Ileus

ILEUS, intestinal obstruction; represents a condition in which an obstacle arises along the intestine to the movement of its contents. Left to its own course, ileus, depending on the type of obstruction, leads in a shorter or longer period of time to severe phenomena threatening death. The study of all the features of ileus leads to a number of complex problems, and first of all to the problem of classification. As a criterion for classification, one can accept 1) the etiological element, 2) the pathological-anatomical element, and 3) the clinical element. A complete classification must group the types of ileus, taking into account all these elements. From the point of view of gross etiology, one can distinguish 3 groups of ileus: 1) congenital ileus (ileus congenitus), 2) ileus based on congenital predisposition (ileus congenito-praedispositus), and 3) acquired (ileus acquisitus). Typical examples of congenital ileus include atresia of the anus (atresia ani) with its varieties, congenital stenosis of the duodenum, and other types. Ileus based on congenital predisposition encompasses a fairly large group of various forms, caused mainly by irregularities in the arrangement and structure of various sections of the intestine. In connection with the doctrine of arterio-mesenteric obstruction of the duodenum, Melnikov studied the arrangement of the named intestine and came to the following conclusions: anatomical-mechanical causes of obstruction in the upper segment of the duodenum can be caused by: 1) mobility of the superior part of the duodenum and imperfection of the shape and position of the entire duodenum, or 2) with a duodenum perfect in shape and position—by adhesions fixing it in an unfavorable position (pathological type of shape and position of the duodenum). Both of these positions of the upper horizontal part of the duodenum contribute to its kinking when the stomach is full. If the kinking resulting from the fixation of the intestine by adhesions can be considered as a case of predisposition to obstruction of an acquired nature, then the kinking of the same intestine due to mobility must be considered a case of predisposition to obstruction of a congenital nature. The same applies to the lower horizontal part of the duodenum. According to Melnikov, the inferior part of the duodenum does not have 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 a supine position, leaves a depression on the duodenum and presses its anterior wall against the posterior. "On a series of specimens, such a depression (impressio mesenterialis) is so significant that the entire section of the duodenum lying above is sharply dilated." From this, it follows with certainty that arterio-mesenteric obstruction represents an ileus on the basis of congenital predisposition, and it is only unclear why it manifests itself relatively rarely. Studies by Kupriyanov and the summary of data on the position of the large intestine by Melnikov fully confirm the observations of clinicians about the significance for obstruction of the large intestine of its bends—such as the hepatic flexure of the colon, and especially the splenic flexure of the colon. It is obvious that a portion of cases of ileus of the large intestine belongs to the group of ileus on the basis of congenital predisposition, since the ileus is often caused by the sagging of the transverse colon, for example, to the symphysis, and the sagging depends on a congenitally long transverse colon (colon transversum longum congenitum). A long mesentery of the small intestine, a common mesentery of the ileum and cecum, and a long mesentery of the sigmoid colon serve as further examples of congenital predisposition to subsequent volvulus of the intestines, i.e., a predisposition to one of the most severe forms of ileus. Besides cases of congenital ileus and ileus on the basis of congenital predisposition, many cases of acquired ileus are known. This includes ileus 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 about ileus with congenital predisposition, it should be remembered that for the appearance of ileus, an acquired element causing the ileus is often added to the congenital-predisposing element. For example, a long mesentery of the intestine predisposes to volvulus of the sigmoid colon; however, for the occurrence of volvulus, it is necessary that inflammation of the mesentery or cicatricial changes be added, i.e., an acquired element. Meckel's diverticulum is often accompanied by strangulation of the intestines and therefore serves as a predisposition to strangulation. However, strangulation 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, strangulation can be caused by purely acquired conditions, such as the formation of inflammatory and gradually organized bands in the abdominal cavity. The pathological-anatomical classification is easily reconciled with the etiological one. From the point of view of pathological anatomy, it is necessary to distinguish volvulus, internal strangulations, intestinal kinks, strictures of various characters, and compression of the intestines by growing tumors (e.g., tumors of the mesentery). In each individual case, to the pathological-anatomical characteristic, if possible, it is desirable to add an etiological characteristic, noting whether the ileus was caused by a congenital condition, a congenital predisposition, or was purely acquired. From the point of view of pathological anatomy, a group of ileus stands out clearly, which proceeds with a disorder of mesenteric circulation and usually leads to hemorrhagic infarction of the intestine with an outcome in gangrene. From an etiological point of view, in these cases, one only has to worry about clarifying the question of whether the circulatory disorder occurred from an embolism of the artery, from its thrombosis, or from compression of the vessels (primarily veins) in the strangulating ring, or from twisting of the mesentery. It is more difficult to reconcile the etiological and pathological-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 captured to a certain extent 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, containing within itself both the pathological-anatomical and etiological classifications, but building a superstructure upon them that is important for understanding the processes occurring in the patient. From a clinical point of view, one distinguishes first of all: 1) dynamic ileus (ileus dynamicus) and 2) mechanical ileus (ileus mechanicus). Dynamic ileus, in turn, falls into a) spastic (ileus spasticus) and b) paralytic (ileus paralyticus). In the former, the spasm of the intestine, most often the small intestine, reaches such a degree that the lumen of the intestine disappears. In the latter, on the contrary, the intestines lose the ability to contract; they fall into a state of paralysis. The most formidable form of paralytic ileus is paralysis of the intestines during acute peritonitis. Since the time of Wahl (v. Wahl; 1889), the division of mechanical ileus into a) ileus due to constriction (ileus per strangulationem) and b) ileus due to obstruction (ileus per obturationem) has taken root in surgery. This classification was supported in Russia primarily by Zeidler (1898) and Zege-Manteuffel (1913), and it is still used by many surgeons today. Yutsevich modified the classification; he calls ileus per strangulationem loop obstruction (cleyaansae) and includes here all cases where, along with the mesentery, the loop also suffers, whether it be twisting of the loop together with the mesentery, its compression by a band, strangulation in a hernial orifice, etc. He calls ileus per obturationem luminal obstruction (devia luminis) and refers to this category all cases with narrowing of the intestinal lumen (according to Studzinsky). Some surgeons are not satisfied with either Wahl's classification or the more complex classification of Wilms and prefer to use, in essence, a purely pathological-anatomical classification, distinguishing ileus from volvulus, kinking, strangulation, compression, adhesion, cancer, etc. But with such a classification, one important moment is missed, which is precisely what Wahl wanted to capture—the moment characterizing a whole group of ileus and consisting of a disorder of blood circulation. However, Wahl's nomenclature is not entirely successful due to the insufficiently clear characterization of individual groups. Oppel proposes to distinguish the following 4 groups of mechanical ileus: 1) ileus per obturationem, 2) ileus per flexionem-compressionem, 3) ileus per incarcerationem, and 4) ileus per torsionem. Invagination (invaginatio), which in other classifications was difficult to assign to any of the groups of ileus, easily fits into the proposed classification: invagination primarily causes a more or less pronounced obstruction of the intestinal lumen and therefore belongs to the group of obturations. At the same time, invagination is always accompanied by more or less sharply expressed phenomena of incarceration and therefore, depending on the greater or lesser expression of either the phenomena of obstruction or strangulation, invagination will be assigned to one or the other group. Both in the case of strangulation of the intestine and in its twisting, blood circulation is disrupted in the intestinal loop.

Ultimately, blood circulation ceases, and hemostasis occurs. Wahl was fundamentally correct in wishing to distinguish a group of Ileus with circulatory disturbance, because circulatory disturbance leads to morphological changes in the intestine, to its gangrene, and even before that, it causes functional changes in the intestine—first spasm, and then paralysis. Therefore, mechanical Ileus should be divided into two groups: 1) simple Ileus (Ileus simplex) and 2) Ileus with hemostasis (Ileus cum haemostase). The second group must be distinguished because it represents a transitional stage to a special form of Ileus caused solely by circulatory disturbance. Embolism of the large mesenteric artery and thrombosis of the mesenteric veins clinically cause all the phenomena of Ileus, accompanied even by a symptom complex of shock. Functionally, sharp disturbances of blood circulation in the intestine under the influence of arterial embolism or venous thrombosis lead to spasm and then paralysis of a loop or loops of the intestines. Morphologically, this circulatory disturbance leads to hemorrhagic infarction of the intestine and then to its gangrene. It is clear that both arterial embolism and thrombophlebitis lead to a typical form of Ileus from hemostasis (Ileus per haemostasin). Thus, a coherent system is obtained, starting from cases with functional changes, moving to cases caused only by circulatory disturbance, and further to cases of mechanical Ileus leading to circulatory disturbances, and ending with the group of simple Ileus. Classification of Ileus: 1. Dynamic (Ileus dynamicus): a) spastic (Ileus spasticus), b) paralytic (Ileus paralyticus). 2. Hemostatic (Ileus haemostaticus): a) embolic (Ileus embolicus), b) thrombophlebitic (Ileus thrombophlebiticus). 3. Mechanical (Ileus mechanicus): 1) with hemostasis (cum haemostase): a) incarceration (incarceratio), b) torsion (torsio); 2) simple (Ileus simplex): a) obstruction (obturatio), b) kinking-compression (flexio-compressio). Thus, all types of Ileus fit into the framework of the presented classification, and it remains simple and fully meets clinical goals. For the completeness of the clinical characterization, one must speak of complete Ileus (Ileus completus) and incomplete (Ileus incompletus), or partial (ileus partialis). Furthermore, one should take into account acute, subacute, and chronic forms, and these forms will again find their place in the presented classification. If one has in mind, for example, obstruction, it can be complete and incomplete. If one focuses attention on torsion, it can also be complete and incomplete. Depending mainly on the completeness or incompleteness of the Ileus, the course of the disease is more stormy or more calm, which occurs even in such a relatively rare form of Ileus as mesenteric-arterial obstruction of the duodenum. It is easiest to begin examining the pathogenesis with cases of chronic partial obstruction, gradually reaching complete obstruction. Such Ileus is caused, for example, by scirrhus of the intestines, 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 in front of the place of narrowing, orally from it, stagnation of the contents occurs. The afferent segment of the intestine expands, and its wall thickens, but this thickening is caused not only by hypertrophy, but partly also by inflammatory edema. Such a wall becomes less soft, less pliable: it cannot be gathered into folds; sometimes one can press a dimple into it with a finger; it becomes more brittle; the peritoneum over it tears easily, as a result of which sutures cut through. The expansion of the afferent segment of the intestine gradually moves higher in the oral direction, but sharp morphological changes are present primarily in the afferent segment of the intestine closest to the place of narrowing. As stated above, the pressure of the contents in the afferent segment increases. As long as the intestinal contents are pushed through the place of narrowing, as long as the pressure in the entire afferent segment does not exceed the force of the closed pylorus, the phenomena of intestinal obstruction can be considered compensated. But finally, a moment arrives when the pressure in the entire afferent segment of the small intestine overcomes the resistance of the pylorus, and the intestinal contents begin to enter the stomach. It overfills the stomach, overcomes the resistance of the cardiac sphincter, and begins to be ejected through the mouth. That formidable phenomenon occurs, which has long been called miserere, and the most severe symptom of which is fecal vomiting. The correctness of the presented explanation of fecal vomiting is confirmed by the following facts: fecal vomiting occurs the sooner, the higher the obstruction is located in the intestine, because the higher the obstruction in the intestine, the smaller the capacity of the afferent segment and the sooner the pressure in it overcomes the resistance of the pylorus. The lower the obstruction is located 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 in obstruction of the large intestine, starting from the ascending and ending with the rectum, the Bauhin valve does not allow contents to pass back into the small intestine. One can see in obstruction of the large intestine its colossal dimensions, while the small intestines are not stretched significantly. This explains the absence of fecal vomiting. For the appearance of miserere in obstruction of the large intestine, it is necessary either that the large intestine be completely clogged with contents, and as a result, the small intestines would also begin to stretch, or that (as sometimes happens) the Bauhin valve be insufficient and allow the contents of the cecum to pass back into the small intestines. Under such conditions, miserere may begin earlier than is usually observed in obstruction of the large intestine. The third proof consists of the following: if, in the presence of already existing fecal vomiting, one provides an exit for the contents from the overfilled afferent segment of the intestine, then fecal vomiting stops instantly; of course, this happens in the case when the afferent segment has not yet fallen into a state of paralysis. This means that restoring the ability to drive contents to the place of least resistance, when that is the anal part of the intestine, stops the miserere. Further study of the pathogenesis of chronic Ileus reveals that after a certain interval of time, an effusion appears in the peritoneal 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 lumen of the intestine reaches the peritoneum, to which the peritoneum responds with the formation of an effusion containing leukocytes. It has long been noted (Kocher et al.) that in far-advanced chronic obstruction of the large intestine, ulcerations of the mucosa and "stercoral ulcers" (ulcers from distension) appear in its oral segment. Sometimes they end in perforation of the intestinal wall. In obstruction of, for example, the sigmoid colon, ulcers appear in the cecum. Sometimes ulceration with subsequent perforation affects a section of the intestine lying closer to the place of obstruction. Rufanov subjected the question of "stercoral ulcers" 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 Rufanov, "but in chemical-toxic, partly biochemical ingredients acting on the vessels similarly to the action of activated trypsin." One must obviously imagine the matter in the following way: as a result of the stretching of the afferent intestine, its vessels and especially the veins are compressed, the pushing of blood through them is hindered, slowed down; to this is added from the side of the intestinal lumen the influence of toxins, which, possibly, damage the endothelium of the vessels. In places, the vessels, especially the veins, become thrombosed. Over the thrombi, surfaces and ulcerations form, which then spread along the course of the thrombosed vessels to the deep layers of the intestine and sometimes end in perforation. Through the perforation hole, the contents of the intestine are emptied into the peritoneal cavity under high pressure. To the mechanical Ileus is added acute peritonitis, accompanied by paralytic Ileus. Many patients suffering from Ileus die from peritonitis. Chronic Ileus also ends in peritonitis if perforation of the intestine occurs. Some acute forms of Ileus proceeding with hemostasis, e.g., volvulus, incarcerations, end in peritonitis; in these cases, peritonitis is a consequence of gangrene of the intestine, and in the latter type of Ileus, an effusion forms in the peritoneal cavity, which is initially transparent, and then takes on a hemorrhagic character due to the transudation of blood from the surface of the intestine affected by hemorrhagic infarction. Finally, at the onset of gangrene of the intestine, the effusion takes on a purulent and putrid character. However, sometimes patients with acute Ileus die before the phenomena of peritonitis. It is known that death occurs the earlier, the higher the obstruction is located. Grekov emphasizes that patients with intestinal knots die particularly quickly. Since the small intestines are usually involved along with the large intestines in intestinal knots, most knots belong to high obstructions. Most modern authors stand firmly on the point of view that death in acute Ileus before the development of peritonitis is explained by intoxication of the organism.

To clarify the issue, one should first examine the pathogenesis of intestinal obstruction from strangulation and volvulus. Both manifest clinically immediately with severe pain. These pains are of a severe nature even when there is no hemorrhagic infarction in the intestine yet. Pains occur when the strangulation and volvulus involve the mesentery of the intestine; consequently, they are of mesenteric origin. When only the intestinal wall is subjected to strangulation (Richter's hernia), there is no sharp pain. Mesenteric pains can, of course, be explained by 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 a disturbance of blood circulation in the mesentery—they are of ischemic origin. As a result of the pain, incarceration or torsion shock occurs. The phenomena of shock are often very severe. Grekov, Kozyrev, and a number of other surgeons attach great importance to shock. It is precisely by shock that Grekov explains early death in cases of intestinal knots. Undoubtedly, a certain number of patients die precisely from shock. It was stated above that late death in I. is usually death from peritonitis. Beyond all this, there remains a certain number of patients who survive the shock but die even before the development of peritonitis. It is precisely those patients with high obstruction who die. It is possible that the death of these patients is caused by intoxication, but some serious objections can be raised against the theory of intoxication. First of all, it is difficult to imagine that a distended 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 proponents of the intoxication theory (Kozyrev). Furthermore, with constant vomiting, the organism becomes depleted of chlorides. American surgeons, in particular, emphasize the significance of the drop in chlorides in the blood of patients with I. With vomiting, bile is expelled, and along with the bile, calcium salts. Finally, with vomiting, proteins, enzymes, and everything necessary for nutrition, tissue building, and maintaining the functions of both the nervous system and endocrine glands are lost. This is why, without resorting to the theory of intoxication, one can consider the death of people suffering from high intestinal obstruction to be death from exhaustion. Exhaustion in I. occurs even faster than with an 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 precisely by the fact that the fistula supposedly removes from the intestine those toxins which, without it, would be absorbed into the blood and poison the organism. It appears to Oppel that the significance of the fistula lies in the diametrically opposite direction: with a distended intestine, all contents are expelled via vomiting, and the intestine absorbs nothing, but as soon as a fistula is created, the intestine collapses and begins to absorb, and the organism begins to be nourished. True, even with a fistula, a portion of useful material is expelled from the intestine, but in the absence of a fistula in I., everything is thrown out, and furthermore, 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 depletion of the blood of water, chlorides, calcium salts, proteins, enzymes, and fats, as a consequence of which the endocrine glands, mainly, fall into a state of severe hypofunction. The brain in patients functions properly: loss of consciousness comes in the very last minutes of life. As for the pathogenesis of dynamic I. and primarily I. spasticus, an example can be I. verminosus, specifically that form where only one "worm" is found in the small intestine, and above this worm, the intestine is contracted to the point of complete obliteration of the lumen. Gallstone intestinal obstruction also manifests sometimes by the fact that above a small-sized stone, the intestine is spasmodically contracted. A large ball of ascarids or a large gallstone can cause, and do cause, a typical intestinal blockage. In another series of cases, a single worm or a relatively small stone causes spasms of the intestine above it. The irritation of the intestine in this case is caused from within, but whether the spasm develops due to the irritation itself or due to the fact that the irritability of the intestine is increased—this remains not entirely clear. The spasms of the pylorus and the spasms of the ileocecal valve described by Grekov can occur, and do occur, without a definable irritant from within. Sometimes an irritant in the form of a small adhesion is found outside the intestine. In relation to the entire group of spastic I., one can think of increased irritability of the intestines. Such increased irritability, which is the result of reduced function of the parathyroid glands, exists in tetany (spasmophilia); but increased irritability of the intestines, reaching the point of typical spastic I., also occurs in hysteria. In Studzinsky's work, an interesting observation by Wohlgemuth is cited, where in a patient undergoing surgery, the abdomen was distended like a mountain. As soon as the patient fell asleep, the abdomen subsided. The same was observed in some hysterical patients who were operated on for I. What explains the increased excitability of the intestines in hysterical women is difficult to say. In any case, one can think that spastic I. is an expression of increased excitability of the intestines, and their 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 produces phenomena of obstruction. It is clear, therefore, that the phenomena in infectious peritonitis are conditioned by two factors: 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. The frequency of I. in general is difficult to determine. Zolotarev believes that in Russia, approximately 30,000 people fell ill with I. annually. The frequency of all types of I. in relation to volvulus is determined much more accurately. Savkov (1925) provides the following data on this matter. Authors: Total number of obstructions, Quantity of volvulus, Percentage of volvulus: Spasokukotsky 49.0, Zolotarev 22.0, Britske 67.0, Savkov 40.0, Balashev 52.0, Soinov 35.0, Alipov 47.5. Savkov's statistics can be significantly supplemented. Gordon and Zykova provide summary statistics of Russian authors and statistics from Uspensky's department (Hospital town in Tver). Summary statistics: Total number of obstructions 991, Volvulus 71, in percent 47.5... By the XIX Congress (1927) of Russian surgeons, the statistics had grown significantly. The following material was reported. Authors... Krasintsev... Gregory... Rozanov... Total... On average, in our country, volvulus with knots accounts for 40% of all I. Knots (according to Grekov's statistics) make up 10% of volvulus cases. Kotomanov, over 25 years, collected 60 cases of intestinal knot in Russian literature. Intussusceptions, judging by the data presented in the table, make up 5% of I. Out of 1,107 cases of I., there are 246 "obturations," i.e., 22%. A certain confusion regarding the issue of "strangulations" and internal strangulations depends on the shortcomings of the classification. Grekov, out of 511 operated cases of I., reports 4 cases of gallstone obstruction, 5 cases of embolism of the mesenteric arteries, and 7 cases of spastic I. According to the summary data of Moscow prosectoriums for the years 1923-27, out of 33,609 autopsies (including newborns), 214 obstructions were noted, not counting strangulated hernias; the latter for the years 1925-1927 (out of 23,039 autopsies) were noted 56 times. Volvulus in the indicated data accounts for about 60%. It is interesting to compare Russian statistics with foreign ones. For this purpose, one can take the statistics of London hospitals for the year 1925. Gallstones. ..........

In London, volvulus accounts for slightly more than 4% of all obstructions, i.e., approximately the same as intussusceptions account for here. On the other hand, in London, 37% of ileus cases are attributed to pure intussusceptions, i.e., intussusceptions without tumors. In short, intussusceptions in London occupy the place that volvulus occupies here, and volvulus occupies the place that intussusceptions occupy here. Ileus caused by the presence of a diverticulum is usually classified as a strangulation. Lopatin-Baatz from the Razumovsky clinic provides a summary of the frequency of ileus from a diverticulum in relation to ileus in general. In the Razumovsky clinic, out of 28 cases of ileus, 6 are counted as depending on Meckel's diverticulum (about 24%). In foreign literature, the frequency of ileus depending on a diverticulum fluctuates within the range of 5–7% to 20%. Symptomatology and diagnosis. The symptoms of ileus are quite distinct in acute forms accompanied by hemostasis, and in chronic forms developing as a result of a gradual decrease in the intestinal lumen. The first form is characterized by the suddenness of onset, the sudden appearance of severe pain sensations that bring the patient to a state of shock: pallor, coldness, weakness, cold sweat, increased heart rate, and a drop in blood pressure. Just as suddenly, the passage of feces and gas ceases. The pains are constant in nature, periodically intensifying due to increased peristalsis of the afferent segment of the intestine. In the very first hours, local symptoms from the abdomen do not yield anything definite: the abdomen is even retracted, there is no local contraction of the abdominal muscles. Vomiting, which appears at the beginning of acute ileus, also does not present anything characteristic, as it is (as is thought) reflex vomiting. Subsequently, the symptoms become more characteristic: with high-located ileus, vomiting appears early, which becomes more frequent and acquires a fecal character. Uneven distension of the abdomen is determined: either the intestine that has undergone volvulus (Wahl's sign) or the intestine leading to the site of strangulation becomes distended. Sklyarov, Yukelson, and others rightly draw attention to the diagnostic and symptomatic significance of the splashing sound: the latter can arise either in the twisted intestine or in the afferent distended segment of the intestine. In the peritoneal cavity, in its dependent areas (lumbar regions), the presence of effusion is detected by percussion; it is easy to prove that it is mobile (change in dullness upon changes in the patient's position). The amount of blood chlorides falls. English surgeons (e.g., Taylor) correctly distinguish three periods in the course and symptomatology of acute ileus. Two of them have already been described above. In the third period, a picture of peritonitis and paralytic intestinal obstruction is added. The abdomen is uniformly distended and quiet, the diaphragm is pushed upward, dyspnea, incessant regurgitation, dry lips covered with crusts, sunken facial features, sharply increased pulse, low blood pressure, sharp limitation or even cessation of urination (in hopeless cases); consciousness is preserved. From the onset of the disease to death, several days pass if surgical aid is not provided. Rarely does the disease drag on for weeks, which happens when the volvulus or strangulation is partial, the influx of arterial blood to the intestine suffers little, 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 during surgery. One can suspect the hemostatic form, and specifically the embolic one, by examining the heart—the presence of chronic or acute endocarditis. It is almost impossible to make an exact diagnosis of the cause of acute ileus in the very first hours. Sometimes, by the localization of pain and with the help of additional examinations (washing the intestines with a siphon enema, inflating the intestine through the anus), it is possible to determine a volvulus of the sigmoid colon specifically. Practically, one can be satisfied with recognizing acute ileus, leaving the clarification of detailed diagnostics to the operation: the first act of the operation—opening the abdominal cavity—is the last act of the examination. A precise diagnosis is made more easily, and symptoms are clearer, in chronic ileus caused by a gradually developing narrowing of the intestinal lumen. Cramp-like pains gradually and slowly increase in both their frequency and intensity. They are localized in a specific place. With the pain, the patient feels a transfusion of fluid (gurgling) or the passage of gas as if with a whistle. In one or another part of the abdomen, local distensions appear, periodic, of a peristaltic nature. Usually, bowel evacuation is hindered: constipation increases. An exception to the general rule is tuberculous strictures of the intestines, in which there is frequent bowel evacuation of a mucous-bloody character. Mucous-bloody stools also occur with cancers of the intestines, but only with cancers that usually do not cause significant phenomena of ileus. Palpation of the abdominal cavity in chronic ileus often determines a tumor that is sometimes more, sometimes less mobile, sometimes more, sometimes less nodular, sometimes more, sometimes less dense. Around the tumor, a peristaltic wave of the intestine (afferent) is observed, raising the abdominal wall from time to time. 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 obstruction, 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, in the presence of peristalsis, a splashing sound is rarely caused, as the contents of the large intestine are dense. Based on the location of the tumor and other symptoms of chronic intestinal obstruction, it is possible and necessary to draw a conclusion about both the location of the narrowing and 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 the large intestine is usually located, e.g., into the right or left iliac region. For a more precise recognition of chronic ileus, one can resort to 1) fluoroscopy and radiographs of the intestines after giving a contrast mass per os, 2) fluoroscopy and radiographs after introducing a contrast mass into the rectum. The latter type of examination is unsuitable for determining the level of obstruction of the small intestine, as the contrast mass does not spread beyond the ileocecal valve. From typical cases, where at least the recognition of ileus does not meet with difficulties, there are a number of deviations where intestinal obstruction is relative and comparatively small (adhesions, slight kinks). Then, prolonged observation and examination with X-rays allow one to arrive at a more definite diagnostic conclusion. Recognition of spastic ileus sometimes meets with insurmountable difficulties. A diagnosis of mechanical ileus is often made, and the diagnosis is essentially correct, as the spasm of the intestine creates a mechanical obstruction. During the operation, the essence of the matter is clarified. It is easier to make a diagnosis when the patient has already undergone an operation previously and a spastic form of ileus was found during it. But even here one must be careful, as after an operation for spastic ileus, a typical mechanical ileus can arise. One has to study the patient and make a diagnosis based on the sum of data from subjective and objective examinations. Spastic ileus of hysterical origin is characterized by the duration of the course without stormy phenomena, without phenomena of increasing intestinal obstruction. Hysterical ileus has a seemingly stationary character, with the presence of phenomena of hysteria. Regarding the signs of ileus paralyticus, see Peritonitis. Here, only the symptoms of paralytic postoperative ileus, which develops without the presence of signs of peritonitis, will be indicated. The most constant symptom is severe distension of the abdomen with cessation of gas passage. Along with this, there is pain, though not very intense. Sometimes vomiting is added. The patient does not give the grave impression that peritonitis gives. The patient's temperature is usually unchanged, the pulse is not accelerated or only slightly accelerated. It should be noted that in the postoperative period, not only paralytic ileus can develop, but also mechanical ileus in the form of volvulus, strangulation, kinking of the intestine, etc. Therefore, ileus as an "accidental" complication of the postoperative period should be strictly distinguished from temporary postoperative paralytic ileus. The distinction lies in the fact that acute ileus always begins suddenly, stormily, and is accompanied by severe pain up to and including phenomena of shock. The treatment of ileus from a fundamental point of view is clear and simple: if the intestine is completely obstructed or its patency is significantly reduced, then it is necessary to either 1) restore its patency or 2) provide an outlet for the contents from the afferent segment of the intestine. The clarity of the fundamental formulation of the question of treating ileus is obscured by spastic ileus, since in it the intestinal obstruction has a functional character; influencing it by operation, i.e., by mechanical action on a functional disorder, is quite difficult if we are talking about purely local operations on the intestines. In acute complete ileus, vital indications come first.

In the very earliest stages, one may attempt lavage via the anus using siphon enemas; if a volvulus of the sigmoid colon is suspected, careful inflation of the intestine via the anus may be attempted. Under no circumstances should laxatives be given. Surgery should be performed as early as possible, even before the appearance of local abdominal distension. With an accurate diagnosis of the site of obstruction, any incision of the abdominal wall that is most advantageous 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 the intestinal obstruction. There is no need to fear evisceration of the intestine. The intestines are placed between hot towels. In early surgery for internal strangulations, volvulus, and kinks of the intestine, the operation ends quickly: the intestine is freed from strangulation, untwisted, and extracted from the site of strangulation. If the strangulation occurred in a peritoneal sac, the opening of the sac is sutured; if the strangulation or kink occurred under a peritoneal band or under a diverticulum, the band and diverticulum are resected. The abdominal cavity is closed tightly. The later the operation is performed, the more difficult it is. The altered intestine can be either bypassed, resected, or bypassed and then resected (Grekov's 2nd method). The choice of method is left to the discretion of the surgeon, depending on 1) the general condition of the patient, 2) the degree of alteration of the diseased intestine, and 3) the technical capabilities of the surgeon. It is advantageous to either resect or bypass an infarcted intestine or an intestine with a strangulation groove, but not to return it to the abdominal cavity under the assumption that it will recover: the infarct may affect only the mucous membrane, but a stricture may form at the site of the infarct after necrosis of the infarcted mucosa. Depending on the degree of the infarct, a bypassed infarcted intestine is either returned to the abdominal cavity or, if it is suspected of gangrene, left outside the abdominal cavity on tampons (after some time, it returns to the abdominal cavity on its own). A gangrenous intestine is either resected or bypassed, but after bypassing, it must be left on tampons outside the abdomen. Resection of the intestine can be performed 1) in one stage, with the ends of the intestine sutured either end-to-end or side-to-side; 2) in two stages—the intestine is brought out of the wound, the base of the intestine is sutured into the wound, and after a day or two, the intestine is cut off; 3) in two stages according to Grekov: bypassing the intestine to be resected with a side-to-side anastomosis, bringing it out of the wound, suturing it into the wound, and cutting it off after 1-2 days; the 2nd method of handling the intestine entails subsequent treatment of the anus. When the small intestines are overfilled in acute intestinal obstruction, puncture with a trocar is permissible for their evacuation. The loop of the intestine to be punctured is brought out of the wound, isolated from the peritoneal cavity, and a purse-string suture is placed at the site of the future puncture to tighten the formed opening. After evacuation of the intestine, the purse-string suture is tightened, and another row of sutures is applied (transversely to the axis of the intestine). Chronic ileus is also treated with all three operative measures mentioned above, i.e., 1) resection of the site of narrowing, 2) bypassing the site of obstruction, and 3) bypassing with subsequent resection. Both single-stage and two-stage resection are used, with the latter being used both with the creation of an anus and with preliminary bypassing of the site of obstruction. The choice of method depends on the patient's strength, local conditions, and the surgeon's qualifications. It must be kept in mind that: two-stage resection with the creation of an anus is applicable to all parts of the large intestine, even to the lower part of the ileum, but not to the jejunum (emaciation!). In benign strictures of the intestine (kinks, scars, pericolitis), bypasses should be as economical as possible: the anastomosis should be located closer to the site of obstruction. In tuberculous strictures, if a bypass is performed, the anastomosis should be placed in sections of the intestine that appear healthy externally. In both types of strictures, bypassing is best achieved with the help of a side-to-side anastomosis (incomplete bypass). In strictures of a malignant nature, if a bypass is involved, one can perform either a partial incomplete bypass or a complete bilateral bypass, whereby one of the ends of the bilaterally bypassed intestine must necessarily be sutured to the integument for the evacuation of the bypassed section of the intestine (mucous fistula). Ileus caused by foreign bodies (worms, gallstones, other objects) indicates the use of enterotomy. Complete ileus as an outcome of chronic ileus often indicates the creation of an anus praeternaturalis. Far-advanced mechanical ileus that has caused severe distension of the small intestines or paralytic infectious ileus indicates the use of fistulas on the ileum, or even on the jejunum (its initial loops). Such fistulas relieve the intestines from overdistension and allow a certain amount of contents to be absorbed into the blood. In view of the depletion of chlorides in the body during ileus, the intravenous administration of a three-percent NaCl solution in an amount of 500-1,000 cm³ is recommended. Outcome of surgical treatment. Operative treatment of acute mechanical ileus yields the following results (according to the statistics of treatment outcomes of Russian surgeons, collected by Gordon and Zykova). The cited statistics can now be significantly supplemented. From a comparison of the tables, it is evident that in a large body of material (Grekov, Ogloblina, Perelman, Yukelson), the mortality rate fluctuates between 55 and 60 percent. In small bodies of material, the mortality rate naturally fluctuates more. Kozyrev has an exceptionally fortunate percentage (28). Rozov in 1907 reported on 58 patients operated on for ileus; of these, 36 died, i.e., 62%. Tseidler in 1898 presented his material—17 cases of ileus, of which 9 died. The statistics of London hospitals from 1925 are as follows: Internal strangulations—28 cases, 50.0% mortality; Intussusceptions—358 cases, 43.5% mortality; Intussusceptions with tumor—342 cases, 31.0% mortality; [Other data points omitted in source]. From these data, it is evident that the successes of surgical treatment of ileus, both in the USSR and abroad, are not brilliant. The main reason for the poor results of operative treatment of ileus lies in the delayed application of the operation. Early operation for kinks of the intestine, strangulation, or volvulus is easy and effective in its result. An operation that is too late (when a gangrenous intestine surrounded by putrid effusion lies in the abdominal cavity) is hopeless. Intermediate operations are technically more or less difficult and heavy in their outcomes. Of course, here too one must strive to improve results by creating fistulas (temporary), infusions of hypertonic solutions, etc., but the center of gravity of the issue lies in early operations. It is better to perform a laparotomy even if one only suspects 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 they were operated on; in the second case, the person is condemned to almost certain death. Postoperative paralytic ileus is treated with siphon enemas, subcutaneous injections of physostigmine, intravenous infusions of hypertonic solutions, and intravenous or subcutaneous infusions of glucose solutions. It must be kept in mind that paralytic ileus can persist for several days and, as stated above, is sometimes accompanied by vomiting. If intravenous infusions of a hypertonic NaCl solution restore the balance of chlorides, then intravenous or subcutaneous infusions of glucose solutions (5-3%) restore the balance of water metabolism and nourish the body.