum,
drawing with them the end of the ileum; in this case the valve forms
the lowest point of the invagination. If the invagination continues,
the end of the cæcum is next inverted; and if the process still goes
on, more and more of the colon is invaginated, until in some rare cases
it traverses the whole of the large intestine, appearing just above or
even protruding through the anus. In this variety the vermiform
appendix lies between the middle and inner layers of the
intussusception, and its opening, usually stretched and enlarged by the
inverted cæcum and inflammatory effusion, is found close to the
ileo-cæcal orifice. In this intussusception the cæcum and colon are
large and roomy, and the invaginated portion not so liable, {847} as it
is when the small intestine is alone implicated, to strangulation and
sloughing; nor is there seen in ileo-cæcal intussusception, unless the
portion of bowel involved is very short, the marked curvature of the
invaginated portion so commonly found in the small intestine. In the
ileo-cæcal form it is twisted or much convoluted rather than bent.
Another variety of ileo-cæcal invagination--very rare, however--is
where the ileo-cæcal orifice does not descend into the cavity of the
cæcum, but the lower end of the ileum passes through the valve into the
large intestine. In this instance the invaginated portion is tightly
compressed by the valve, and strangulation is speedy and complete. An
invagination may occur in the lower part of the ileum, and the inner
and middle layers pass on to the ileo-cæcal valve, and be arrested at
that point, and afterward, in consequence of violent peristaltic
action, the whole intussusception, inner, middle, and outer layers, be
invaginated into the colon. In this way the invagination becomes
doubled.
While intussusception may occur in either sex and at all periods of
life, it happens nearly twice as often in males as in females, and is
most frequently seen in childhood. Leichtenstern[6] found in his
statistics of 473 cases that one-half were seen in children under ten
years old, and one-fourth of all intussusceptions occurred in children
from four to twelve months old. Invagination of the small intestine is
found almost exclusively in adults. Brinton from his records gives the
mean age of its occurrence 34.6 years. According to the same author,
the average age of ileo-cæcal invaginations is 18.57 years, and
one-half of all cases of this form of intussusception observed by him
were in children under seven years of age. Leichtenstern states that
the lower part of the ileum is the most frequent site of invagination
in the small intestine, and the descending colon and sigmoid flexure
the most common portion involved in intussusception occurring in the
large intestine.
[Footnote 6: _Op. cit._]
The mechanism of intussusception is probably not always the same. The
following is thought to be the most frequent process: A segment of
bowel becomes paralyzed by local peritonitis, some injury, diarrhoea,
or colic, and while in this state a segment of bowel above is subjected
to violent peristaltic action, and is forced into the unresisting
portion below. In this case the paretic segment forms the outer or
receiving layer of the intussusception. Leichtenstern believes that the
paretic portion is turned in and invaginated into the normal bowel
below, and that the clinical course of intussusception and post-mortem
appearance correspond with this explanation. If such is the case, the
paralyzed portion forms the inner layer, and the active bowel below the
receiving layer. Another theory, which applies with much force to the
most common of all invaginations--viz. the ileo-cæcal--is, that as
violent anal tenesmus produces prolapse of the rectum, so prolonged and
powerful tenesmus at the ileo-cæcal opening may cause prolapse of the
lips of this orifice, and, eventually, invagination of the ileum, or of
both this and the cæcum, into the colon. When we remember that the
ileo-cæcal valve is furnished with a sphincter muscle, the analogy is
complete. The idea so long entertained that intestinal worms may
occasion invagination of the bowel has generally been abandoned. A
polypoid tumor, by dragging down the portion of bowel to which it is
attached, may produce invagination; and {848} Brinton's statistics give
5 per cent. of cases of intussusception from this source. An
examination of a larger number of cases would probably show a much
smaller percentage due to this cause.
A majority of cases of intussusception, however, take place suddenly,
without previous diarrhoea, colic, traumatism, or ill-health of any
kind, and probably occur without any tenesmus or paresis of a portion
of bowel. It may be that the longitudinal fibres of a segment of gut
contract, dilating and shortening a portion of the bowel; while this
part is distended a portion immediately above may be lengthened and
narrowed by contraction of the circular fibres, and violent peristalsis
going on at this moment, aided, possibly, by contraction of the
muscular wall of the abdomen, forces the upper and narrow segment into
the lower and dilated one.
At first the invagination involves a small portion of the bowel, but,
active peristaltic action continuing, it rapidly increases in size.
This increase is made at the expense of the sheath or outer layer,
which turns in to form the middle layer. The length of the invagination
varies from two or three inches to three, four, or five feet.
The symptoms of intussusception generally come on suddenly, and
indicate both intestinal obstruction and inflammation. Pain resembling
violent colic, and referred to the site of the invagination, is a
prominent symptom. The pain is intense, paroxysmal in character, but
after a time it becomes continuous. At first pressure gives relief, but
in a few hours tenderness, denoting peritonitis, appears, limited to
the invagination or spreading gradually over the whole abdomen.
Vomiting soon follows, and, with rare exceptions, is persistent. After
two or three days occasionally blood and sometimes fecal matter are
ejected from the stomach. Diarrhoea, with bloody, mucoid stools, is
rarely ever absent, and is characteristic of invagination. The patient
has from fifteen to twenty passages a day. If the large intestine is
involved, the diarrhoea is accompanied with tenesmus. Above the
obstruction gas and ingesta accumulate, and produce abdominal
distension, sometimes well marked. Generally the tumor formed by the
invagination can be felt through the abdominal wall, and is a symptom
of great importance. Meteorism and peritonitis may render the existence
of the tumor obscure or altogether prevent its recognition, but in
intussusception of the colon and at the ileo-cæcal valve the solid
cylindrical mass can usually be found, and frequently, when the small
bowel alone is implicated, a very careful and patient examination will
enable the observer to detect it. Sometimes it changes its site, size,
and shape; occasionally it can be felt in the rectum or is seen
protruding through the anus.
The urgency of the symptoms of invagination depends upon the portion of
bowel involved and the degree of constriction of the gut and its
attached mesentery. When the bowel is tightly constricted the symptoms
are acute, and the patient may die in a day or two; when the bowel is
not constricted the symptoms are chronic in character, and in the early
stages not urgent. The difference here is like that between
strangulated and incarcerated hernia.