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Part 12

Obstipation · Thomas Charles Martin — chapter 12 of 20 · ~1,740 words · public domain

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To collate in brief:

1. The muscular development of the adult rectum and lower sigmoid is plainly apparent in the plates here exhibited of the fresh specimens. A deficient muscularity is observed in the infant specimens.

2. The peritoneal band of these parts in the adult is observed to be, relatively, very considerably shorter than that in the infant, and the sigmoid flexure is relatively shorter.

3. The rectal valves appear to bear the same proportion to the gut in both adult and infant, but when we remember the difference in muscular development in the two the disproportionately greater resistance of the valve in the infant rectum is obvious.

4. The anal expansibility is remembered as adequate in the adult, and is seen to be deficient in the infant.

Correlative to the facts just stated we must recognize that the adult rectum has resident within its own wall a powerful expulsive muscular mechanism; that the shortening of the mesentery holds the upper rectum steady under the applied auxiliary forces; that the angulations of the normal sigmoid are not necessarily obstructive, though in a desirable measure retardative; that the forward incline of the lower sacrum and coccyx behind, and the development of the uterus and prostate and their inherent supports in front, provide the lower adult rectum with a firm funnel-like arrangement which guides the feces directly upon the os internum of the anus; that the valves divide the feces into portions to facilitate their separate successive discharge, and finally in sequence, that the physiologic descent of the structures of the ischiorectal space reduces this last resistance to the minimum in adult defecation.

Straining, the ruptures and prolapses, obstipation, retention of feces, and the multitudinous consequent ills demand our consideration, though this study forces the conclusion, I believe, that the individual’s escape is ultimately assured by process of development, and that for the normally formed infant, the physician will find the solution of the problem of difficult defecation in the solution of the stool.

TREATMENT.

Diet, hygroscopic suppositories, and fluid injections which may render more fluid the intestinal contents will favor their descent through the convoluted gut, the valvulated rectum, and the contracted anus.

Massage of the abdomen over the region of the colon aids in (1) the development of the auxiliary abdominal muscles of defecation and of the intrinsic expulsory muscles in the intestinal wall; and further, such manipulations (2) directly propel the gut’s contents along the tortuous course of the bowel and hence (3) reduce, inasmuch as they may overcome the obstructive features of the valve.

If there be an overgrowth of the rectal valve and if it form an almost impassable barrier to the descent of the feces it may be in some measure overcome in infants by the dilatation which may be effected through the means of the gently introduced trained finger. In case the defective valves are present in the form of diaphragmatic strictures or membranous septa with circular aperture, the valve may be safely cut by a method described in another place.

As at birth the pelvic bones are not yet united and as the rami of the ischium and pubes are still quite cartilaginous it is obviously possible that a little energy intelligently directed upon the anus from without will spread the pelvic outlet, whereas the infant labors ineffectually with his own forces applied as they are from within. The nurse, therefore, may be directed to pare away her nail-ends, lubricate her fingers and gently introduce the smallest finger through the anus. Daily gradual dilatation of the infant’s pelvic outlet should be practised, graduating from finger to finger until the required degree of dilatation be reached. The introduction of the finger independent of its dilating uses incites the mechanism of defecation to action.

Rachitic subjects with abnormal contraction of the pelvic outlet demand forcible divulsion of the ischial tuberosities.

OBSTIPATION IN THE ADULT.

If it be the function of the normal rectal valve to beneficently retard the descent of the feces it is obviously true that it may be the especial property of the valve in certain other than normal conditions to maliciously obstruct the descent of the feces.

There are three forms of valvular obstruction:

1. Anatomic coarctation of the valves may afford an exaggerated physiologic resistance to the descent of the feces (Fig. 54).

2. Congenital hyperplasia of the rectal valve is a condition classically described as diaphragmatic stricture or membranous septum in the abdominal rectum.

3. Hypertrophy of the rectal valve constitutes the classic annular stricture of the abdominal rectum.

THE SYMPTOMS.

The patient is the subject of more or less chronic obstipation, he sometimes makes frequent partially successful attempts daily at defecation, but may experience an unrequited desire for stool. The patient acquires the reprehensible physic-habit. In time the periods of obstipation are interrupted by diarrhea. There is an ineffectual straining at stool except for fluid feces. Later the diarrhea occurs with greater frequency, and ultimately long periods of diarrhea may ensue which are interrupted by a transitory constipation and obstipation. All these symptoms may be accompanied by increasing degrees of flatulence and borborygmus, and from time to time the patient is subjected to attacks of intestinal autointoxication, and finally he becomes neurasthenic. On account of the especial nonsensitiveness of the rectal valve the patient’s sufferings are not uniformly referred to this region by himself, but in many instances, however, the intelligent patient is prepared to present his physician with a ready-made diagnosis of rectal obstruction. Finally, the symptoms of intestinal obstruction become pronounced, and if the patient be unrelieved the disease proceeds to a fatal termination. Symptoms of pain, aching in the sacral and iliac regions, hemorrhage, proctorrhea, prolapse, hemorrhoids, fistulas, etc., are usually the signs of concomitant sequels of the hypertrophied valve, and these may embrace the entire proctica. For a classic graphic description of the symptoms of rectal stricture, which has never been excelled, the reader is referred to the paper by Dr. Sherwin published in the Transactions of the London County Medical Society in 1787.

PATHOGENESIS.

1. Obstructive anatomic coarctation of the normal rectal valves is a fortuitous embryonic affair, and admits of no amplification in this section.

2. Prenatal hyperplasia: The fibrous and muscular laminas of the rectal valve are developed from the mesoblastic layer of the blastoderm and the mucous membrane is derived from the hypoblast; this latter layer consists of columnar epithelium, and epithelium of this character may be found covering both superior and inferior surfaces of congenital diaphragmatic strictures or membranous septums. When there exists an aperture in this character of stricture it is seldom or never situated centrally. Another distinguishing feature of this obstruction is that it constitutes a cephalad boundary to a rectal chamber. If the lowermost valve be deformed, and if it be situated unusually low down, the lower rectal chamber may be noninflatable. In such an instance the anal or fixed rectum may seem to be of an extraordinary length, but that such is not really the fact may be determined by digitally ascertaining the situation of the anal borders of the levatores ani muscles. Such a stricture has its origin, probably, in the embryonic hyperplasia of the rectal valve. Another form of diaphragmatic stricture is sometimes observed at the anus. It has its origin in an imperfect anorectal coalescence. The salient structures of this septum are hypoblastic enteron and epiblastic proctodeum, and a microscopic inspection of a portion of membrane taken from its inferior surface reveals its epiblastic origin. This anorectal septum is of variable thickness, if there be a perforation it is located centrally. This character of stricture is always situated caudal to the rectal chamber. It is due to an arrest of fetal development.

3. Postnatal hypertrophy: Inflammation of the normally formed rectal valve, infiltration of lymph through its structures and organization of the plastic exudate contract and fix in a state of contraction this normal projection across the lumen of the rectum and constitute the nonmalignant annular stricture of this organ. Abnormal increase of fibrous tissue from any cause may, without contracting the valve-strait, render the valve sufficiently inelastic as to constitute it an obstruction. Extension of the inflammatory processes to an adjacent valve or a general hypertrophic rectitis involving an area occupied by several valves, consequent contraction of the longitudinal muscular bands in the area involved, together with contraction of the circular muscular bands, the infolding of masses of the lax mucous membrane, and the infiltration of plastic lymph into all these tissues between the valves as well as into the valve structure itself, organization of the exudate, degeneration of the muscular elements and increase of fibrous tissue, is the probable sequence of morbid processes which establish the nonmalignant tubular stricture of the rectum. The great thickness of the gut-wall at the situation of the tubular stricture is ordinarily not a new product of the disease. It is the consequence of the infolding of the mucous membrane, fixed in longitudinal corrugations by the organization of the plastic exudate.

The causation of hypertrophy of the rectal valve may be direct infection; a rectitis, dysentery, chancre, chancroid, gonorrhea; or traumatism, irritation or injury by a foreign body; the irritation of scybalums; or, it may be the local expression of some constitutional dyscrasia; syphilis or tuberculosis. The influence of age or of emaciation, through atrophy of the cellular tissues and the hypertrophy of the fibrous, may contribute a relative increase to the tendinous feature of the rectal valve.

Because of the absence of the rectal valve in the rabbit, cat, dog and monkey it was found impossible to do vivisection work for the production of an experimental stricture.

There are many specimens of hypertrophied rectal valves to be seen in the metropolitan museums in Europe, none of which, of course, are classified as such. The cases quoted below were copied by me from the catalog of the Pathological Museum of the Royal College of Surgeons, London, and the specimens which are pictured here may be found on their shelves. These cases are chosen for illustration because their accessibility affords the reader an opportunity for their verification. The pictures were drawn under my direction by Mr. Godart with the aim of illustrating this essay. The specimens immersed in preservative are sealed in cylindric glass jars of the usual laboratory type. Each of these we set into rectangular vessels of water to overcome refraction-errors and afford accurate appearances.

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