Ileus

ILEUS, intestinal obstruction; represents a condition in which an obstacle arises along the intestine preventing the passage of its contents. Left to its own course, I. depending on the type of obstruction leads in a shorter or longer period of time to severe phenomena threatening death. The study of all features of I. raises a number of complex problems and first of all the problem of classification. As a criterion for classification one can take 1) the etiological element, 2) the patho-anatomical element, and 3) the clinical element. A completed classification should group types of I., taking into account all these elements. From the point of view of rough etiology, one can distinguish 3 groups of I.: 1) congenital I. (I. congenitus), 2) I. based on congenital predisposition (I. praedispositus) and 3) acquired (I. acquisitus). Typical examples of congenital I. include atresia of the anus and its varieties, congenital narrowing of the duodenum and other types. Ileus based on congenital predisposition encompasses a rather large group of various forms caused mainly by abnormalities in the position and structure of different parts of the intestine. In connection with the doctrine of arterial-mesenteric obstruction of the duodenum, Melnikov studied the position of the said intestine and came to the following conclusions: anatomomechanical causes of obstruction in the upper segment of the duodenum can be caused: 1) by the mobility of the superior part of the duodenum and the imperfection of the form and position of the entire duodenum or 2) in a duodenum perfect in form and position-by adhesions fixing it in an unfavorable position (pathological type of form and position of the duodenum). Both positions of the upper horizontal part of the duodenum contribute to its bending when the stomach is full. If the bending as a result of fixation of the intestine by adhesions can be considered as a case of predisposition to acquired obstruction, then the bending of the same intestine due to mobility should be considered as a case of predisposition to congenital obstruction. The same applies to the lower horizontal part of the duodenum. According to Melnikov's data, the inferior part of the duodenum has no sharp bends, but along its anterior surface in the thickness of the mesentery passes the superior mesenteric artery, which as a rule on all specimens fixed in the supine position leaves an impression on the duodenum and presses its anterior wall to the posterior one. "In a series of specimens such an impression (impressio mesenterialis) is so significant that the entire part of the duodenum lying above is markedly dilated". From this it undoubtedly follows that arterial-mesenteric obstruction represents an I. based on congenital predisposition, and only its relatively rare manifestation is incomprehensible. - Researches of Kupryanov, a summary of data on the position of the large intestine by Melnikov fully confirm the observations of clinicians regarding the significance for obstruction of the large intestine of its bends-both the hepatic flexure of the colon and especially the lienal flexure of the colon. Obviously, a part of cases of I. of the large intestine belongs to the group of I. based on congenital predisposition, since I. is often caused by the sagging of the transverse intestine for example to the symphysis, and this sagging depends on the congenitally long transverse intestine (colon transversum longum congenitum). A long mesentery of the small intestine, a common mesentery of the ileum and cecum, a long mesentery of the sigmoid intestine serve as further examples of congenital predisposition to subsequent volvulus of the intestines, i.e. predisposition to one of the most severe forms of ileus. In addition to cases of congenital I. and I. based on congenital predisposition, many cases of acquired I. are known. This includes I. caused by inflammatory adhesions, neoplasms, especially malignant ones, tuberculosis, actinomycosis, syphilis and a whole series of other causes, up to spasm and paralysis of the intestines. When speaking of I. with congenital predisposition, one should remember that for the appearance of I. to the congenital-predisposing-element an acquired element causing I. is often added. For example, a long mesentery of the intestine predisposes to volvulus of the sigmoid intestine; however, for the occurrence of volvulus it is necessary that inflammation of the mesentery, its scar changes be added, i.e. an acquired element. Meckel's diverticulum is often accompanied by incarceration of the intestines and thus serves as a predisposition to incarceration. However, incarceration usually occurs when the diverticulum becomes inflamed (diverticulitis) and adheres either to the mesentery of the small intestine, or to the cecum, or to the abdominal wall, i.e. when the diverticulum forms a ring into which loops of the small intestine slip. Finally, incarceration can be caused by purely acquired conditions, such as the formation of inflammatory and gradually organized strands in the abdominal cavity. Patho-anatomical classification easily agrees with etiological. From the point of view of pathological anatomy one has to distinguish volvulus, internal incarcerations, bends of the intestines, their strictures of various nature and compression of the intestines by growing tumors (for example tumors of the mesentery). In each individual case to the patho-anatomical characteristic, if possible, it is desirable to add an etiological characteristic, noting whether I. is caused by a congenital condition, congenital predisposition or purely acquired. From the point of view of pathological anatomy a group of I. going with disturbance of mesenteric circulation and usually leading to hemorrhagic infarction of the intestine with outcome in gangrene is clearly distinguished. From the etiological point of view in these cases one has to be concerned only with clarifying the question of whether the circulatory disturbance occurred from embolism of the artery, from its thrombosis or from compression of the vessels (first of all veins) in the incarcerating ring or from twisting of the mesentery. It is more difficult to reconcile the etiological and patho-anatomical classification with the clinical one, since in the clinical classification one has to take into account the functional element as well. If the latter can be to a certain extent captured in the etiological classification, it cannot be captured in the morphological classification. Therefore for surgeons the clinical classification turns out to be the most valuable, which includes in itself the classification and patho-anatomical and etiological but builds upon them a superstructure important for understanding the processes occurring in the patient. From the clinical point of view one distinguishes first of all: 1) dynamic I. (I. dynamicus) and 2) mechanical I. (I. mechanicus). Dynamic in turn breaks down into a) spastic (I. spasticus) and b) paralytic (I. paralyticus). In the first the spasm of the intestine, most often of the small intestine, reaches such a degree that the lumen of the intestine disappears. In the second, on the contrary, the ability of the intestines to contract disappears, they fall into a state of paralysis. The most formidable form of paralytic I. is paralysis of the intestines in acute peritonitis. Since the time of Wahl (v. Wahl; 1889) in surgery the division of mechanical I. into a) I. due to strangulation (I. per strangulationem) and b) I. due to obstruction (I. per obturationem) has taken root. In Russia this classification was supported above all by Tseydler (1898) and Tseyge-Manteifel (1913), and many surgeons still use it. Yutsevich modified the classification; he calls I. per strangulationem loop obstruction (claustransae) and includes here all cases where together with the mesentery the loop also suffers, whether it is twisting of the loop together with the mesentery, its compression by a strand, incarceration in a hernial opening etc. I. per obturationem he calls lumen obstruction (devia luminis) and attributes to this category all cases with narrowing of the intestinal lumen (according to Studzinsky). Some surgeons are not satisfied with either Wahl's classification nor the more complex classification of Wilms and prefer to use in essence a purely patho-anatomical classification, distinguishing I. from volvulus, bend, incarceration, compression, adhesion, cancer etc. But with such a classification one omits one important moment which as a matter of fact Wahl wanted to capture-the moment characterizing a whole group of I. and consisting in disturbance of circulation. However Wahl's nomenclature is not quite successful due to the insufficiently clear characterization of individual groups. Oppel proposes to distinguish the following 4 groups of mechanical I.: 1) I. per obturationem, 2) I. per flexionem-compressionem, 3) I. per incarcerationem and 4) I. per torsionem. Intussusception (invaginatio), which in other classifications was difficult to attribute to any of the groups of I., easily fits into the given classification: intussusception first of all causes more or less expressed obstruction of the intestinal lumen and therefore belongs to the group of obstructions. At the same time intussusception is always accompanied by phenomena of incarceration more or less sharply expressed and therefore depending on the greater or lesser expression of the phenomena of obstruction or incarceration intussusception will belong either to one or the other group. As in incarceration of the intestine as in its rotation in the loop of the intestine circulation is disturbed.

Ultimately, circulation ceases and hemostasis occurs. Val' was fundamentally correct in wanting to isolate a group of I. with circulatory disorders, since circulatory disorders lead to morphological changes in the intestine, to its gangrene, and even before that cause functional changes in the intestine—first spasm, and then paralysis. Therefore, mechanical ileus should be divided into two groups: 1) simple I. (I. simplex) and 2) I. with hemostasis (I. cum haemostase). The second group should be isolated because it represents a transitional stage to a special form of I. caused solely by circulatory disorders. Embolism of the mesenteric artery, thrombosis of the mesenteric veins clinically cause all the phenomena of I., accompanied even by a shock symptom complex. Functionally, severe circulatory disorders in the intestine under the influence of arterial embolism or venous thrombosis lead to spasm and then paralysis of a loop or loops of intestine. Morphologically, this circulatory disorder leads to hemorrhagic infarction of the intestine and then to its gangrene. It is clear that both arterial embolism and thrombophlebitis lead to the typical form of I. from hemostasis (I. per haemostasin). Thus, a coherent system is obtained, starting from cases with functional changes, passing to cases caused only by circulatory disorders, then to cases of mechanical I. leading to circulatory disorders, and ending with the group of simple ileus. Classification of I. 1. Dynamic (I. dynamicus): a) spastic (I. spasticus), b) paralytic (I. paralyticus). 2. Hemostatic (I. haemostaticus): a) embolic (I. embolicus), b) thrombophlebitic (I. thrombophlebiticus). 3. Mechanical (I. mechanicus): 1) with hemostasis (cum haemostase): a) incarceration (incarceratio), b) torsion (torsio); 2) simple (I. simplex): a) obstruction (obturatio), b) flexion-compression (flexio-compressio). Thus, all forms of I. fit into the framework of the given classification, and it remains simple and fully meets clinical objectives. For completeness of clinical characterization, it is necessary to speak of complete I. (I. completus) and incomplete (I. incompletus), or partial (ileus partialis). In addition, acute, subacute, and chronic forms should be taken into account, and these forms will in turn find their place in the given classification. If, for example, obstruction is meant, it can be complete and incomplete. If attention is fixed on torsion, it can also be complete and incomplete. Depending mainly on the completeness or incompleteness of I., there is a more severe and a more calm course of the disease, which occurs even in such a relatively rare form of I. as mesenteric-arterial obstruction of the duodenum. The pathogenesis is simplest to begin considering with cases of chronic partial obstruction that gradually progresses to complete obstruction. Such I. are caused, for example, by strictures of the intestine, compression of the intestine by a tumor from the outside. When the lumen of the intestine is narrowed at a certain place, and the intestine cannot immediately push all its contents in the anal direction, then before the narrowing, orally from it, stagnation of contents occurs. The proximal segment of the intestine dilates, and its wall thickens, but this thickening is caused not only by hypertrophy, but also partly by inflammatory edema. Such a wall becomes less soft, less pliable: it cannot be gathered into folds; sometimes a dimple can be pressed out on it with a finger; it becomes more brittle; the peritoneum over it easily tears, as a result of which sutures are cut through. The dilation of the proximal segment of the intestine gradually extends higher in the oral direction, but sharp morphological changes are mainly present in the proximal segment of the intestine closest to the narrowing. As stated above, the pressure of contents in the proximal segment increases. As long as the intestinal contents are pushed through the narrowing, as long as the pressure in the entire proximal segment does not exceed the force of the closed pylorus, the phenomena of intestinal obstruction can be considered compensated. But finally comes a moment when the pressure in the entire proximal segment of the small intestine overcomes the resistance of the pylorus, and intestinal contents begin to enter the stomach. It fills the stomach, overcomes the resistance of the cardiac sphincter, and begins to be expelled through the mouth. That formidable phenomenon occurs, which has since ancient times been called miserere, and the most severe symptom of which is fecal vomiting. The correctness of the given explanation of fecal vomiting is confirmed by the following facts: fecal vomiting occurs the sooner, the higher the obstacle in the intestine, because the higher the obstacle in the intestine, the smaller the capacity of the proximal segment and the sooner the pressure in it overcomes the resistance of the pylorus. The lower the obstacle in the small intestine, the later fecal vomiting occurs. With narrowing of the large intestine, even with its complete obstruction, there may be no fecal vomiting at all, because with obstruction of the large intestine, starting from the ascending and ending with the rectum, the Bauhin's valve does not allow contents to pass back into the small intestine. One can see in obstruction of the large intestine its colossal size, while the small intestines are not dilated to a significant extent. This explains the absence of fecal vomiting. For miserere to appear in obstruction of the large intestine, it is necessary either that the large intestine be completely filled with contents, and as a result the small intestines begin to dilate, or that (as sometimes happens) Bauhin's valve is insufficient and would allow contents from the cecum to pass back into the small intestine. Under such conditions, miserere can begin earlier than is usually observed in obstruction of the large intestine. The third proof is as follows: if, when fecal vomiting is already present, an outlet is given for the contents from the dilated proximal segment of the intestine, then fecal vomiting stops instantly; of course this happens in the case when the proximal segment has not yet fallen into a state of paralysis. Thus, restoration of the ability to push contents to the place of least resistance, when such is the anal part of the intestine, stops miserere. Further study of the pathogenesis of chronic I. reveals that in it, after a certain period of time, an effusion appears in the abdominal cavity, indicating the beginning of irritation of the peritoneum, the beginning of peritonitis. This is explained by the fact that the inflammatory process from the intestinal lumen reaches the peritoneum, to which the peritoneum responds by forming an effusion containing leukocytes. It has long been noted (Kocher and others) that in far-advanced chronic obstruction of the large intestine, in its oral segment, ulcers of the mucosa and 'ulcers from stretching' appear. Sometimes they end in perforation of the intestinal wall. For example, in obstruction of the sigmoid colon, ulcers appear in the cecum. Sometimes ulceration with subsequent perforation affects a segment of the intestine lying closer to the site of obstruction. Rufan subjected the question of 'ulcers from stretching' to experimental study. He explains the appearance of ulcers by the influence of the intestinal contents on its vascular-nervous apparatus. 'The main moment of this vascular disorder lies not in the mechanical stretching of the intestine,' says Rufan, 'but in the chemico-toxic, partly biochemical ingredients acting on the vessels similarly to the action of activated trypsin.' It is necessary obviously to imagine the matter as follows: due to the stretching of the proximal intestine, its vessels and especially the veins are compressed, the pushing of blood through them is difficult, slowed down; to this is added from the side of the intestinal lumen the influence of toxins, which may damage the endothelium of the vessels. In places, vessels, especially veins, thrombose. Over the thrombi, surfaces, ulcers form, which then spread along the course of the thrombosed vessels to the deeper layers of the intestine and sometimes end in perforation. Through the perforation hole, under great pressure, the intestinal contents empties into the abdominal cavity. Acute peritonitis, accompanied by paralytic I., joins the mechanical I. Many patients suffering from I. die from peritonitis. Chronic I. also ends in peritonitis if perforation of the intestine occurs. Some acute forms of I. going with hemostasis, for example, volvuli, incarcerations, also end in peritonitis; in these cases peritonitis is a consequence of gangrene of the intestine, and in this type of I. an effusion forms in the abdominal cavity, which is initially transparent, and then takes on a hemorrhagic character due to the oozing of blood from the surface of the intestine affected by hemorrhagic infarction. Finally, at the beginning of gangrene of the intestine, the effusion takes on a purulent and putrefactive character. However, sometimes patients with acute I. die before the phenomena of peritonitis appear. It is known that death occurs the sooner the higher the obstruction is located. Grekov emphasizes that patients with intestinal knots die especially quickly. Since intestinal knots usually involve both the large and small intestines, most of the knots belong to high obstructions. Most modern authors firmly hold the point of view that death in acute I. before the development of peritonitis is explained by intoxication of the organism.

To clarify the question, one should first analyze the pathogenesis of intestinal obstruction from strangulation and volvulus. Both are clinically manifested by the most severe pains immediately. These pains are of a cruel character even before there is a hemorrhagic infarction in the intestine. The pains occur when the strangulation and volvulus affect the mesentery of the intestine, therefore they are of mesenteric origin. When only the intestinal wall is strangulated (Richter's hernias), there are no severe pains. Mesenteric pains can of course be explained by the strangulation of the mesentery, however, pains of the same character occur in purely hemostatic ileus (see above). From this it is evident that mesenteric pains must be explained mainly by the disturbance of blood circulation in the mesentery - they have an ischemic origin. As a result of the pains, an incarceration or torsion shock occurs. The phenomena of shock are often very severe. Grekov, Kozirev and a number of other surgeons attribute great importance to shock. Grekov precisely explains the early death in intestinal knots by shock. Undoubtedly, a certain number of patients die from shock. It was stated above that late death in I. is usually death from peritonitis. By this remains a certain number of patients who survive the shock but die before the development of peritonitis. Those patients die who have high obstruction. It is possible that the death of these patients is caused by intoxication, but against the theory of intoxication some serious objections can be raised. First of all it is difficult to imagine that a dilated afferent intestine could absorb contents at all, including toxins. On the other hand, patients suffering from high intestinal obstruction usually suffer from severe vomiting. Many surgeons draw attention to the fact that patients become dehydrated due to vomiting, which is also acknowledged by the defenders of the theory of intoxication (Kozirev). Moreover, with constant vomiting the organism becomes impoverished of chlorides. Especially American surgeons emphasize the importance of the decrease in chlorides in the blood of patients with I. With vomiting, bile is expelled, and along with bile - calcium salts. Finally, with vomiting, proteins, enzymes, everything that is needed for nutrition, tissue building and maintenance of functions of both the nervous system and endocrine glands is excreted. That is why, without resorting to the theory of intoxication, one can consider the death of people suffering from high intestinal obstruction as death from exhaustion. Exhaustion in I. occurs even more quickly than in accidentally formed anus praeternaturalis in the upper part of the jejunum or in the duodenum. Some Russian authors (Nazarov), and especially American surgeons, draw attention to the life-saving role in I. of intestinal fistulas created in the upper part of the jejunum. Some surgeons try to explain the beneficial effect of fistulas by the fact that the fistula supposedly removes from the intestine those toxins which would otherwise be absorbed into the blood and poison the organism. It seems to me that the significance of the fistula lies in the diametrically opposite direction: in a dilated intestine all contents are expelled with vomiting, and the intestine absorbs nothing, and as soon as a fistula is created, the intestine collapses and begins to absorb, and the organism begins to be nourished. Indeed, with a fistula, part of the useful material is expelled from the intestine outward, but in the absence of a fistula in I. everything is expelled, and moreover the intestine, due to overdistension, is deprived of the ability to absorb. As a result, the death of patients with high intestinal obstruction can be explained by the impoverishment of the blood with water, chlorides, lime salts, proteins, enzymes, fats, as a result of which the endocrine glands fall into a state of sharp hypofunction. The brain of patients works properly: loss of consciousness comes in the last minutes of life. As for the pathogenesis of dynamic I. and first of all I. spasticus, an example can be I. verminosus, namely that form when in the small intestine there is only one 'worm', and above this worm the intestine is contracted to the complete obliteration of the lumen. Gallstone intestinal obstruction also sometimes manifests itself in that the intestine is convulsively contracted above a small stone. A large ascarid knot, a large gallstone can cause and do cause typical intestinal obstruction. In another series of cases, one parasite, one relatively small stone cause spasms of the intestine above them. The irritation of the intestine in this case is caused from within, but it is not quite clear whether the spasm develops due to the irritation itself or due to the fact that the excitability of the intestine is increased. The pyloric spasms described by Grekov, the spasms of the Bauhinian valve can be and are without a definite internal irritant. Sometimes the irritant in the form of a small adhesion is located outside the intestine. With respect to the whole group of spastic I., one can think of increased excitability of the intestines. Such increased excitability, which is the result of decreased function of the epithelial bodies, is present in tetany (spasmophilia); but increased excitability of the intestines, reaching typical spastic I., also occurs in hysteria. In the work of Studzinsky there is an interesting observation by Wohlgemut, when a patient who underwent surgery had a mountainous abdomen. As soon as the patient fell asleep, the abdomen subsided. The same thing was observed in some hysterical patients who were operated on for I. It is difficult to say what explains the increased excitability of the intestines in hysterical women. In any case, one can think that spastic I. is an expression of increased excitability of the intestines, and this increased excitability turns out to be of general, not local origin. The pathogenesis of I. paralyticus is also gradually being clarified. Inflammation of the peritoneum always causes paralysis of the intestine at the site of inflammation. General peritonitis causes paralysis of all intestines. Paralysis of the intestine gives phenomena of obstruction. It is therefore clear that the phenomena in infectious peritonitis are determined by two moments: 1) intoxication from the absorption of poisonous substances from the peritoneum (Speransky believes that in peritonitis toxins spread along the branches of the vagus nerves to the centers of the medulla oblongata and poison it) and 2) obstruction of the intestines due to their paralysis. Frequency of I. in general is difficult to determine. Zoltarev believes that in Russia annually about 30,000 people contracted I. The frequency of all types of I. in relation to volvuli is determined much more accurately. Savkov (1925) gives the following data on this matter. Authors Total number of Volvuli Percentage of obstruction volvuli Spasokukotsky 49.0 Zoltarev . . 22.0 Britsky. . . . 67.0 Savkov .... 40.0 Balashev . . . 52.0 Soinov.... 35.0 Alypov .... 47.5 Savkov's statistics can be significantly supplemented. Gordon and Zykov give a summary statistics of Russian authors and statistics of the department of Uspensky (Hospital town in Tver). Statistics Combined . . Hospital town . . Total number of obstructions sigj Volvuli И га £ <-------------------------------^^^- »«o тон- еле- S-Ro-i B ^{m a}| ких пой I mani I 991 71 in percent 47.5 I 51.2 36.6 58.0 6.1 19.0 43.7 23.0 ; To the XIX Congress (1927) of Russian surgeons the statistics has grown significantly even more. The following material was reported. U3 Authors o o Я o,2 к S «FT e X O, н o. в co >> Mi» в o Krasintsev . . - Gregory . . . - Rozanov .... - . Total . .' On average in our country volvuli with knots give 40% of all I. Knots (according to Grekov's statistics) constitute 10% of volvuli. Kotomanov in 25 years collected 60 cases of intestinal knot in Russian literature. Intussusceptions, judging by the data given in the table, constitute 5% of I. In 1,107 cases of I. there are 246 'obstructions', i.e. 22%. Some confusion in the question of 'strangulations' and internal strangulations depends on the shortcomings of classification. Grekov in 511 operated cases of I. gives 4 cases of gallstone obstruction, 5 cases of embolism of mesenteric arteries and 7 cases of spastic I. According to the summary data of Moscow morgues for 1923-27 years in 33,609 autopsies (counting also newborns) 214 obstructions were noted, not counting strangulated hernias; the latter for 1925-1927 years (in 23,039 autopsies) were noted 56 times. Volvuli in the indicated data constitute about 60%. Russian statistics is interesting to compare with foreign. For this purpose one can take the statistics of London hospitals for 1925. Gallstones. ..........

74 Total...... 1.655 In London, volvulus accounts for slightly more than 4% of all obstructions, i.e., approximately the same as intussusceptions account for us. However, in London, 37% of ileus is due to pure intussusceptions, i.e., intussusceptions without tumors. In short, intussusceptions in London occupy the place that volvulus occupies in our statistics, while volvulus occupies the place that intussusceptions occupy in ours. Ileus caused by the presence of a diverticulum is usually classified as a strangulation. Lopatnikova-Bats from the Razumovsky clinic provides a summary of the frequency of ileus from diverticulum in relation to ileus in general. In the Razumovsky clinic, out of 28 cases of ileus, 6 are due to Meckel's diverticulum (about 24%). In foreign literature, the frequency of ileus due to diverticulum ranges from 5-7% to 20%. Symptomatology and diagnosis. The symptoms of ileus are quite clear in acute forms accompanied by hemostasis and in chronic forms developing due to gradual narrowing of the intestinal lumen. The first form is characterized by the suddenness of onset, the sudden appearance of severe pain that brings the patient to a state of shock: pallor, coldness, weakness, cold sweat, increased heart activity, falling blood pressure. The passage of feces and the expulsion of gas also cease suddenly. The pains are constant, periodically intensifying due to increased peristalsis of the leading segment of the intestine. In the very first hours, local symptoms from the abdomen give nothing definite: the abdomen is even drawn in, there is no local contraction of the abdominal muscles. Vomiting that appears at the beginning of acute ileus also presents nothing characteristic, as it is (as is believed) reflex vomiting. Later the symptoms become more characteristic: with a high-located ileus, vomiting appears early, which becomes more frequent and takes on a fecal character. Uneven bloating of the abdomen is determined: either the intestine subjected to volvulus (Val's symptom) or the intestine leading to the site of strangulation bulges. Sklyarov, Yukelson and others rightly draw attention to the diagnostic and symptomatic significance of the splashing sound: the latter may occur either in the twisted intestine or in the leading bulging segment of the intestine. In the abdominal cavity, in its dependent areas (lumbar regions), percussion reveals the presence of effusion; it is easy to prove that it is mobile (change in dullness with changes in the patient's position). The amount of chlorides in the blood falls. - English surgeons (e.g., Taylor) correctly distinguish in the course and symptomatology of acute ileus three periods. Two of them have been described above. In the third period, the picture of peritonitis, paralytic intestinal obstruction, is added. The abdomen is uniformly swollen and calm, the diaphragm is pushed upward, shortness of breath, continuous regurgitation, dry, crusted lips, sunken facial features, markedly rapid pulse, low blood pressure, sharp restriction or even cessation of urination (in hopeless cases); consciousness is preserved. From the onset of the disease to death passes several days, if surgical help is not given. Rarely the disease drags on for weeks, which happens when the volvulus or strangulation is partial, the inflow of arterial blood to the intestine is little affected, and therefore gangrene of the intestine develops slowly. Ileus with hemostasis does not differ symptomatically from the typical hemostatic form. Recognition of the typical hemostatic form is usually made at operation. The hemostatic form, and specifically the embolic one, can be suspected by examination of the heart - presence of chronic or acute endocarditis. To establish an accurate diagnosis of the cause of acute ileus in the very first hours is almost impossible. Sometimes by the localization of pains and with the help of additional studies (irrigation of the intestines with a siphon enema, inflation of the intestine through the anus) it is possible to determine volvulus of the sigmoid colon. In practice, one can be satisfied with the recognition of acute ileus, leaving the clarification of detailed diagnosis to the operation: the first act of the operation - opening of the abdominal cavity - is the last act of the examination. A more accurate diagnosis is made more easily, the symptoms are clearer in chronic ileus caused by gradually developing narrowing of the intestinal lumen. Colicky pains gradually and slowly increase both in frequency and intensity. They are localized in a specific place. During pains the patient feels the pouring of liquid (gurgling) or the passage of gases as if with a whistle. Localized swellings appear in one or another part of the abdomen, periodic, of peristaltic character. Usually emptying of the intestine is difficult: constipation increases. An exception to the general rule are tuberculous strictures of the intestines, in which there is frequent emptying of the intestine of a mucous-bloody character. Mucous-bloody stools also occur in intestinal cancers, but only in cancers that usually do not cause significant phenomena of ileus. Palpation of the abdomen in chronic ileus often determines a tumor, more or less movable, more or less uneven, more or less dense. Near the tumor a peristaltic wave of the intestine (leading) is observed, which from time to time raises the abdominal wall. In the area of the peristaltic intestine, a splashing sound can be caused by shaking the abdominal wall. It is usually caused in the small intestine, dilated before the obstacle, i.e., in the ileum, when the stricture is in the cecum, and in any part of the small intestine when the stricture also involves the small intestine. In the large intestine, when peristalsis is present, a splashing sound is rarely caused, because the contents of the large intestine are dense. From the location of the tumor, from other symptoms of chronic intestinal obstruction, it is possible and necessary to conclude both about the location of the narrowing and about its nature. However, it must be taken into account that the small intestine with a tumor can shift under the influence of the weight of the tumor to a place where usually the large intestine is located, e.g., in the right or left iliac region. For more accurate recognition of chronic ileus, one can resort to 1) X-ray examination and photographs of the intestines after the administration of a contrast substance per os, 2) X-ray examination and photographs after the introduction of a contrast substance into the rectum. The latter kind of investigation is unsuitable for determining the level of obstruction of the small intestine, because the contrast substance does not pass beyond the Bauhinian valve. From the typical cases, where at least the recognition of ileus presents no difficulties, there are a number of deviations when intestinal obstruction is relative and comparatively small (adhesions, slight bends). Then prolonged observation and X-ray examination allow one to arrive at a more definite diagnostic conclusion. Recognition of spastic ileus sometimes insurmountable difficulties. The diagnosis of mechanical ileus is often made, and the diagnosis is essentially correct, because spasm of the intestine creates mechanical obstruction. At operation the essence of the matter is clarified. It is easier to make a diagnosis when the patient has previously undergone surgery and at it a spastic form of ileus was already found. But even here one must be careful, because after an operation for spastic ileus a typical mechanical ileus may develop. One has to study the patient and make a diagnosis on the basis of the sum of data from subjective and objective research. - Spastic ileus of hysterical origin is characterized by a prolonged course without violent phenomena, without phenomena of increasing intestinal obstruction. Hysterical ileuses have a stationary character, as it were, with hysterical phenomena present. For signs of ileus paralyticus-see Peritonitis. Here only the symptoms of postoperative paralytic ileus will be indicated, which develops without the presence of signs of peritonitis. The most constant symptom is severe bloating of the abdomen with cessation of gas passage. Along with this there are pains, however not very intense. Sometimes vomiting is added. The patient does not produce the heavy impression that peritonitis gives. The temperature of the patient is usually unchanged, the pulse is not accelerated or is slightly accelerated. It should be noted that in the postoperative period a non-paralytic ileus, but a mechanical one in the form of volvulus, strangulation, bend of the intestine, etc., can also develop. Therefore ileus as an 'accidental' complication of the postoperative period should be strictly distinguished from temporary postoperative paralytic ileus. The difference is that acute ileus always begins suddenly, violently, accompanied by severe pains up to and including shock phenomena. The treatment of ileus from a principled side is clear and simple: if the intestine is completely obstructed or its permeability is significantly reduced, then one must either 1) restore its permeability or 2) give an outlet to the contents from the leading segment of the intestine. The clarity of the principled formulation of the question of the treatment of ileus is obscured by spastic ileus, since in it the intestinal obstruction has a functional character; to influence it by operation, i.e., by mechanical action on a functional disorder, is rather difficult, if one speaks of purely local operations on the intestines. In acute complete ileus, vital indications come first.

In the earliest days, irrigation through the anus with siphon enemas may be attempted, and in case of suspicion of volvulus of the sigmoid colon, careful inflation of the intestine through the anus. Under no circumstances should laxatives be given. The operation should be performed as early as possible, even before the appearance of local abdominal distension. With precise diagnosis of the site of obstruction, any most advantageous incision of the abdominal wall is made. The rule is a wide incision along the midline. From this incision, it is possible to quickly orient oneself and find both the site and the cause of intestinal obstruction. Evisceration of the intestine need not be feared. The intestines are placed between hot towels. In early operations for internal hernias, volvuli, and kinks of the intestine, the operation ends quickly: the intestine is freed from the constriction, untwisted, and extracted from the site of constriction. If the constriction occurred in the peritoneal sac, the opening of the sac is sutured; if the constriction or kink occurred under a peritoneal band or under a diverticulum, the band and diverticulum are resected. The abdominal cavity is closed hermetically. The later the operation is performed, the more difficult it is. The altered intestine may be either excluded, or resected, or excluded and then resected (Grekov's second method). The choice of method is left to the surgeon's discretion depending on 1) the general condition of the patient, 2) the degree of alteration of the diseased intestine, 3) the technical abilities of the surgeon. An infarcted intestine, an intestine with a strangulation groove, is best either resected or excluded, but not returned to the abdominal cavity, assuming it will recover: the infarct may only involve the mucous membrane, but at the site of the infarct, a stricture may form after necrosis of the infarcted mucosa. An excluded infarcted intestine, depending on the degree of infarction, is either returned to the abdominal cavity or, if it is suspected of being gangrenous, is left outside the abdominal cavity on tampons (after a certain interval, it itself retracts into the abdominal cavity). A gangrenous intestine is either resected or excluded, but after exclusion it is necessarily left on tampons outside the abdomen. Resection of the intestine can be performed 1) in one stage, with the ends of the intestine being sutured either end to end or side to side; 2) in two stages - the intestine is brought out through the wound, the base of the intestine is sutured into the wound, and after one or two days the intestine is cut off; 3) in two stages according to Grekov: exclusion by lateral anastomosis of the intestine to be resected, bringing it out through the wound, suturing it into the wound, and cutting it off after 1-2 days. The second method of dealing with the intestine leads to subsequent treatment of the anus. When in acute intestinal obstruction the small intestines are distended, puncture with a trocar is permissible for their emptying. The loop of intestine to be punctured is brought out through the wound, isolated from the peritoneal cavity, a purse-string suture is placed at the future puncture site to close the opening formed. After emptying the intestine, the purse-string suture is tightened, and another series of sutures is applied (transverse to the axis of the intestine). Chronic ileus is also treated by all three of the above-mentioned operative measures, i.e. 1) resection of the narrowed area, 2) exclusion of the obstructed area, and 3) exclusion with subsequent resection. Both one-stage and two-stage resection are used, with the latter being applied both with the creation of an anus and with preliminary exclusion of the obstructed area. The choice of method depends on the patient's strength, the local conditions, and the surgeon's qualification. It should be borne in mind that: two-stage resection with the creation of an anus is applicable to all large intestines, even to the lower part of the ileum, but not to the jejunum (emaciation!). For benign strictures of the intestine (kinks, scars, pericolitis), exclusions should be as economical as possible: the anastomosis should be placed closer to the site of obstruction. For tuberculous strictures, if exclusion is performed, the anastomosis should be in areas that appear healthy. In both types of strictures, exclusion is best achieved by lateral anastomosis (incomplete exclusion). For malignant strictures, if exclusion is to be performed, either partial incomplete exclusion or complete bilateral exclusion can be done, with one end of the bilaterally excluded intestine necessarily being sutured into the body wall for emptying of the excluded segment (mucous fistula). Ileus caused by foreign bodies (worms, gallstones, other objects) indicates the use of enterotomy. Complete ileus as a result of chronic ileus often indicates the creation of a praeter natural anus. Advanced mechanical ileus, causing severe distension of the small intestines, paralytic infectious ileus indicates the use of fistulas in the ileum, even in the jejunum (its initial loops). Such fistulas relieve the intestines from overdistension and allow some of the contents to be absorbed into the blood. Due to the depletion of the body's chlorides in ileus, intravenous administration of a 3% solution of NaCl in an amount of 500-1,000 cm³ is recommended. Outcome of surgical treatment. Surgical treatment of acute mechanical ileus gives the following results (according to statistics of treatment outcomes by Russian surgeons collected by Gordon and Zykovova). Authors Number of cases Percentage of mortality 58.0 42.7 28.8 57.7 The presented statistics can now be significantly supplemented. Authors Sklyarov Grekov Ogloblin Gregory Rozanov Krasintsev Mambre Number of cases Percentage of mortality 41.5 56.0 60.0 35.5 51.0 56.0 58.0 From comparison of the tables, it is seen that on a large material (Grekov, Ogloblin, Perelman, Yukelson), the percentage of mortality fluctuates between 55 and 60. On a small material, the percentage of mortality of course fluctuates more. Kozirev has an exceptionally favorable percentage (28). Rozov in 1907 reported on 58 patients operated on for ileus; of these 36 died, i.e. 62%. Seidler in 1898 presented his material - 17 cases of ileus, of which 9 died. Statistics of London hospitals from 1925 are as follows: | Causes of ileus Total cases Percentage of mortality 28 358 342 223 613 17 74 50.0 43.5 31.0 Internal hernias Invaginations Invaginations with tumor 33.0 22.0 35.0 51.0 t From these data, it is evident that the successes in surgical treatment of ileus in the USSR and abroad are not brilliant. The main reason for poor results of surgical treatment of ileus lies in the delayed application of the operation. Early operation for kinks of the intestine, constriction, volvulus is easy and effective in result. Too late an operation (when a gangrenous intestine surrounded by putrefactive exudate lies in the abdominal cavity) is hopeless. Intermediate operations are more or less difficult technically and have grave outcomes. Of course, here too one must strive to improve results by creating fistulas (temporary), infusions of hypertonic solutions, etc., but the main weight of the question lies in early operations. It is better to perform laparotomy even only on suspicion of acute ileus and not find it, than to miss an existing ileus. In the first case, the patient risks very little and is cured of the disease for which he was operated on, in the second case, the person is doomed to almost certain death. Postoperative paralytic ileus is treated with siphon enemas, subcutaneous injections of physostigmine, intravenous infusions of hypertonic solutions, intravenous or subcutaneous infusions of glucose solutions. It should be borne in mind that paralytic ileus may persist for several days and, as stated above, is sometimes accompanied by vomiting. If intravenous infusions of hypertonic NaCl solution restore chloride balance, then intravenous or subcutaneous infusions of glucose solutions (5-3%) restore water balance and nourish the body.