Pylorospasm

PYLOROSPASM, a disease of infancy, the essence of which consists in temporary or permanent narrowing of the exit portion of the stomach, as a result of which the walls of the latter become distended and vomiting occurs, which represents the main symptom of the disease. The most typical example of diseases of this kind is hypertrophic P., first described by Hirschsprung in 1887. The clinical picture of the disease is extremely uniform. In completely healthy, well-developing infants on the 2nd-3rd week of life without any apparent causes, vomiting begins and remains the dominant symptom throughout the entire course of the disease. A sharp deterioration in nutritional status, up to transition into severe atrophy, a significant decrease in the amount of urine, and persistent constipation are the natural consequences of this persistent vomiting. The first descriptions of this disease appeared in Denmark, Germany, Austria. In France and in our country until recently, the literature on this question was extremely poor, which is probably explained by insufficient familiarity of pediatricians with this disease. An extremely curious fact, which has not yet found a satisfactory explanation, is the significantly greater incidence of the disease in boys than in girls (the percentage of boys ranges from 75% to 90%). Several cases in the same family is a phenomenon described by many pediatricians. Relatively often such 'familial' cases are observed in twins. The character of feeding apparently has no significance in the etiology and pathogenesis of P. Symptomatology. Among the general symptoms of the disease, attention is drawn to some kind of concentrated, restless, tense expression of the face in these children. Wrinkles on the forehead Feer even considers a very characteristic sign of P. Hypertrichosis is also a very frequent symptom. Hair extends far onto the forehead, eyebrows are dense, often fused together on the bridge of the nose. Often children assume a forced position, throwing their head back. The most characteristic symptom of the disease is vomiting. Sometimes it begins already from the first days of the child's life (4% of all cases, Holt), in the vast majority of cases however on the 2nd-3rd week. Later it appears only rarely. Vomiting is initially expressed very mildly, however over the course of several days it intensifies so much that it becomes the central symptom of the disease. Vomiting is often noted even during eating; in other cases it appears not long after feeding. Sometimes vomiting is noted several hours after food intake and in these cases it usually has an especially violent character. Sometimes vomiting causes cyanosis in the child. Vomitus is expelled in a strong stream not only through the mouth but also through the nose ('fountain vomiting'). In some children, the slightest attempt to give them food causes the strongest swallowing spasm. In these cases, children after a few gulps with a piercing cry and with signs of severe pain push away the breast or bottle. Vomiting in especially severe cases occurs 30-40 times a day, in milder cases 5-10 times. The amount of vomitus in some cases exceeds the amount of milk sucked shortly before this; this is explained by the fact that the stomach becomes distended and food remains in it for a long time. The character of the vomitus varies; as a rule we have an acidic food mush consisting of curdled, and sometimes unchanged milk and gastric secretions. In not quite fresh cases, a large amount of mucus is often found. Sometimes the vomitus contains brownish streaks of clotted blood. Much less frequently an admixture of larger or smaller amounts of fresh, unchanged blood is noted. Finkel'shtein explains this by superficial submucosal hemorrhages, small erosions or even ulcers. Vomiting of coffee grounds is considered a sign prognostically unfavorable, indicating, as most believe, the presence of ulcers or large erosions. These ulcers are often localized in the area of the hypertroph pyloric sphincter. Klein-schmidt assumes that spasm of the pyloric sphincter can cause ischemia of adjacent areas due to compression of arteries with subsequent ulceration. The vomitus as a rule does not contain bile. If in some cases an admixture of bile can be found, then it is usually very little and it appears far from in every case of vomiting. Such severe vomiting is naturally associated with loss of significant amounts of food and therefore the nutritional status deteriorates. In some cases children lose weight slowly, gradually, in others a rapid, rapid fall in weight is noted. Over a relatively short period of time the child can turn into a very severe atrophic case. It is extremely important to note that the frequency and intensity of vomiting by no means always correspond to the state of the weight curve. Since the child loses large amounts of fluid with vomitus, the amount of urine decreases significantly. Instead of 400-500 cm³ of urine per day, which the child usually excretes on the 2nd month of life, in some cases in a child with P. only 16 cm³ of urine per day was observed (Vol'mer and Serebriy). Freydenberg even observed anuria. The urine becomes concentrated, often contains protein and formed elements. Albuminuria and pyuria should probably be explained by the significant dehydration of the body (Schiff's dehydration pyuria). Very characteristic for children suffering from P. is constipation; once every few days a scanty greenish 'hungry' stool appears. In some cases P. is accompanied by frequent liquid stool, which as a rule retains its 'hungry' character: its amount is small, the color is dark green, sometimes it contains a certain amount of mucus. On examination, the child's abdomen attracts attention. Usually it is sunken, and the sinking is mainly expressed in the lower part of the abdomen. Only the area of the stomach protrudes, and often the stomach is visible through the abdominal walls, along which powerful peristaltic waves periodically pass. This peristalsis begins on the left, moves toward the right hypochondrium and disappears in the area of the liver. Peristalsis is best observed with oblique lighting. Most often it can be noted immediately after eating. Light tapping of the abdomen in the stomach area with the fingertips also often promotes the appearance of peristalsis. This peristalsis can be explained by the presence of an obstacle in the exit part of the stomach in the form of a narrowed pyloric sphincter. On palpation of the abdomen, it is often possible to feel to the right of the midline under the liver a small dense rod-shaped tumor the size of the little finger phalanx, which corresponds, as operations and autopsies show, to the thickened, hypertrophied pyloric sphincter. Although with careful examination this tumor can often be felt, it must however be noted that there are unquestionable cases of hypertrophic P. in which the pyloric sphincter cannot be felt. The density of the palpable pyloric sphincter and the nutritional status of the child have essential significance. The more the abdominal walls are thinned, the more atrophic the musculature, the easier it is to feel the pyloric sphincter. In X-ray examination of fresh cases, the size of the stomach is found to be little changed; in prolonged cases the stomach may be distended and dilated. Most attention is drawn to the powerful peristalsis and the prolonged retention of food in the stomach. Sometimes even after 6 hours a significant part of food remains in the stomach; only very small amounts of contrast medium are visible in the intestine. Metabolism in P. is sharply disturbed, and it is completely natural that the persistent vomiting observed in this disease leads to a series of pathological changes. A detailed study on this topic was published by Vol'mer and Serebriy, whose data were subsequently confirmed by many researchers (Phelizot, Maize Is and others). In the study of gastric secretion, many found acidity significantly increased, but studies conducted by Vol'mer and Serebriy showed that there are no grounds to speak of a regular increase in acidity of gastric juice in P. On the contrary, cases with hypochlorhydria are often encountered. The nitrogen balance in P. is difficult to study, since it is practically impossible to account for all the amounts of food that the child retains. Existing studies allow one to think that there are no significant deviations from normal in P. Excretion of ammonia is as a rule significantly decreased; in severe cases of P. the urine does not contain ammonia at all. The sharp decrease in the amount of formed ammonia is especially clearly manifested in the decrease of the ammonia coefficient; instead of the normal 14 it sometimes reaches 0. From the side of the blood, attention is drawn to significant hypercapnia, exceeding in some cases 100 volume % CO₂ [maximum 114, normal 45-55 (Vol'mer, Serebriy)]. Apparently the activity of the kidneys, which excrete a relative excess of alkaline valences, is insufficient, and this explains such a significant increase in the alkaline reserve of the blood.

The ion concentration of the blood in all severe cases is found to be reduced, i.e., there is a shift toward alkalosis (pH up to 7.51). In mild cases of P. the blood pH is unchanged. The chloride exchange is severely disrupted. The loss of chloride by the body with vomitus leads to a significant decrease in the level of chloride in the blood (down to 300 mg% instead of the normal 550-600 mg%) and presumably also a decrease in chloride content in the tissues. The amount of chloride in the urine sharply decreases, sometimes it is absent altogether. The content of Ca, K, and P in the blood serum does not change. Since in P. alkalosis is almost always present, theoretically one could expect the presence of signs of tetany (spasmophilia). The latter, however, are observed exclusively rarely. The reasons for this are not yet entirely clear. It is necessary to note here that the indications sometimes found in the literature according to which P. is one of the symptoms of tetany are not entirely correct. Course of the disease. All the phenomena described above, characteristic of P., usually last for weeks. In some cases the clinical picture remains severe throughout, while in other, much more frequent cases, remissions occur during which vomiting is not so frequent and as a result the general condition of the child noticeably improves. This cyclical, wave-like course of the disease is a sign very frequently encountered in P. It undoubtedly indicates that in pylorospasm, along with hypertrophy of the pylorus, spasm of the exit part of the stomach has very great pathogenetic significance. In some children suffering from P., vomiting is not very pronounced; these children retain a significant portion of the food introduced and as a result their nutritional state does not suffer very much. Sometimes one can even speak of a rudimentary form of P. The disease does not always proceed so easily. In some children vomiting is so severe that the introduction of any sufficient quantities of food becomes completely impossible. The child begins to lose weight very quickly; often in a short time (2-3 weeks) he turns into a severe atrophic patient, often losing 1/5 and sometimes more of his original weight. The child is very listless, drowsy, his temperature is below normal. In some cases of these children, sudden increases in temperature to 39°-40° are observed, and no clinical basis for explaining these increases can be found. Most likely they are connected with the severe disruption of intermediate metabolism observed in P., in particular with alkalosis. In these cases it often creates the impression that death is inevitable. However, with the creation of an appropriate environment, with proper care and nutrition, a turn for the better often occurs. This improvement sometimes occurs suddenly, in other cases it appears gradually. Vomiting becomes not so violent, not so frequent, the child begins to retain ever larger quantities of food. One of the first signs of improvement is the disappearance of constipation. But even when vomiting has ceased and the child has begun to gain weight, peristalsis of the stomach can still be observed for a long time. In other cases this improvement does not occur and the child dies. Relatively rarely is starvation as such the cause of death; much more often the child dies from an accidentally acquired infection. However, even where a known improvement has already occurred, where vomiting has begun to weaken, it is still premature to speak of recovery. One must remember that the tolerance of these children to food is sharply reduced. When too large quantities of food are administered, signs of intoxication can easily appear in them. A turn for the better, where it has occurred, is usually observed at the 4-5th month of the child's life. Feer therefore asserts that in conservative treatment it is important to bring the child to 3-4 months. Pathological anatomy. On autopsy of children who died from P., marked changes are found in the pylorus. It represents a very dense, often cartilaginous consistency cylindrical body 2-3.5 cm in length and 1.5-2.0 cm in width, inserted between the stomach and the duodenum. Heile draws attention to the fact that the typical 'tumor' of the pylorus represents a very dense muscular cylinder, which crunches when cut and contains very little blood. Along with this, there are also cases of P. in which the pylorus is less firm to the touch and contains much more blood. Into the lumen of the duodenum the hypertrophied pylorus protrudes in the form of a fleshy funnel with an opening in the middle, resembling the portio vaginalis uteri. The lumen of the hypertrophied pylorus - when viewed from the duodenal side - usually has the shape of a rosette or a star. This is explained by the fact that the mucous membrane lining the pylorus is folded into longitudinal folds. On the prepared specimen in addition to longitudinal folds, transverse folds can often be noticed. The latter have particularly great importance, as they can close the lumen like a valve and make it completely impassable at times. The lumen of the pylorus is always significantly narrowed, although very unevenly. In rare cases a catheter can be passed through it, a thin probe passes with difficulty, and finally in some cases liquid barely passes through (Skvortsov). On microscopic examination it turns out that the hypertrophy of the pylorus is caused by an increase in the muscular layer, and as a rule the normal quantitative relationships between the longitudinal and transverse musculature are preserved. The hypertrophy of the musculature, being most pronounced in the region of the pylorus, also extends to the walls of the stomach. Dilatation of the stomach is usually observed only in protracted cases. As for the mucous membrane of the stomach, no particularly marked changes are present; sometimes slight petechiae, erosions or even ulcers are described. Pfaundler was the first to draw attention to the fact that sometimes on autopsy of children who never during life suffered from gastro-intestinal phenomena, the stomach is in a contracted state and these 'systolic' stomachs (Pfaundler) closely resemble the picture of pylorospasm. The question is decided by the absence or presence of muscular hypertrophy. While the thickness of the contracted wall of a normal pylorus does not exceed 3 mm, in P. its thickness is 5-7 mm. On autopsy of children who died from P., it was noted that hypertrophic stenosis of the pylorus in 4% of all cases is combined with other congenital malformations: constrictions, stenosis (infra- or suprapapillary) of the duodenum or other segments of the intestine, dilatation of the lower third of the esophagus, dilatation of the renal pelvis, enterocystoma, etc. (Pfaundler). b.m.e. sr. xxiv. o<> Practically this has a certain significance, as it explains some failures observed in the surgical (and to some extent conservative) treatment of P. The etiology and pathogenesis of P. remain to this time not yet entirely clarified. Hirschsprung, and then a whole series of other researchers (Finkelstein, Ibragim and others), who published works on this topic, believed that they were dealing with a congenital organic defect of development, consisting in a primary pathological increase in the muscular mass of the pylorus; this hypertrophy of the pylorus causes the phenomena of stenosis. Flynn, Murray and some others were inclined to consider the hypertrophy of the pylorus a manifestation of phylogenetic atavism. They pointed out that in some mammals the relationship between the thickness of the muscular layer of the pylorus and other parts of the stomach very closely approaches what is observed in hypertrophic P. This view could be considered to a certain degree justified only if it could be proven that man stands in a direct genetic connection with these animal groups and not on different branches of one common phylogenetic trunk (Skvortsov). Finally, the opinion was expressed that hypertrophy of the pylorus is an atavism not phylogenetic but ontogenetic. In this connection reference was made to research (Retzius, Müller) according to which in embryos the pyloric canal, in contrast to what we find in children and adults, is characterized by a much more powerful development of the musculature than the other parts of the intestine. None of these theories, explaining in one way or another the origin of hypertrophy of the pylorus, gained widespread acceptance at that time (the 90s of the 19th century). The most complete and detailed critique of the view of P. as an organic congenital defect was given by Thomson (Thomson, 1895), as well as Pfaundler, Wernstedt and others. The main objections of these authors amounted to the following. 1) No cases of congenital P. have been described in either the fetus or the newborn. 2) The disease in the vast majority of cases begins at the 2-3rd week. 3) During the disease remissions are very often observed without any apparent causes, during which all phenomena subside or even disappear completely. 4) A considerable number of cases of hypertrophic P. end in recovery with conservative treatment, or even without any treatment. For a long time after the disappearance of all symptoms of the disease, a hypertrophied pylorus can still be palpated.

Sometimes it can also be confirmed anatomically in cases of accidental death of a child who, during the first months of life, suffered from P. 5) There are cases in which, despite the presence of quite definite, severe clinical symptoms of P., we do not find hypertrophy of the pylorus on autopsy. This discrepancy between clinical symptomatology and patho-anatomical data can only be explained by the possibility of the appearance of the symptom complex of pylorostenosis on the basis of pyloric spasm, i.e., pylorospasm. Thomson draws an extremely important conclusion from this: where hypertrophy of the pylorus exists, it is a consequence of primary spasm, resp. a violation of the coordination of activity of the stomach muscles; hypertrophy of the pylorus is a kind of working hypertrophy. Thus, Thomson denies the presence of a congenital developmental defect and considers the entire disease as a special kind of neurosis. Very prominent pediatricians (Feer, Geibner, Bendix, Cherny and Keller) have joined Thomson's point of view. Be that as it may, the presence of spastic phenomena in pylorostenosis is beyond any doubt. Finkelstein even believes that vomiting in pylorostenosis is very often not a consequence¹ of stenosis; to a large extent it is explained by processes of a spastic nature that have nothing to do with stenosis. In purely organic stenoses, vomiting never has such a violent character. It is also rare in organic stenoses to observe the powerful, characteristic of P. peristalsis, which gave some authors reason to speak of gastrospsam. However, even Thomson's hypothesis, which considered that hypertrophy of the pylorus is always a secondary phenomenon depending on spasm, met with a number of very substantial objections. The most probable is that the spasm is primary and congenitally hypertrophied pylorus. Clinical manifestations of pylorostenosis appear only when a spasm is secondarily superimposed on the hypertrophied pylorus. At the same time, it is well known that there exists a picture of the disease that extremely resembles pylorostenosis, in which we do not find hypertrophy of the pylorus on autopsy, so obviously in this latter case we are dealing with P. Does this last concept rule out the possibility of secondary working hypertrophy of the pylorus on the basis of primary spasm? It is impossible to prove the possibility of such working hypertrophy appearing, since in each individual case it cannot be established whether the pylorus was already hypertrophic in the child at the moment of birth. The hypotheses of recent times concerning the etiology, and partly also the pathogenesis of P., are little probable. According to the views according to which P. represents a manifestation of avitaminosis B* (Brodie) or combined avitaminosis B+C (Reyher), are little substantiated. The immediate disappearance of all symptoms of P. after a successful operation without the introduction of any vitamins is sufficiently weighty to refute the opinion just presented. The view of Cohen and Breitbart (Cohen_r Breitbart), who consider P. a manifestation of allergy, finds no confirmation in the material of European authors. Stolte's hypothesis, according to which hypertrophy of the pylorus is explained by the action of maternal hormones, does not withstand criticism. Pylorostenosis and pylorospasm. At the present time, many authors [Pfaundler, Feer, Heile, Nobel, Langovoy, Andrews] strictly distinguish pylorostenosis from P. in the narrow sense, attaching very great importance to differential diagnosis for deciding the question of the therapy of the disease (surgical or therapeutic treatment). Nobel and Priesel also differentiate pylorostenosis* from P., using both the clinical picture and X-ray examination [see separate table (to the article Heart Defects), fig. 8]. Heile also stands on the same point of view; if after 3 hours a significant part of the food remains in the stomach, then the child has pylorostenosis and needs to be operated on. Andrews somewhat extends the period and believes that the diagnosis of pylorostenosis can only be made when after 6 hours about V-2 of the barium mush remains in the stomach. All the symptoms characterizing one or the other disease are so inconsistent, unstable, that the compiled schemes for differential diagnosis only emphasize this inadequacy. The course of the disease usually quite clearly shows the predominance of spasm over stenotic phenomena or vice versa. The indication for surgery is the severity of the disease, the rapid exhaustion of the child, and not only the presence of stenosis, which may be relatively small. In each individual case, it is of course desirable to differentiate pylorostenosis from P.; however, it must be pointed out that this is not always possible. In general, P. proceeds more easily. At the same time, one has to observe and indisputable cases of pylorostenosis (fountain vomiting, powerful peristalsis, palpable pylorus), which proceed comparatively easily. And this is understandable: the degree of narrowing can be very different, and this largely determines the course of the disease. Finkelstein, carefully weighing all clinical data, points out that the antemortem diagnosis is not always possible. Despite all the difficulties, wherever possible, it is necessary to differentiate the degree of pylorostenosis and P. In addition, it is necessary to take into account the possibility of confusing pylorospasm with some other diseases: namely 1) with habitual vomiting; the latter proceeds comparatively easily, peristalsis is always absent, the pylorus is never palpable, constipation is less common; 2) with rumination; in this disease there is actually no vomiting; food comes back from the stomach into the mouth, and the child with visible pleasure "chews" it, while food slowly flows from the corners of the mouth; 3) with starvation, which can also cause a picture resembling the most severe P. (fountain vomiting, even stomach peristalsis, constipation); the introduction of sufficient quantities of food quickly eliminates all phenomena. Some rare gastric diseases (spasm of the middle part of the stomach, "catarrhal gastritis" of French authors) can give a picture similar to P. They are observed in children older than 6 months, exclusively on artificial feeding, and develop very gradually. It is extremely difficult to distinguish hypertrophic P. from stenosis of the pylorus caused by a congenital anomaly (Landerer-Meyer type), or stenosis of the duodenum, localized above the opening of the bile duct. These diseases are generally rare. The combination of P. with cardio- or esophagospasm can only be recognized radiologically. Treatment. A huge number of works have been published on the question of treating P. Basically, there are 2 "methods of treatment-conservative and surgical. From the works of recent years, it is evident that very great successes have been achieved in the conservative treatment of P. It can be considered indisputably established that with skillful treatment and good care in favorable conditions, mortality from P. is relatively small. One of the basic conditions for successful conservative treatment is the feeding of the child with mother's milk. Most often, at the beginning of the appearance of the disease, the child is breastfed by the mother. In the first days of the disease, the child can be left at the mother's breast, and transferred to 10 feedings. If this does not help, fountain vomiting continues and the child quickly loses weight, then it is necessary to take the child off the breast and feed it with expressed mother's milk. During the day, no more than 10 feedings should be prescribed. Assigning 20-24 feedings a day to the child (i.e., every hour with a few teaspoons) is completely inappropriate, as the child is completely deprived of rest. The amount of food should not be too large; it is better to give less, but with the calculation that the child will retain this amount of food. Initially, the child is prescribed 100 g of mother's milk per 1 kg of body weight per day. At the same time, the child receives about 70 calories per 1 kg of body weight, i.e., its energy minimum. If the child vomits even with these small amounts of food, it is advisable to give the child an additional amount of food that he lost by vomiting. The use of skimmed milk is theoretically not justified and practically gives no results. In P., we are interested in the opposite, i.e., in the introduction of concentrated food. It is best to concentrate mother's milk with carbohydrates (beet sugar, nutritive sugar, mondamkn), and at the same time it should not be boiled. It is advisable to use thick porridges prepared with a small amount of milk. Where P. is combined with aerophagia, porridges help especially well; where there is no aerophagia and the stenosis is particularly pronounced, porridges give no good results. Porridges, whatever they may be, can only be supplementary food; the child cannot be fed exclusively with them. As for the use of ordinary artificial mixtures, none of them is suitable for the dietary treatment of P. In severe cases, some advise introducing food through a tube: gastric (Pfaundler) or duodenal (Hess, Putzig). Hess and Putzig indicate that the use of a duodenal tube gives excellent results.

Due to purely technical difficulties, this method did not receive widespread adoption. The introduction of an adequate amount of fluid is of great importance in the conservative treatment of P. Where possible, it is necessary to administer fluid per os. Where this is difficult, ordinary enemas are used (3-4 times a day with 30-40 g), Ringer's solution or 5% glucose, or drip enemas (1 drop per second, 90 g in 1/2 hour). If these measures do not achieve the desired effect, it becomes necessary to resort to subcutaneous infusions of Ringer's solution (1-2 times a day with 90-120 g; larger amounts are difficult to administer in one dose). Gastric lavage is recommended by many authors (Ibrahim, Pfaundler, etc.). It is performed 1-2, and sometimes more times a day, but usually does not yield good results. Sometimes the use of a pacifier immediately after feeding is of great service (Korolev). Of medications, atropine (Atropinum sulfuricum 1:1,000) is most widely used. It is usually given 10 minutes before feeding, starting with 1 drop before each feeding, increasing on average to 25 drops per day. It is important to know that children tolerate atropine better than adults, but cases of poisoning (dry mucous membranes, dilated pupils, scarlet fever-like rash) have been described even with relatively small doses. Atropine does not always have a beneficial effect. By slowing peristalsis, it only reduces compensatory gastrospsam; according to some authors, atropine has no effect on the tone of the pylorus at all (Salomon, Freydenberg). Favorable results are sometimes obtained from the use (especially subcutaneous) of adrenaline (2 decigrams under the skin). Opium and papaverine can also be included in this category of remedies. Folmer and Serebrysky, based on the presence of alkalosis, proposed the use of hydrochloric acid (1/10 solution up to 30-40 cm³ per day). This remedy is purely symptomatic in nature and in its action can be compared with atropine. Among other measures, the application of dry heat (1/2 hour with a hot water bottle, 1/2 hour rest, etc.) is of great importance. A favorable effect from the use of diathermy was observed by Tobler. According to Rossi, satisfactory results are obtained by exposing the child to a mercury-quartz lamp. Radiotherapy, which gives satisfactory results according to Wiener, has not yet been sufficiently studied. The creation of an appropriate environment (well-ventilated, bright room, quiet, prevention of influenza infections) and care are of great importance. Surgical treatment of P. If the old method of surgical treatment of P., which consisted in stretching the pylorus (Loreta, Foramitti), resulted in 60-80% mortality, then the introduction of extramucous pylorotomy (Ramstedt's operation) has radically changed the entire picture. Ramstedt's operation, which Feer calls the Columbus's egg in the surgical treatment of P., consists of the following: through a longitudinal incision of the rectus abdominis muscle, 3-4 cm long, the abdominal cavity is opened in the region of the pylorus. The stomach usually protrudes through the incision. The pylorus is extracted and all layers are cut longitudinally down to the mucosa. When cutting, the hard pylorus makes a crunch similar to cartilage. Without suturing or even closing the pylorus, the abdominal cavity is tightly closed with the mesentery. The operation is not associated with the loss of any significant amount of blood. Its duration is 3-10 minutes. The operation is best performed under local anesthesia. The postoperative period is very important. The operated child should be managed as in severe dyspepsia, namely, a tea diet should be prescribed (for 8 hours) and then, starting with 200 g of maternal milk (20 g per feeding), gradually increase (by about 100 g daily) the amount of food. In the first 1-2 days after the operation, the temperature may be elevated even to 39°-40°. Vomiting usually stops immediately after the operation, but Ramstedt points out that it may persist for 1-2 days; he explains this either by the anesthesia or by the atonic state of the stomach. If vomiting persists longer, a second operation is necessary. Experience shows that in such cases not all muscle bundles were cut and therefore the stenosis remained uneliminated. Cases have also been described in which vomiting that did not stop after Ramstedt's operation was explained by duodenal stenosis that existed along with P. Such cases, however, are very rare. The question of which method of treatment to prefer—surgical (as some Americans and English do) or conservative (as some Germans and Danes do)—is decided depending on the severity of the disease, the conditions in which the child has to be treated, and the resources at our disposal. If the case is severe, the child is rapidly losing weight, then after an attempt at conservative treatment lasting 3-5-8 days, it is better to turn the child over to a surgeon for the operation, and then again take him under the care of a pediatrician. One should not delay the operation for too long. The less weight the child has lost, the easier he will tolerate the operation. If the disease is relatively responsive to conservative treatment, then surgical intervention cannot be considered. The further development of children who have undergone P. in the first months of their lives proceeds quite satisfactorily. They do not differ from normal children in any way. Pylorospasm in adults—see Stomach, motor and secretory disorders.