Intestinal Obstruction.*

INTESTINAL OBSTRUCTION.* The Results of Recent Experiment applied to Clinical Practice. By IAN AIRD, Ch.M., F.R.C.S. Ed. {From the Surgery Research Department, University of Edinburgh.) Acute intestinal obstruction is so easily reproduced in the experimental animal that the study of its effects on the organism has been an important field in recent surgical research. From the thousands of animal experiments performed during the last ten years, a wide knowledge has been gained which has not yet enjoyed much application in treatment. For example, blood transfusion, unquestionably a life-saving measure as a preliminary to operation in cases of extensive strangulation, is not yet performed as a routine measure in such typical examples of this condition as superior mesenteric thrombosis and volvulus of the newborn, and saline administrations for high obstruction are still inadequate, haphazard and uncon- trolled, though they are capable of easy standardisation. Since the beginning of this century the operative mortality in cases of intestinal obstruction has remained steady at the high level of 40 per cent. The time seems overdue for a reconsideration of our present treatment, and for a close examination of the wealth of experiment at our disposal for modification or elaboration of that treatment. The present paper is an attempt to relate to clinical practice those recent experimental findings which seem immediately applicable. Classification of Acute Intestinal Obstruction.?The following classification of acute intestinal obstruction is simple and inclusive :? A. Simple occlusion. (i) High small intestine obstruction ; (ii) low small intestine obstruction ; (iii) colonic obstruction. B. Closed loop obstruction. (i) Loops with sterile content ; (ii) loops with heavily infected content ; (iii) loops with mildly infected content. PapCr iS a condensation of the author's thesis, "The Morbid Ph lysio*-ThlS ogy of Intestinal Obstruction," submitted for the degree of Master o urgery of Edinburgh University and sustained and highly commended by the Senatus. 375 Ian Aird C. Strangulation. (i) Sudden anaemia ; (ii) venous congestion (a) short loop, (b) long loop, (c) loops of medium size. D. Neurogenic obstruction. (i) Spastic ileus ; (ii) Adynamic (paralytic) ileus. It must be understood that these categories are purely arbitrary. While pure forms of these varieties of obstruction can be produced experimentally, in clinical practice pure forms are rare. In a clinical case of short loop strangulation, for instance, is the strangulated loop coincidentally a closed loop ; above the strangulation, the bowel dilates as above a low simple occlusion ; ultimately the distention involves the duodenum, and in a single case the effects of strangulation, closed loop low obstruction, occlusion, and high occlusion may be present in together varying degree, and demand in treatment a multiplicity of methods. A. Simple Occlusion.?(i) High Intestinal Obstruction.?As a result of the work of Wilkie, Haden and Orr, Draper-Maury, and Elman Hartmann, and a host of others, it is now recognised that all the phenomena of high intestinal obstruction are dependent on the loss to the organism of water and of inorganic ions which, poured into the stomach and duodenum in enormous as quantities digestive juice, fail to pass beyond the obstruction to be reabsorbed, as they are in the absence of obstruction, by the intestine below. The heavy and progressive loss of water leads to an increasing dehydration, whose degree can be measured clinically by the dryness of the patient's skin, the increasing thirst, and the diminution in the output of urine. The blood becomes increasingly concentrated, the erythrocyte and the count haemoglobin rise, there is an increase in blood a viscosity, prolongation of the sedimentation rate, and a reduction of the total blood volume. The accompanying loss of the inorganic ions of the gastric, pancreatic, biliary and duodenal juices leads to a lessened electrolyte content of the blood, and a fall occurs in the blood chlorides, the blood sodium, and the blood potassium. An attempt is made by the organism to maintain the choloride level by the complete retention of the chlorides from urine, and by a passage of chlorides from to the the tissue fluids blood. Even these measures fail to keep the loss of pace with chloride in the digestive juices, yet the 376 A Intestinal Obstruction electrolytic content of the blood must be maintained, and the lost chloride must be replaced by some other electrolyte. The only electrolyte on which the organism can draw to an almost unlimited degree is bicarbonate : as the blood chloride falls, the bicarbonate content rises, and alkalaemia results. (That the alkalaemia is not due purely to loss of acid in the gastric juice is clearly demonstrated by the continued rise in alkali reserve of the blood, even in the later stages of high obstruction when all free acid has long disappeared from the vomitus.) Coincident and parallel with the fall in blood chloride is a rise in the non-protein nitrogen and blood urea. This increase in N.P.N, is not wholly explained by the increased concentra- tion of the blood by dehydration, nor by the diminished output of urine, for the total twenty-four hour urea output may be actually increased. It is probably due to increased cell destruction in the parched tissues, to increased breaking-down of protein molecules deprived of their water of hydration, and to an attempt to maintain the osmotic pressure of the plasma by utilising urea to replace some part of the lost chloride. All these phenomena?dehydration, hypochloraemia, alkalaemia, and azotaemia?thus depend primarily on the loss of water and sodium chloride in the digestive juices, and the most severe and rapidly fatal form of simple occlusion is where the obstruction is located directly below the entrance of the biliary " and pancreatic ducts?the lethal line of Draper-Maury." The severity of an obstruction and the rapidity of its course, vary inversely as its distance above or below this line. The symptoms of high obstruction can be exactly duplicated when the digestive secretions are drained by a complete duodenal fistula, or by pilocarpine salivation, or by apomorphine vomiting. In its pure form, high simple occlusion is best seen clinically in post-gastro-enterostomy vomiting and in acute duodenal ileus, but also in less degree in complete pyloric stenosis (congenital or acquired), in acute dilatation of the stomach, and in the very highest jejunal obstructions. In low simple occlusion, dehydration and hypochloraemia may be absent. If present, they occur only at a late stage, when the duodenum and whole small intestine are dilated, and vomiting is continual. The high obstruction of the clinician is the low obstruction of the experimentalist. The high obstruction of the experimentalist is hardly considered an intestinal obstruction by the clinician. Since the symptom complex of high (duodeno-jejunal) 377 Ian Aird occlusion is due to loss of water and inorganic ions, complete relief follows the administration of saline solution. Wilkie 33 first showed the value of saline in high obstruction, and a host of later workers have shown that an animal with a duodeno- jejunal occlusion can be kept alive indefinitely by the adminis- 18,14 tration of sodium chloride solution either parenterally or 23 into the bowel below an obstruction6' 22, provided the stomach be kept empty.16 Salts other than sodium chloride are useless. The diversion of digestive juices to the bowel below the obstruction by anastomosis also prevents dehydration and hypochloraemia and their sequelae. treatment of The duodeno-jejunal occlusion is well recognised?gastric lavage, the intravenous administration of saline, of and removal the obstruction or a short-circuiting operation only when dehydration and hypochloraemia are relieved. Two features of importance in this treatment have received insufficient attention. (1) Hypertonic saline solutions have no place in the treatment of high occlusion. The obstructed organism requires water as well as salt, and only physiological saline should be administered. That hypertonic saline may actually have a harmful effect will be shown later. The (2) quantities of saline given are still usually inadequate. A patient suffering from high obstruction may lose eight litres of fluid to (2 3 times the total plasma volume) in 24 hours, and can absorb no fluid taken by mouth. An intravenous infusion of 500 c.c. or even of a litre of saline is quite inadequate to replace this loss. Saline should be given until the blood chlorides closely approach the normal level. A safe technique of chloride restitution is to wash out the stomach and infuse two litres of saline intravenously on admission to hospital. The degree of hypochloraemia is then measured. If this is slight, immediate relief of operative the obstruction can be safely undertaken. If hypochloraemia is still considerable, saline administration should be continued by intravenous drip, and the degree of hypochloraemia re-estimated at intervals of two hours until the blood chlorides reach a safe level. What methods should be used to estimate hypochloraemia ? Such laboratory aids as estimation of blood chlorides, estimation of alkali reserve, estimation of non-protein nitrogen will give the degree of hypochloraemia, and a haemoglobin estimation will indicate the amount of dehydration, but these 378 Intestinal Obstruction methods are elaborate and not always convenient. Ready evidence

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