BUFFALO MEDICAL JOURNAL.

VOL. LXII.

IN

JUNE, 1907.

ORIGINAL COMMUNICATIONS.

Obstruction of the Bowel.

BY MARSHALL CLINTON, M.D., Buffalo, N. Y.

No. II

N meeting with cases of obstruction of the bowel the physician is always confronted with the question as to whether the condition is one depending upon some acute inflammatory process, or due to some mechanical obstruction, gradual or sudden in its onset. Stenosis of the intestine or gradual narrowing of the lumen of the intestine is of slow development. Among the common causes of stenosis of the intestine we find stricture as a result of cicatricial contraction, malignant disease or, more rarely, benign growths within the bowel and compression from without, as pressure by a tumor.

Irrespective of the development of the stenosis itself we find that the symptoms may develop very gradually or may occur suddenly when the patient is in apparent health. The primary cause of all the fundamental symptoms of narrowing of the lumen is interference with the onward passage of intestinal contents. As soon as the passage of bowel contents becomes difficult, so that the normal peristaltic wave is insufficient to force these contents through the point of constriction, symptoms appear. The severity of the symptoms and the time of their appearance will depend largely on the location of the stenosis, as we know that almost complete obstruction may exist in the small intestine before any symptoms are noticed, while slight narrowing of the lumen of the large intestine, particularly the latter half, will be followed by early symptoms.

In stenosis of the large intestine and rectum constipation is an early symptom; gradually this becomes more intractable and patients complain of a feeling of distention and swelling in the abdomen; then of loss of appetite and occasional attacks of nausea. One of the characteristic early symptoms of stenosis of the large intestine are these alternating attacks of constipation followed

by diarrhea. After a time, irrespective of the location of the stenosis, paroxysmal attacks of colic occur. The time in the development of stenosis that colic appears varies widely, as hypertrophy of the bowel wall above the stenosed area will delay the onset of this symptom. Many patients complain of colic as the first symptom. The colic may be localised or diffused over the abdomen and even the chest, the colic being frequently accompanied by vomiting.

In all cases during paroxysms of colic absolute constipation exists. If the abdomen of a patient with stenosis be examined during a paroxysm, tonic contraction of the intestine, above the stenosis, may be seen and felt. The picture present on inspection of the abdomen is typical of this condition-that is, coils of intestine stiff from tetanic contraction, which rise above the level of the abdomen. The attacks of colic may recur after a few days or not for many weeks. When stenosis is far advanced and the attacks recur with great frequency, the abdomen remains permanently distended and the patient suffers from dyspnea. As stenosis progresses, attacks of colic occur every day until ultimately the symptom picture of complete obstruction develops. In cases of stenosis there is frequently a feeling of fluctuation on palpation, and occasionally distinct succussion sounds can be produced, particularly in the intestine above the stenosis.

When loops become much distended and filled with fluid the percussion note in the abdominal flank may be dull, changing its level with change in position of the patient as seen frequently in ascites. However, this may be differentiated from ascites by making rapid taps against the dull area, which will reveal distinct succussion sounds. To attempt to differentiate clinically between the various forms of stenosis of the bowel, is too hard a problem to be readily mastered. We know, however, that irrespective of the cause of the stenosis this condition generally tends to result in complete occlusion. Given then any case in which we find the prominent symptoms as outlined, we are reasonably sure that unless that patient is relieved, there will ultimately result an occlusion or, as it is more commonly known, an acute intestinal obstruction.

Surgical experience and medical practice show no class of cases more to be dreaded than that of acute intestinal obstruction. The mortality under any method of treatment is alarmingly high. Surgical intervention in a developed case of intestinal obstruction is the best hope these patients have; and unless this be offered to them at an earlier period than happens commonly, our statistics will not improve. No accident as a post-operative complication, except peritonitis, is so feared as this.

In the majority of post-operative obstruction cases of course a localised or general peritonitis is the initial cause, and the subsequent obstruction is but a part of the symptom complex. This is shown in every case of peritonitis that goes progressively from bad to worse. It is undoubtedly extremely hard at times. to differentiate between cases of post-operative intestinal obstruction due to peritonitis, and cases in which peritonitis develops secondarily to a mechanical obstruction.

In following post-mortem work it has often chanced that a patient has been thus examined, who died of a post-operative obstructive lesion with a secondary peritonitis, when the history. of that particular case showed that the patient had been treated as one suffering from a spreading peritonitis and not as a case of intestinal obstruction. It is important to remember that in every case of intestinal obstruction the symptoms are not due simply to the interruption of the flow of intestinal contents through the bowel. Complications, such as circulatory disturbances in the intestinal wall and mesentery and alterations in functions of these structures, are in large measure responsible for the symptoms seen.

As soon as the occlusion of the bowel occurs the appetite is lost, and the patient begins to complain of nausea and belch gas. Nausea persists until vomiting finally occurs. At first the stomach contents are vomited mixed with bile, and then fecal vomiting occurs. Fecal vomiting is only absent in very acute and very rapidly fatal cases of strangulation of the bowel. In these cases death ensues before the formation of feculent bodies can occur in the upper intestinal tract. The act of retching and vomiting determines whether fecal vomiting occurs and not the antiperistaltic movement of the bowel; for cases may go on to fatal termination with the entire gastrointestinal tract filled with fecal material, while no fecal vomiting may have occurred.

As an illustration of excessive retrostalsis in a case of incomplete obstruction, with a spreading peritonitis, the writer has seen an olive oil enema vomited up several hours after its injection into the rectum. With the onset of early pain which is so often seen, an evacuation of the bowels may occur, associated with a great deal of tenesmus; all of the expelled material coming from the lower bowel, beyond the point of obstruction. This symptom is often misleading as naturally an obstruction of the bowel is not suspected when a bowel movement occurs. After this movement, however, nothing further passes the bowel as the result of either cathartics or enemata, unless it be a little fecal material mixed with the enema that has over-distended the rectum. No flatus or real feces from now on are passed; the

belly begins to distend, the distention depending upon the anatomic character of obstruction and its situation in the intestine.

At this time the most serious symptom may develop,-that of shock and collapse. The face of the patient becomes distorted with pain, and a frightened expression appears; extremities become cold and bluish; pulse becomes rapid, small and compressible. Gradually the gastrointestinal symptoms increase in severity and hiccough becomes violent; nausea becomes very distressing and fecal vomiting continues. In addition the patient suffers from an unquenchable thirst; the abdomen becomes more and more distended; respiration becomes more rapid and shallow, and the patient is tortured with a terrible feeling of oppression. The urinary secretion is partially or completely arrested; the patient becomes weaker and weaker, and the picture is rendered more distressing by the fact that the mental condition is almost unaffected, while experiencing great pain.

In the last stages the skin is sallow and flaccid, cool, livid, and frequently covered with a cold sweat. The eyes of the patient are sunken and surrounded by dark circles; the face looks pinched; the nose sharp and pointed; the voice weak, and the pulse feeble and threadlike.

In the early stage the degree of pain the patient suffers depends largely upon the extent of the involved intestine; the larger the amount of intestine involved in the process the greater the pain. In acute obstruction of the small intestine, as a rule. there is more pain than in obstruction of the larger gut. The pain and obstruction is constant, as in peritonitis; is increased by pressure, remit. and becomes exacerbated, due to violent peristaltic movement above the point of obstruction. When pain ceases without relief of the obstruction it indicates a fatal ending.

One symptom that varies greatly in different parts is the increase in intraabdominal pressure. This occurs as a result of the distention of the gut, and as a result of the reflex action of the abdominal and diaphragmatic muscles. This increased pressure causes an embarrassed heart action, and also what is an extremely important matter, it may prevent the intestines from regaining their normal position, by reason of peristaltic pull. It favors the development of new areas of stasis so that a compromised bowel will be held as if in a vise, by this increased pressure. Some patients cannot recover after an obstruction is relieved surgically; this being the case particularly when there is a tremendous increase of abdominal pressure, unless this, in turn, be relieved by an enterostomy or colostomy.

In differentiating between the stenosis that occurs in normal or healthy gut and that which occurs as the result of a gradual

narrowing of the intestinal lumen, it should be remembered that in chronic stenosis we see the wave-like movement of energetic, resistant intestine against the belly wall; while in acute obstruction the abdominal wall will be tense, resistant, and rarely shows any intestinal movement. In intestinal strangulation the intestinal and peritoneal branches of the pneumogastric and the sympathetic are first stimulated. Irritation of these fibers leads to alteration of the heart's action and, by causing reflex paralysis of the cardiac branches of the pneumogastric and the splanchnic nerves, further produces alterations in the general distribution of the blood throughout the general circulation. When reflex paralysis of the splanchnics occurs there will be an enormous distention of the abdominal organs with blood. The temperature of the skin and the rectum is lowered until peritonitis ensues. This latter condition occurs by reason of the passage of bacteria through the wall of the intestine as soon as the bowel wall becomes edematous, or there is any interference with the local circulation.

The prognosis of acute intestinal obstruction depends on a variety of factors aside from the time it may be operated upon for relief. As a general rule, we may say that the life of these patients is not threatened so much by the interference with the onward passage of the feces and the intestinal occlusion, as by the symptom of collapse. Here is the key to the surgical prognosis of any operated case. If there is marked collapse and great increase in abdominal rigidity the patient's chances are extremely small, even if the condition has existed but a short time. On the other hand, patients may have an intestinal ob struction of several days and yet recover with operation. The most interesting although the most rapidly fatal case of acute obstruction that has come under the writer's notice occurred last August.

A young man, 26 years old, was seized with cramps in the afternoon about 2 o'clock. His condition did not improve under anodynes or enemas so about midnight he walked from his bed into an automobile, and was driven 22 miles to the hospital. He was seen by me at 4:30 A.M., after his arrival at the hospital and I found him in a state of collapse-no radial pulse: nausea, and vomiting: no abdominal rigidity, although there was slight distention and some pain on pressure. His condition did not warrant anything being done except hot packs, with small repeated doses of morphine and stimulants. His collapse did not let up for an instant and he died before noon. Total duration of illness, less than 24 hours. An immediate post-mortem showed an intusseption with over two feet of strangulated ileum in the cecum. There was no peritonitis whatever, except in the peritoneum lining the invaginated intestine. This represents one