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A System of Practical Medicine. by American Authors. Vol. 2 · William Pepper — chapter 147 of 249 · ~2,859 words · public domain

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PROGNOSIS.--Intestinal cancer always proves fatal. Death may result from the debility resulting from the cancerous cachexia or from intestinal occlusion or from peritonitis. The duration of the malady is usually not long. It runs its course in from several months to one, rarely to two, years.

{874} TREATMENT.--Treatment must be directed to the alleviation of the distress caused by the disease. No curative treatment is known. When the cancer is situated in the colon, especially in the sigmoid flexure, the operation for artificial anus often affords great though temporary relief. The diet should consist of such articles in the digestion of which a large residue is not formed. Milk, eggs, soups, etc. should compose the principal articles of food. Mild laxatives will be required to secure the proper evacuation of the bowels, and to relieve pain and discomfort opium is invaluable and should be freely used. When obstruction is imminent nutrient enemata afford the most efficient means of administering nourishment.

Lardaceous Degeneration of the Intestines.

SYNONYMS.--Albuminoid degeneration, Waxy degeneration, Amyloid degeneration, etc.

Lardaceous degeneration of the intestines is an affection of quite frequent occurrence in those persons who are the subjects of a like change elsewhere; for although it has been asserted that it may be present as a primary affection, it almost always succeeds the same form of degeneration in other organs. Since, for the most part, it only makes itself manifest at an advanced stage of the disease, its importance is usually masked by the grave constitutional condition of the patient, whose vital forces are wellnigh exhausted by the already advanced degenerations present elsewhere. The extensive implication of other organs and tissues in the same degenerative process also creates great obscurity in the symptomatology of intestinal lardaceous disease, and is doubtless the cause of the existing dearth of definite knowledge upon the subject.

That the intestines are comparatively frequently involved in lardaceous disease is shown by dead-house statistics. Thus, Charlewood Turner reported from the London Hospital that in 58 cases of lardaceous disease the intestines were affected 10 times; and Goodhart in 150 consecutive necropsies of lardaceous disease at Guy's Hospital reported implication of the intestines 63 times.

Although the bowels do not become affected as early as several other parts, they will almost certainly become involved should the patient's life be prolonged; and in those cases where death is a direct result of the degeneration the intestines share with the kidneys the chief responsibility. It is not, however, until an advanced stage of lardaceous degeneration that its presence in the alimentary canal is revealed by symptoms; indeed, many cases do not, throughout life, betray evidences of the pronounced alterations that are to be discovered after death. Even in extreme cases there are no symptoms that would, even with probability, be referred to lardaceous disease of the bowels in the absence of the same degeneration in other organs and parts. There are, then, no specific symptoms following lardaceous degeneration of the bowels.

Where the normal functions of the intestines can no longer be properly performed in consequences of the changes that have taken place in them, there results a moderate diarrhoea. At first the number of movements {875} may not be increased; the evacuated matters are fluid and of a greenish or pale color. Usually, little or no pain is experienced, though at times and in certain individuals this may be severe and colicky. The diarrhoea is not always steadily progressive, but may from time to time disappear. With the progress of the disease it may become more free and persistent, and in the later stages hemorrhage from the bowels may be superadded. This may vary in amount, and where, as is often the case, the stomach participates in the degeneration, hæmatemesis may also appear. These hemorrhages may be insignificant, or may at once assume alarming proportions, and even bring to an unexpected termination the life of the individual. Already, at the outset of the intestinal symptoms, the general health will have shown evidences of profound alteration, but upon the supervention of the diarrhoea more rapid progress will be observed, consequent upon the increased nutritive disturbance. The use of remedies in temporarily controlling this diarrhoea may prolong for months the life they are powerless to save.

So far as concerns the intestinal affection, there is no special tendency toward febrile excitement. It must not be forgotten, however, that acute inflammatory attacks of various tissues and organs frequently arise in the course of lardaceous disease.

Though there seems to be reason to believe that mild degrees of lardaceous degeneration may sometimes be cured, especially when dependent on syphilis, there is but little hope of arresting its progress at the late stage when the bowels become implicated. Indeed, when pronounced degeneration of the bowels takes place the disease is usually nearing the end of its course; for it is a well-settled fact that in this degeneration extensive implications of organs may occur without markedly reducing the patient's general condition, so long as the kidneys and intestines remain unaffected. The cause of death is usually to be traced to these organs. Dickinson found that in 35 cases where death was apparently due to renal lardaceous disorder, the immediate result was brought about by diarrhoea in 13 cases. Presumably, in a large proportion of these lardaceous disease of the bowel was present.

The degeneration usually affects the lower portion of the small and the upper part of the large intestine. Occasionally it will be found to have invaded the whole alimentary tract. As in lardaceous degeneration generally, the process begins in the small arteries and capillaries and veins, affecting primarily the arterial and venous muscular coats--not, however, according to the latest authorities, the muscular fibres themselves, but their perimysium and the cement substance, the degeneration being one limited to the connective tissues. In the mildest cases only some of the small vessels of the mucous membrane are involved, and no naked-eye changes can be detected. In more advanced stages the mucous membrane is pale and shows evidence of catarrh. Thickening occurs, and as the process advances a peculiar appearance is revealed which has been compared to that of wet wash-leather (Wilks). The iodine test now gives the mahogany-colored reaction of lardaceous matter, with the tissues affected, or, if the methyl-aniline-violet test of Cornil be employed, the lardaceous material will display a red-violet color, while {876} normal structures will be tinged blue-violet. It is said to be better to make the test near a Peyer's patch, since the latter is seldom affected by the degeneration, and brings out, by contrast, the surrounding lardaceous material. This distribution of the material cannot be considered as constant, however, since Hayem found the patches of Peyer most frequently affected.

In more advanced stages the surface may become irregular from glandular enlargement, and ulceration may occur. Microscopic examination shows the lardaceous material in the vessels, and also in the stroma of the mucous membrane and villi. The epithelium is not involved. The degeneration, at first confined to the mucous membrane, extends to the submucous tissue, the proper muscular coat of the intestines being often implicated--so far, at least, as concerns its connective tissue. In the more severe cases Hayem found the agminated and solitary glands extensively involved. Fine branches from affected vessels penetrate to the interior of the glands. In such cases the mesenteric glands will be found implicated. The degeneration of the vessels running through the gland structure causes disappearance of this substance by fatty degeneration, and occasions a reticulated arrangement of the lardaceous material, and, secondarily, ulceration. In a similar manner ulcers may arise in any part of the affected tract. Finally, the lardaceous material may involve the whole thickness of the gut.

The diagnosis of lardaceous disease of the bowels can only be made with certainty in the presence of pronounced albuminoid disease of other parts in association with the symptoms of intestinal disorder. It possesses no characteristic symptoms.

Inasmuch as the disorder invades the bowels only at a late stage of its existence, the prognosis acquires additional gravity. It is probable that advanced albuminoid disease is never cured; so much the more hopeless is it when affecting this tract. If unchecked, the diarrhoea rapidly saps the powers of life; if temporarily alleviated, the approach of death is more gradual.

Whatever attempts are to be made to cure the disease, they must be through the general system, and are identical with those directed toward the cure of lardaceous disease generally. Treatment directed to the intestines must be palliative. The diarrhoea must be combated by appropriate diet and the administration of such remedies as protect the surface of the mucous membrane and control the intestinal movement. Bismuth subnitrate in large doses is therefore indicated. Various astringents may be employed, while the use of opium often secures most gratifying relief. It should be given in generous doses. Preparations of the crude drug seem to answer better than its salts. The necessity of keeping the gut free from undigestible matters that may irritate the already badly-damaged mucous membrane is apparent. Patients with this form of lardaceous degeneration usually show the cachexia resulting from profound modifications of nutrition, and their intestinal symptoms can only be regarded as links in a long pathological chain. Hemorrhage will call for remedies that under ordinary circumstances are employed to control bleeding from the bowels.

{877}

DISEASES OF THE RECTUM AND ANUS.

BY THOMAS G. MORTON, M.D., AND HENRY M. WETHERILL, M.D., PH.G.

Diseases of the inferior and terminal portion of the large intestine may be divided into primary and secondary--the former when the morbid cause is local and independent of disease elsewhere, the latter when it is consequent upon or incident to some other bodily affection. Among the primary lesions may be classed congenital malformations, prolapse of the rectum, hemorrhoids, and some varieties of new growths; also diseases caused by local irritations, infection, or traumatism, such as proctitis, ulceration, fissure, non-malignant stricture, chancroidal invasion and primary syphilis, including obstruction of the bowel by impacted feces and foreign bodies. Thread-worms and various cutaneous eruptions about the anus may also be included among the causes of the primary diseases of this portion of the alimentary canal.

The secondary affections are quite numerous, and may be caused by direct extension of disease from the colon, as in the dysentery following typhoid fever, and follicular enteritis, or entero-colitis of children; by contiguity, from diseases in neighboring organs--e.g. ischio-rectal abscess causing fistula--or by changes in the nervous or vascular supply, such as is seen in spasmodic contraction, paralysis, epidemic dysentery, cholera, and the action of certain remedies.

The rectum, the third or terminal portion of the large intestine, has no sharply-defined upper limits: it is usually understood to begin at the sigmoid flexure, opposite the left sacro-iliac symphysis; it is from six to eight inches in length and terminates in the anus. As the sigmoid flexure is the narrowest portion of the colon, so the calibre of the first part of the rectum is narrower than the portion below, where it gradually becomes more commodious, and near the anus presents a peculiar condition of the walls which gives it a capacity for remarkable distension. The rectum, which is somewhat cone-shaped, in its anatomical and pathological characters retains those of the large intestine with slight variation. Upon the upper or first part of the rectum the duplicature of the peritoneum is continued, forming the meso-rectum, which invests the bowel, attaching it to the sacrum. Below this the middle portion of the rectum (extending to the tip of the coccyx) is attached to the sacrum by connective tissue only, but also has a peritoneal investment on the upper portion of its anterior surface.

{878} The third or terminal part of the rectum, which is only an inch and a half in length, and is entirely without peritoneal covering, terminates at the anus. The circular and transverse muscular fibres, mucous crypts, and appendages throughout the rectum are identical with those above, except that the general muscular tunic is thicker; but the longitudinal fibres are less distinctly aggregated into bands than in the colon, being disposed in a more uniform manner, except that, like the circular fibres, they are especially aggregated between the sacculi. The fact that the meso-rectum limits the mobility of the upper and more narrow part of the rectum has led some to locate a third sphincter at this point, but the existence of such an organ has not been generally admitted. Van Buren characterizes it as an organ which "anatomy and physiology had been equally unsuccessful in assigning either certainty of location or certainty of function."

The anus guards the outlet of the bowel by its double sphincter muscle, which under normal circumstances affords voluntary control, within certain limits, over defecation. The well-known peculiarity of the vascular supply, a sort of erectile tissue being formed by the inferior hemorrhoidal plexus and the passage of some of the efferent veins through the sphincter muscle, by which they are subjected to pressure, is very favorable to the development of certain forms of disease which will be considered among the local disorders. As embryology has thrown considerable light upon the pathology of morbid growths by demonstrating relationships that were previously unsuspected, so a consideration of the development of the lower portion of the intestinal canal may lead to a better understanding of some of its diseases, especially those which are symptomatic or secondary. In early foetal life the third division of the primitive intestine, the pelvic portion, terminates in a cloaca in common with the urachus; subsequently, about the eighth week, a partition (the perineum) is formed which divides the cavity into two portions, the uro-genital sinus and the anal cavity. In the mean time, at an early period a depression occurs on the cutaneous surface at the site of the anus, which deepens progressively until it encounters the primitive intestine, with which it unites at the end of the fourth week, and the continuity of the tube becomes established. It therefore is seen that the rectum in its upper and middle portions is derived from the internal and middle layers of the blastodermic membrane, while its lower third, with the anus, like the buccal cavity, is formed by the external and middle layers.

In its diseases, then, the greater part of the rectum would seem to naturally participate in those of the large intestine, to which it structurally belongs, while its inferior portion and the anus would partake more in the disorders of the general cutaneous system. This peculiarity of development also explains the difference noticed in the vascular supply. The rectal veins are usually divided, like the rectal arteries, into three sets--superior, middle, and inferior. They are arranged so as to form two distinct venous systems, the rectal returning its blood through the inferior mesenteric veins into the portal system, the anal terminating in the internal iliac. The first system is made up of the superior hemorrhoidal, the second of the remaining veins.

The superior hemorrhoidal forms a venous plexus which surrounds the {879} internal sphincter muscle; the inferior hemorrhoidal vein also forms a plexus, but it is subcutaneous and principally below the inferior border of the external sphincter.

There are, however, a number of communicating branches passing along the walls of the rectum from one plexus to the other. The internal hemorrhoidal veins also communicate freely with the branches of the internal iliac around the trigone of the urinary bladder by means of small vessels, which pass through the prostate gland and seminal vesicles. By this method of anastomosis some relief is afforded when there is an obstruction in the portal circulation, which is such a common cause of turgescence of these veins, often resulting in permanent dilatation or hemorrhoids.

At the lower part, or at the junction of the middle and lower third of the rectum, the internal circular fibres of the muscular coat of the intestine become quite numerous, forming what is called the internal sphincter muscle; it is nearly an inch in breadth, and completely surrounds the lowest part of the rectum. It is about an inch above the margin of the anus; its muscular fibres are of the involuntary or unstriped variety; in function it assists the external sphincter in closing the anus and preventing the involuntary escape of the contents of the bowel.

The external sphincter lies directly under the skin and upon the internal sphincter and the levator ani muscle; its fibres encircle the anus: arising from the coccyx, they are inserted into the tendinous centre of the perineum, joining the transversus perinæi, the levator ani, and accelerator urinæ muscles. The sphincter ani is constantly in a state of tonic contraction, but the force of its contraction may be voluntarily increased. In the skin and superficial fascia are found minute branches of the pudic and small sciatic nerves; in the ischio-rectal space the internal pudic nerve; crossing about the centre are the inferior hemorrhoidal nerves, which are distributed to the anus and the lower portion of the rectum; the perineal nerve is especially distributed to the anterior part of the anus.

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