INTESTINAL OBSTRUCTION TREATMENT BY REENFORCED SIPHONAGE A MODIFICATION OF WANGENSTEEN'S METHOD JOHN
L.
CARMICHAEL, M.D., AND
Visiting Surgeon, Birmingham Baptist, St, Vincent's and Hillman's Hospitals
J.
L.
GUFFY, M.D.
Resident in Surgery, Birmingham Baptist Hospital
BIRMINGHAM, ALABAMA
HE use of the duodenal tube as a means of combatting abdominal distension in postoperative obstruction and other abdominal conditions was extended greatly by Wagensteen's1,2 apparatus described below, Fig. 2. A modification of this by one of us (J. L. G.) proved so useful in a case of postoperative obstruction that we believe it warrants reporting and a discussion of some of its mechanics The intestinal tract is composed of approximately twenty-three feet of small and nine feet of large intestine. It has been estimated that normally about 8000 c.c., or approximately eight quarts, of digestive fluids and other secretions are poured daily into this tract. Most of this fluid empties into the first few inches of the small intestine. In the upper intestinal tract digestion is more abundant and absorption is less; but as the contents pass downward, digestion decreases in activity and absorption occurs at an increasingly greater rate. The large bowel is concerned chiefly with the absorption of water and the discharge of solid waste material. The stoppage of intestinal flow past any given point in this tract is a simple but accurate definition of intestinal obstruction. This blockage may be accomplished in three ways: (I) a mechanical closure of the intestinal lumen, as adhesions in peritoneal inflammations, intussusception, volvulus, etc.: (2) a paralysis of the intestinal muscles as in paralytic or adynamic ileus; and (3) closure of the lumen of the bowel from a localized spasm of intestinal
T
muscle, a condition known as dynamic ileus. This latter is rarely seen and is usually limited to cases of lead poisoning. In early postoperative obstruction which occurs within the first two weeks foIIowing operation, the usual cause is the closure of the intestinal lumen in one or more areas by the formation of constricting bands of adhesions. Strangulation is rare because the constricting bands are not firm enough in two weeks to cause the blood supply to be shut off from 'a loop of bowel. Another cause of postoperative obstruction is paralytic ileus which may occur alone but is more apt to be associated with the other form of obstruction just mentioned. The unusual forms of obstruction, such as those due to mesenteric thrombosis or to embolism, are not considered in early postoperative obstruction as they are rare; and when they do occur the results are usually fatal regardless of the method of treatment. One is nearly always justified in treating early postoperative obstruction expectantly. If the integrity of the intestinal wall is maintained for four or five days after the diagnosis of obstruction is proved, it can be accepted that the natural reparative processes will reestablish the continuity of the bowel lumen. As soon as there is an obstruction, regardless of the cause, the intestinal fluids accumulate in the proximal portion of the intestine. As distention and peristalsis increase, the rate of secretion is acceIerated. 3 ,4 If the obstruction is high, there is little absorption of the secretions and the clinical signs of obstruction; i.e.
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cramps, intestinal borborygmi, nausea and vomiting occur early. When the obstruction is low in the intestinal tract there is a
FIG. r •.
considerable absorption of the secretions before distension becomes pronounced; and the signs of obstruction, particularly the nausea and vomiting, occur late, occasionally as long as four or more days. The pouring of fluids into the intestinal tract at the rate of 8000 c.c. in twenty-four hours causes an appalling dehydration if this fluid is not reabsorbed, regardless of whether or not it is vomited. This constitutes the first real danger in obstruction and suggests one of the vital steps in its treatment, the supplying of sufficient fluids. Since this fluid loss also includes an excess of chloride or other acid ions, these should be supplied in the replacement fluid, otherwise an alkalosis will result. 3 ,5,6 This is done best by intravenous or subcutaneous normal or slightly hypertonic saline solution. Sodium bicarbonate solutions are definitely harmful, proved by a priori reasoning and experimental data. Another great danger met in intestinal obstruction because of the distension, is impairment of circulation in the bowel wall even to the point of gangrene. In combating this distension and thus preserving the integrity of the bowel wall the Wangensteen method of reenforced siphonage has found its place. The indwelling duodenal tube has been used for a considerable time. One of its
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chief faults, however, was the irregularity with which it worked. The principle of the siphon explains its unreliability for work. As soon as the outer limb of the siphon (duodenal tube) was filled with air or gas from the intestinal canal the suction stopped, as the reason for the suction was the weight of the column of the liquid in this outer limb of the tube (see Fig. I, na). For this irregular pull in the outer end of the duodenal tube the Wangensteen apparatus substituted the constant pull from the weight of the column of water in that portion of the tube from bottle B to bottle A, Fig. 2, designated as ba. The net suction force would be determined by the weight of a column of fluid equal in length to the distance da, Fig. 2. In other words the difference lies between the level of the duodenal end of the tube and the level of the water in bottle A. On setting up this apparatus in the treatment of the case reported, one of us (J. L. G.) suggested that a third bottle inserted between the patient and the inverted bottle B, would relieve the patient of the annoyance of watching the unseemly contents of bottle B. This bottle (bottle c) was inserted as indicated in Fig. 3. A study of the modification reveals a considerable change in the mechanics of the instrument. In the Wagensteen apparatus the net suction force is always the weight of the column of liquid in the tube from the level of the end of the tube in the duodenum to the level of the liquid in bottle A. This is designated in Fig. 2 as da. This force remains constant regardless of the height of bottle B, and is the same as the suction force in the simple duodenal tube as long as the latter remains filled with fluid. However, in the modified apparatus, Fig. 3, it can be seen that changing the level of bottle B changes the net suction force by a corresponding amount. To compute the suction force obtained by this apparatus we have to add to the weight of the column of water ba, Fig. 3, the net suction force obtained in that part of the apparatus beginning with the tube
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in the duodenum and ending at bottle c. The net suction force here is represented by the weight of the column of water dc,
FIG.
2.
Fig. 3. It will be noted that c designates the end of the tube from the duodenum and not the level of the water in bottle c as should be the case if this tube end were under the level of the water in bottle c as it is in Fig. I. This computation is only approximate since no cognizance is taken of such factors as friction in the tubes or the weight of the air or gas in the tube from bottle c to bottle B, Fig. 3, or the differences in specific gravity between water and intestinal fluids. These, however, are negligible factors. It will be noted that the net suction force in this new apparatus is the column of water, ba, plus the column of liquid, de. Any increase in the height of bottle B will correspondingly increase the amount of this suction force. There is no likely need for the greater suction provided in the modified apparatus; but when the modified apparatus is used it is well to be acquainted with the change in mechanics involved in the altered apparatus. The case in which this modified instru-
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ment was first used by us is reported. Mrs. J. W. T., white, female, age fortyone years, was admitted to the Baptist
FIG. 3.
Hospital, Birmingham, Alabama, July 22, 1933, at 5 :00 P.M. Her chief complaint was a delayed menstrual period, accompanied by sharp pains in the lower abdomen; with onset in the left side and at first referred to the lower bowel and rectum, then radiating across the lower abdomen. Her last menstrual period had begun June I, 1933. Two weeks before admission, she had had the first attack of the pain described and this was accompanied by the first menstruation since her June period, some five or six weeks before. This attack occurred while she was playing bridge. A second attack occurred six days later, awakening her in the middle of the night. The last attack similar to the others occurred the evening before her admission. Menstruation was not profuse with any of these attacks. She had had morning nausea for some weeks. On the day of her admission she had traveled in an automobile for more than one hundred miles. Upon entrance to the hospital she had profuse vaginal bleeding, accompanied by severe lower abdominal pain.
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Her past history was unimportant except for typhoid at twenty-two years of age and a left hernioplasty at thirty-six. The family history was irrelevant. Her menstruation had begun at thirteen and was irregular until she was twenty-one. After that time its occurrence was at twenty-eight-day intervals and its duration four or five days. She was married at twenty-three. There had been only one pregnancy, which terminated normaIIy at fuII term during her twenty-fourth year. At the time of our examination she was comfortable from 0.25 gr. of morphine. She was not in shock and did not appear anemic. The pulse was 86 and her general physical condition seemed good. Three hours after admission the pulse rate increased and she presented other signs of early shock. A diagnosis of ruptured ectopic pregnancy was made and operation was done immediately. The abdomen was fiIIed with blood. The left tube, dilated in its outer half was removed with a mass of blood clot and yeIIow spongy tissue, as weII as a considerable quantity of blood. The abdomen was hurriedly closed with drainage. An infusion of 1000 C.C. of normal saline was given during operation and was repeated every six to eight hours for several days. A transfusion was given within a few hours after operation. On the third postoperative day fecal vomiting began and was accompanied by excruciating pain and abdominal distension. No bowel movement could be obtained. It was felt that there was an obstruction due to fibrinous bands of adhesions which were holding the intestinal loops together and constricting them. On the fourth day after operation suction siphonage was instituted with the described modified Wangensteen apparatus, Fig. 3. This was attached to a nasal tube, which
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had been inserted the third day after operation. With the apparatus attached, the patient was aIIowed to drink water freely. However, 3000 to 4000 C.c. of saline and glucose solutions intravenously or by hypodermoclysis were continued daily. The obstruction was relieved on the fourth day after suction siphonage was instituted, and the nasal tube also removed. Her convalescence was normal afterward and she was discharged from the hospital on the fourteenth postoperative day. We believe an enterostomy would have been necessary in this case if decompression of the obstructed and distended bowel had not been accomplished, thereby moving the intestinal toxins and keeping intact the blood supply to the bowel waIl. SUMMARY 1. The problems of postoperative intestinal obstruction are considered. 2. The use of reenforced siphonage as suggested by Wangensteen is discussed. 3. A modification of the Wangensteen apparatus is described and the physical principles of this and the original apparatus are presented. 4. The use of the modified apparatus in one case is reported.
REFERENCES
I. WANGENSTEEN, O. H. Therapeutic consideration in
the management of acute intestinal obstruction, Arch. oj Surg., 26: 933--961 (June), 1933. 2. WANGENSTEEN, O. H., and PAINE, J. R. Treatment of acute intestinal obstruction by suction with the duodenal tube, J. A. M. A., 101: 1532-1539 (Nov. I I), 1933. 3. DRAGSTEDT, L. R. Proc. Soc. oj Exp. Bioi. and Med.,
XXV; 239-241, 1928. 4. RAINE, F. and PARRY, M. C. Arch. oj Surg., 19: 478-511 (Sept.), 1928. 5. MORTON, J. J. Ann. oj Surg., 95: 856-877 (June), 193 2 . 6. DIXON, C. F. N. O. Med. and Surg. J., 85: No. n; 87--97 (Aug.), 1932.