Part 143

{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 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.

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 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.

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 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.

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.

In acute cases the attack is sudden, obstruction complete, and the symptoms those of internal strangulation of the bowel, often followed by collapse, which may destroy life in a few hours. These cases are {849} chiefly jejunal and iliac invaginations, and the higher up in the small intestine the seat of obstruction the more violent and urgent the symptoms. Constriction, being great, is followed by engorgement and inflammation of the invaginated bowel, and if the patient lives long enough gangrene ensues, by which the obstructing mass is separated and discharged en masse or in fragments through the anus. Not unfrequently life is saved in this way. That gangrene has taken place and separation of the invaginated segments is in progress are often known by the very fetid character of the evacuations and by their admixture with blood and shreds of necrosed bowel. When the sequestrum has been detached entire, it is often passed with difficulty. Frequently it lodges at some point in the bowel, producing temporary obstruction and giving rise to tenesmus and pain as it passes along the large intestine. There is no doubt that the continuity of the intestine above and below the neck of the invagination has been established, and complete cures effected in the way already mentioned. Usually, however, the patient dies from collapse, peritonitis, or perforation of the bowel before the obstructing mass can be removed by gangrene. Children almost invariably die before this can take place, and adults live from the seventh to the fourteenth day, according to the greater or less violence and acuteness of the symptoms. When the slough has been discharged and the continuity of intestine established, recovery is still uncertain, and death very often happens for reasons referred to in speaking of the separation of the sequestrum.

Separation of the invaginated portion and its expulsion, according to Leichtenstern, in the majority of cases takes place from the eleventh to the twenty-first day, but in chronic cases it is often delayed for months. According to Brinton, separation of the sequestrum occurs between the eighth and fifteenth in intussuscepted small intestine, and between the fifteenth and twenty-second days in acute cases of ileo-cæcal and colic invaginations.

In chronic cases of intussusception, which usually embrace the ileo-cæcal and colic varieties, strangulation is not common and the course of the disease is protracted. These cases often last for several months, and the symptoms are not always well defined. At first the pain is paroxysmal, with long intervals of ease. Vomiting succeeds, but is not persistent; discharge of the contents of the bowel below the seat of lesion takes place and afterward fecal matter from above this point, because the permeability of the bowel is not usually lost in chronic cases. Eventually the alvine discharges become bloody, mucoid, and characteristic of intussusception; the severity of the symptoms may gradually increase, the pain becoming greater, more constant, the vomiting more incessant, the discharges from the bowels more frequent, and in one, two, or three months the patient dies from asthenia. Several authentic cases are related where the disease lasted one or two years before terminating fatally. Very often some days before death the pain and tenderness cease, and the operations become free from blood and normal in character.

{850} Constipation.

Constipation is a prominent symptom in all of the conditions which give rise to intestinal obstruction, and habitual constipation or loss of the powers provided for the advance of the contents of the intestines not unfrequently leads to permanent occlusion of the canal. It is impossible to fix any definite rule as a standard of health for the number and quantity of alvine evacuations. Some individuals have a passage from the bowels once every day; others, in the enjoyment of as good general health, suffer from the ordinary inconveniences of constipation if they have less than two or three daily fecal discharges; others, again, apparently equally as well, have a movement from their bowels once in two or three days or once a week, or even once in two weeks. Habershon records the case of a "woman sixty years old who from youth upward had had a passage from the bowels only every six or eight days, and whose health had been perfect." A lady under my own observation, for twenty years never had an alvine discharge oftener than once in two weeks, and three times in her life had passed two months without a movement of her bowels. This lady was the mother of several children, and, although not in perfect health, was able to attend to her ordinary household duties. Such cases are not very uncommon, and occur, as far as I have been able to ascertain, more frequently in women than in men.

The number of fecal evacuations and the quantity discharged have been shown by Bischoff and Voit to depend, to some extent, upon the character of the food ingested, vegetable diet producing abundant, and animal diet scanty, stools. Doubtless, the quality of the food partly explains the quantity of the alvine evacuation, although, to some extent, this must depend upon the time that the feces remain in the colon, a long residence there taking away a greater part of the watery constituents and making the fecal mass thicker and harder; but the variations in the number of stools in persons living on the same diet can only be explained by the variations in the activity of the peristaltic action in different individuals, or in the same individual at different periods and under different surroundings.

The causes of habitual constipation are of the most varied and diversified character, and it is not always possible in an individual case to point out the original or primary one. Not unfrequently several causes are in operation at the same time to produce sluggishness of the intestinal canal and constipation. Very often it begins with change of scene and habits, by which the daily visit to the water-closet is interfered with, or after confinement to bed with some temporary indisposition. It is more likely to occur in men and women whose habits are sedentary and who are constitutionally lazy and indolent. The feces are allowed to remain in the rectum and colon, and every hour after the ordinary time for going to stool diminishes the watery parts of the fecal mass and makes it harder and more consistent. Many cases of chronic constipation, begun in this way, have ended in dilatation and thickening of the intestine, ulceration of the mucous membrane, and, eventually, perforation of the coats and escape of the contents of the gut into the peritoneal cavity. Rapid {851} excretion of water by the kidneys, lungs, and skin produces constipation by withdrawing a large proportion of the water from the fecal mass, rendering it unnaturally dry and of diminished bulk. In diabetes, constipation arises from this cause unless the patient makes up the loss by drinking an unusually large quantity of water. Constipation in nursing-women is explained by the loss of water in the secretion of milk. The profuse sweating which attends malarial fever, phthisis, and other diseases readily accounts for the constipation which often accompanies these disorders.