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. Flint⁴ 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.

⁴ Practice of Medicine.

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 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 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. Aitken⁵ 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.

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, 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. Leichtenstern⁶ 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.

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 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 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.

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. Habershon⁷ 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.

⁷ On Diseases of the Abdomen, quoted by Leichtenstern in Ziemssen's Cyc. P. of Med., vol. vii. p. 588.

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 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.

Certain articles of food not necessary to mention here produce constipation. They fail to excite peristaltic action; or articles of diet which at first act as a stimulus to the bowels, and even provoke temporary diarrhoea, lose their power if kept up too long—just as certain purgative medicines lose their force if continued for too long a period. Gradually they cease to increase the peristaltic action, and rather add than otherwise to the inactivity of the intestines. Eating the same kind of food day after day is very apt, sooner or later, to result in diminished sensibility of the intestinal canal, a reduction of the peristaltic force, and deficiency in the secretion of the digestive juices, which in itself is a common cause of constipation. Frequent change of diet is generally needed to supply the stimulus necessary for that intestinal motion which relieves the bowels.

Bile is looked upon as one of the most powerful agents in stimulating peristaltic action, and when, from any cause, mechanical or otherwise, it is not poured into the bowel, constipation ensues. Unnatural flexures, congenital or acquired, of the large intestine are not unfrequently the source of chronic constipation. These flexures, normal or factitious, favor accumulation of feces, especially in subjects who have diminished sensibility of the bowel and a paretic state of the muscular coat. Certain injuries and diseases of the brain and spinal cord reduce, and sometimes altogether prevent, intestinal activity. Hysteria, if it exist for any length of time, is generally attended by sluggishness of the bowels, and great mental depression (melancholia) is sometimes preceded and sometimes followed by habitual constipation. In treating such a case it is important to make the distinction.

Temporary paralysis of the muscular coat of the bowel, followed by symptoms of intestinal constriction, with insuperable constipation, sometimes attends violent contusion of the abdomen. In some cases prolonged functional weakness of the muscular coat follows the injury. Many chronic diseases leave the bowel in a sluggish condition by the pathological changes produced in the intestine. The function of the muscular coat is frequently injured by the infiltration which accompanies peritonitis. The fibres are separated by the serous effusion which attends this inflammation; they become overstretched, and, losing their contractility, end in paralysis and obstinate constipation. Occlusion of the canal from this cause may last for days, and be accompanied with tympanitis, stercoraceous vomiting, and all the signs of internal strangulation, ending in death. Post-mortem examinations in such cases show no stricture or unnatural diminution in the size of the canal, but that the fatal occlusion was due to paralysis of the muscular coat of the bowel and arrest of its power.

The normal advance of the contents of the bowel is interfered with by any cause which lessens the contractility of the muscular coat. Chronic diseases which debilitate the general muscular system affect at the same time the contractile power of the muscular coat of the canal, and the debility and degeneration of old age are felt here, and sometimes occasion the constipation which often accompanies this period of life. Leichtenstern⁸ says that chronic intestinal catarrh is a common factor of constipation—that when this catarrh is of long standing it produces relaxation of the muscular coat and diminishes the elasticity of the intestinal walls. He believes that this pathological condition exists in a large proportion of the cases of habitual constipation attended with mental depression, that the hypochondriasis makes its appearance after the constipation has become chronic, and that it is a secondary symptom. This affection is located chiefly in the small intestine, and does not usually involve the colon.

⁸ Op. cit.

Probably the most common form of chronic constipation is that which accompanies loss of sensibility and muscular inactivity of the colon and rectum. The large bowel becomes sometimes so distended by the accumulated fecal masses that it has been found after death to measure ten or fifteen inches in circumference and to contain an astonishing quantity of feces. Any part of the canal, except the last two inches of the rectum, which is kept empty by the contraction of the sphincters, may be occupied by the mass, but the accumulation is greatest in the rectum, cæcum, and sigmoid flexure. At the last-named location the distension is so great that the mass can be readily felt through the abdominal walls. The tumor may be as large as a foetal head, and may be mistaken for a simple or malignant tumor of the omentum, stomach, or other organ, or for pregnancy or ovarian growth. The dilatation may be so enormous as to push the small intestines into the back part of the abdominal cavity and to interfere with the function of any organ upon which it encroaches. It may press upon the concave surface of the liver, and, arresting the flow of bile, produce jaundice or mechanically interfere with some portion of the track of the urinary organs and cripple their functions. When situated in a portion of the canal not tightly attached to the abdominal walls it is slightly movable, more or less hard and consistent, according to its duration, for it remains often for months unchanged, sometimes giving to the fingers the impression of a rather soft, easily-indented swelling with a uniform smooth surface—more often feeling like a hard, irregular, elongated, and corrugated mass of fecal balls. Contraction here and there of bundles of the circular muscular fibres of the gut produces the irregular, corrugated impression imparted to the fingers. Their shape and position may sometimes be changed by pressure through the abdominal wall. If the accumulation occurs in the rectum, the introduction of a tube or bougie is prevented by the impacted mass, which can be gotten away only by the fingers or by some instrument. The colon and rectum may be dilated to their utmost capacity with an enormous amount of feces, enough to fill a common-sized pail, and both the patient and medical attendant be deceived as to the sufferer's condition by the fact that he has his daily number of stools. The semi-fluid contents of the small intestines find their way through this mass by some irregular and uncertain track, undermining and breaking down sometimes a lump of the old fecal accumulation, which, if small in size or broken up, may pass on and escape by the anus, but if large and hard may drop into the irregular and uncertain passage and permanently close it; then sudden and complete intestinal occlusion takes place, with all of its fearful consequences. If this, however, should not occur, and the accumulation is not recognized and removed, the enormous dilatation may go on until complete paralysis of the muscular coat is produced, and entire stoppage of the current of feces, with permanent occlusion of the bowel; or before this takes place ulceration may set in, partly because of the great pressure of the fecal mass upon the mucous membrane, and partly from the irritating character of the contents of the bowel. Ulceration begins, most likely, at some point where resistance is greatest, and perforation of the bowel may ensue.

SYMPTOMS.—If the accumulation occupies only a portion of the colon, as the cæcum or sigmoid flexure, the distended part may become displaced and twisted on its long axis. This condition scarcely ever happens in the large intestines except at the parts mentioned. Torsion of the cæcum rarely takes place except in persons of from forty-five to sixty years of age, while twisting of the sigmoid flexure may happen at any period of life. When distended and very heavy from the weight of feces, with probably some congenital defect about its mesenteric attachment, the sigmoid flexure may become twisted and drop into the pelvis, producing at once symptoms of internal strangulation.

Individuals accustomed to having one or more alvine evacuations a day are made uncomfortable by two or three days of constipation. A feeling of distension about the abdomen, with flatulence and heat, follows this condition, and soon afterward headache, loss of appetite, and symptoms of indigestion supervene. If this state of the bowels continues unrelieved, pressure upon the hemorrhoidal veins takes place and interference with venous return, producing congestion in the lower end of the rectum. This is attended by straining, diarrhoea, evolution of gaseous matter, colicky pains, and possibly sympathetic disturbance of the genito-urinary organs. When at last the hardened and enlarged mass is discharged, it produces some pain and burning about the anus, with possibly rupture of the mucous membrane in that region. Fissure of the anus may thus originate. In the case of a lad aged about nine years under my care fissure of the anus began in this way, and after its formation the pain of defecation was so intense that he resisted for ten days every attempt of his bowels to move. After this time he passed every day or two one or more hardened fecal balls, but always with such atrocious pain that he looked forward to the next attempt with terror. This case ended in fecal impaction, which nearly proved fatal.

Not unfrequently persons who habitually go two or three days without having a passage from the bowels are not apparently inconvenienced, and after a time any of the discomforts ordinarily felt from constipation are not noticed, if indeed any exist.

Generally, however, chronic constipation leads to a host of troubles of the most varied character. There is not an organ in the body that is not more or less influenced by it. The generation of gas in the intestines produces a sense of fulness of the abdomen and elevation of the diaphragm which interferes with the action of the lungs and heart. The sufferer is oppressed, sighs, and has difficult respiration and attacks of palpitation of the heart. The influence of the abdominal pressure is conducted by the sympathetic nerves to the brain, and the patient frequently has vertigo, headache, ringing in the ears, faintness, etc., and in consequence of the pressure upon other nerves or of hyperæmia of the spinal cord and its membranes he has dull aching pains in his back, groins, genitals, or extremities. I have seen in several instances pain in the legs, coming on after the patient has retired and lasting until morning, violent enough to prevent sleep, at once permanently relieved by an active cathartic after antiperiodics, alteratives, and anodynes had failed to do any good.

A patient suffering from habitual constipation usually obtains temporary relief by the bowels acting either spontaneously or after a dose of medicine; but, the causes of constipation continuing, the physical discomforts and suffering continue, varied in every conceivable way. His digestion being disturbed, appetite poor, and assimilation imperfect, he gradually loses flesh and his complexion becomes sallow and unhealthy. In addition to this, he soon grows irritable and fretful, trifling affairs trouble him, he has fits of great mental depression, and soon settles down into hypochondriasis, his life becoming a burden to himself and a nuisance to his friends.

If the constipation ends in fecal accumulation, the worst symptoms of mechanical obstruction may present themselves at any time, and death of the individual follow. The practitioner should always keep this fact in mind in treating every case of intestinal obstruction, and search for fecal impaction by examining the rectum and the whole length of the large intestine through the anterior abdominal wall. Very often symptoms of impaction come on gradually in one who has been ailing for some weeks or months, but sometimes the onset is as sudden as in a case of acute occlusion of the intestines. The patient is seized with pain like that of colic and an urgent desire to empty his bowels, but all attempts to do this are futile, and the straining is followed by great exhaustion; borborygmus, nausea, vomiting, and possibly hiccough, soon come on, with tympanitic distension of the belly. If the impaction is not overcome, death by collapse or from peritonitis follows. Post-mortem examination shows enormous fecal accumulation, peritonitis as a consequence of the obstruction, perforating ulcer in some part of the large bowel, more often the sigmoid flexure, or, in some cases, absolute rupture of the cæcum itself, and escape of its contents into the peritoneal cavity.

Stricture of the Bowel.

In a report by George Pollock⁹ of 127 cases of intestinal obstruction, 77 belonged to the above class; and Brinton, in his analysis of the whole group of cases collected by him, says stricture constitutes about 73 per cent. In 124 cases of intestinal obstruction reported by Mr. Bryant¹⁰ from the post-mortem records of Guy's Hospital, 47 were found to be stricture of the bowel. The above statements show that stricture, or diminution of the calibre of the bowel, is the most frequent cause of intestinal obstruction, and the subject is worthy of our earnest consideration.

⁹ Medico-Chirurgical Review, 1853.

¹⁰ Practice of Surgery.

While stricture of the bowel may be found in any portion of the intestinal canal, it occurs most frequently in the sigmoid flexure and rectum. Brinton found in 100 fatal cases of stricture 30 in the rectum and 30 in the sigmoid flexure; only 8 cases in 100 were in the small intestine. Brinton's statistics correspond very nearly with those of other writers. The affection is more common in men than women, and the average age at death is about forty-four years.

The most common cause of stricture is contraction following cicatrization of ulcers of the mucous and submucous coats of the intestine. The ulcer may involve the circumference of the bowel, and the resulting cicatrix terminate in uniform constriction of its lumen, or the ulceration may extend several inches along the side of the intestine, ultimately causing contraction in the direction of its longitudinal axis, marked stenosis, and kinking of the gut. When ulceration, continuous or in patches, involves a large extent of bowel, it may reduce the gut to a mass of indistinguishable cicatricial tissue. Bristowe¹¹ says he has seen the whole cæcum thus contracted "into a channel barely capable of admitting a goose's quill."

¹¹ Reynolds's System of Medicine.

Stricture of the intestine often follows dysentery or tubercular and syphilitic ulceration of the bowel. Follicular or hemorrhoidal ulceration is sometimes the beginning of a stenosis which ends in stricture of the rectum. Stercoral ulcers of the colon are not unfrequently the starting-point of cicatricial contraction of the calibre of the bowel. Sometimes, but rarely, ulcers of typhoid fever end in constriction of the intestinal tube. The diameter of the gut is also contracted by the effects of caustic substances, by ulceration following the lodgment of foreign bodies, and by effusion of lymph or thickening attendant upon long-standing hernia. Very often after death it is impossible to determine what particular kind of inflammation and ulceration caused the stricture. Generally, the cause which provokes the ulceration sets up chronic peritonitis, which materially aids in producing the obstruction. Spasm of the circular muscular fibres usually accompanies these lesions, and materially contributes in many cases to fatal intestinal obstruction. Some authors assert that spasm without organic change can produce acute obstruction: such an occurrence, except possibly in the rectum, must be very rare, if indeed it ever happens.

The most common cause of stricture is cancer. This disease may originate in the bowel itself, or, beginning in some neighboring organ or tissue, gradually spreads and involves the gut. It may extend around the bowel or be infiltrated along the sides of the canal for several inches, and may be scirrhous, medullary, or epithelial in character. Eighty per cent. of the cases of cancer of the bowel are situated in the rectum. Usually, but not invariably, cancerous deposits are found in persons who have passed middle age.

An impediment to the passage of fecal matter is invariably produced in constriction of the intestine from the above causes, and it frequently continues until fatal occlusion occurs. The contents of the bowel accumulate above the block, producing distension of the gut and thickening of the muscular coats above the stricture, with contraction and atrophy of the portion of intestine below. Dilatation of the bowel above the seat of lesion is sometimes great enough to cause rupture and peritoneal extravasation, or distension and stretching of the coats of the canal may be sufficient to interfere with its circulation, and ulceration ensue.

Occasionally cases of stricture or well-marked circumscribed contraction of the bowel are seen which give rise to no marked symptoms of constriction during life. Such was the case in the instance related by Bristowe and referred to above. These instances are, however, exceptional in the large intestine.

Symptoms of stricture vary according to the site, cause, and extent of the lesion. They are gradually developed, and in this respect are unlike the symptoms of internal strangulation or of intussusception, which are generally acute and rapid in their course. When the obstruction in stricture is complete, progress toward death is comparatively slow. If the stricture is seated in the small intestine, the symptoms are often so obscure that for a long time the presence of the contraction may not be suspected; the contents of the small bowel are usually fluid, and in this state readily pass through the constricted part. The more solid the contents of the bowel, the greater the difficulty in passing a contracted and narrow orifice, and the more conclusive and characteristic the assemblage of symptoms of obstruction from stricture.

The history of a case of intestinal obstruction from stricture is often instructive. For weeks or months there have been colicky pains and intestinal disorder; possibly, in the early stages, diarrhoea, but later marked constipation, and probably previous attacks where constipation was for a time insuperable and death from obstruction imminent. Hemorrhage, except in cancer or when complicated with piles, is rare. The attack may come on suddenly, or constipation become more and more difficult to overcome; violent peristalsis presents itself, accompanied by pain and abdominal distension, and followed by nausea and vomiting, the latter often being stercoraceous. During the throes of pain—for it is paroxysmal—the outline of the distended gut can be felt and seen through the abdominal walls if they are thin and free from fat. Unless the stricture is relieved the patient gradually dies from asthenia. Inflammation is often absent throughout, but enteritis or peritonitis may come on, or perforation and peritoneal extravasation ensue and hasten the fatal termination.

When the obstruction is in the rectum it can be felt with the finger; if in the sigmoid flexure, it may be felt with a gum bougie or probe, but the use of the former is unreliable, and the latter, unless carefully employed, dangerous. Obstruction at this point, however, is attended with marked distension of the descending and transverse colon. If seated in the small bowel, the large intestine is flaccid and collapsed. Careful manual exploration often enables the practitioner to determine the site of the contraction. Weight, pain, dulness, and fulness are usually found about the stricture, but these signs may be of little value when the abdominal wall is thick and unyielding, or peritonitis or tumor is present, or the contracted portion of bowel is compressed or drawn out of its proper site. Brinton suggests that the site of stricture may be determined by the quantity of water which can be injected through the anus into the bowel. Such an estimation must often be erroneous, as stricture is rarely ever complete and fluid may be forced through the constricted part. Indeed, Battey of Georgia has demonstrated upon dead and living subjects that fluid may be made to pass through the entire canal from the anus to the stomach.

Obstruction due to cancer of the rectum can be determined by digital examination. When seated in the small intestine or higher up in the large bowel, the presence of a painful tumor, preceded for weeks by evidences of impaired nutrition, emaciation, and followed by lancinating pain, cancerous cachexia, etc., will indicate the character of the trouble.