Ultrasound of the fetal duodenum. Diagnosis of duodenal atresia in the fetus. Congenital intestinal obstruction

I want to tell you our story, maybe it will be useful to someone, because when I found out that my daughter had duodenal atresia, I found very little information on the Internet, much less stories with a good ending.

I’ll say right away that this is my first pregnancy, very long-awaited and desired. At 6 weeks I registered for a consultation and everything was fine - I had no toxicosis or any unpleasant moments associated with pregnancy until 23 weeks. At 23 weeks, my husband and I decided to do a 3D ultrasound in order to see our baby doll in all its glory, especially since the doctor - an ultrasound specialist does this type judging by the reviews on the Internet, the best one in our city, we went to the ultrasound as if it were a holiday - we were sure that there were no problems. The doctor examined the baby for a long time, showed us, told us that we were having a girl, she was about to finish the study when she noticed an enlarged stomach in the fetus. This began the biggest nightmare of my life. She identified a double-bubble in a child, that is, a double bubble in abdominal cavity and strongly recommended going to geneticists as soon as possible. Which is what we did the next day. A “wonderful” woman - a geneticist, for some reason, with special pleasure, almost with a smile (seriously, I’m not exaggerating) told us that this malformation in the fetus is a marker for Down syndrome, that such defects, as a rule, are not isolated and most likely more multiple accompanying vices will come out, that the vice is incompatible with life and many, many other “pleasant” things, to say that we were in shock is an understatement. She suggested that I undergo cordocentesis and terminate the pregnancy. Let me remind you that the due date was already 23 weeks, the nearest date for cordocentesis was in a week, and the result would have to wait 10 working days, that is, by the time I received the test result, I should have been 26 weeks! And I had to terminate the pregnancy at such a time when modern world children born at this stage are already being nursed. Nevertheless, we agreed to the analysis in order to know in advance whether the baby has chromosomal abnormalities; of course, there was no talk of termination. After going to genetics, I had a terrible hysteria (they’ll try to make you feel so bad that life doesn’t seem so bad), after which my kidneys were severely seized and I was taken by ambulance to the hospital, so until the end of my pregnancy I was almost constantly in hospitals with my kidneys, in total 6 times - I was even given a nephrostomy (((but this is not about me. The result of the cordocentesis was good, that is, all the karyotypes of the baby are normal, after which the same geneticist woman, having learned about the problems with the kidneys, told me: “So anything can happen.” Shall we interrupt it? Why do you need all this? ". Tough. My husband and I started searching for all kinds of information on this issue, there wasn’t much of it, we went for a consultation with pediatric surgeons, a million ultrasounds from different specialists and everyone told us one thing - we have to wait childbirth, only after delivery will the picture be clear, how and what next will depend on where the intestinal blockage occurred. We waited and prayed for our girl. I had a very difficult - terrible polyhydramnios (due to a developmental defect), plus constant problems with kidneys, nephrostomy (you constantly carry a bag with your contents). The doctors unanimously insisted that a favorable outcome is possible only with a full-term pregnancy and that I was unlikely to carry it to term due to polyhydramnios (at the end of pregnancy, 8 liters and that’s just water). But I carried my daughter to 38 weeks, the birth was more or less successful, not counting the fact that the ultrasound on the day of birth told me that the baby weighed 3800, and my daughter was born only 2900. Because of this, they did an episiotomy.

So Lisa was born! 2920 and 51 cm. She didn’t scream right away, since all the paths were clogged with secretions from the stomach. She was immediately put in intensive care and in an incubator; of course she was not allowed to eat, only intravenously, and I was not allowed to feed her. On the second day, the daughter was transferred to the regional children's hospital, to the intensive care unit, and began to prepare for surgery. We had the operation on the 4th day of life, it was very complex and difficult, since operations on the intestines are considered one of the most difficult for recovery period. Operation was successfully completed. 18 days of intensive care - we went every day - several hours of waiting and a few minutes of meeting with my daughter. Finally, after 18 days, Lisa was transferred to the surgical department and I was allowed to go to bed with her! And 18 days after the birth of my daughter, I finally took her in my arms. She was very, very weak, they fed her a little at a time, starting at 3 grams! a special mixture and then through a probe. The days in the hospital were a real hell, round-the-clock IVs, injections, a probe, all possible sensors - it was very difficult to take it in your hands, even to feed it, so as not to pull out or knock anything off. Endless catheter replacements - I wasn’t even allowed into procedures so that I wouldn’t see this and the long-awaited discharge. Almost 2 months later we were finally home! Of course, you can’t write everything, but I tried to write the main thing, I know that for someone it can be important, as it was for me once when the slightest information was important. Many thanks to the uzist doctor who diagnosed a defect of such early stage. We were ready and almost nothing was a shock for us. We were initially armed with information and therefore everything ended well. My daughter is developing according to her age, we have no restrictions in anything, an ordinary child is as if nothing had happened, only a small scar on his tummy reminds of what he has experienced. Fight for your babies to the end! This is 2 hours after birth)))

Page 11 of 107

Accurate data on the number of cases of atresia duodenum Not yet. The initial figure was 1: 50 thousand births, but in all likelihood, too low. The estimate of 1: 20 thousand births is also low (Amerson, Ihle, 1954) and the most probable ratio seems to be 1: 10 thousand births (Rickham, 1970). More than half of the cases relate to immature children with many concomitant other defects and disorders, in particular with mongolism (up to 50%), malrotation, heart defects, esophageal atresia, abnormal anorectal and skeletal formations. An excellent work is devoted to duodenal atresia by Salonen (1978).
Both Lynn (1972) and Rickham (1970) unanimously point out that the first description of this disease was given by Calder (1733); this, of course, was a selective diagnosis concerning a 7-day-old boy. Attempts to treat it did not come until much later, at the end of the 19th century, and since only gastrostomies or duodenostomies were performed, it is not surprising that the mortality rate reached a full 100%. Probably only Ernst (1916) managed to successfully perform duodenojejunostomy on a newborn girl. As late as 1951, Benson and Soigou noted only 57 cases of survivors - these data span a period of 36 years. During 1950-1962. Only 39% of those operated on, i.e. 18 children, survived the operation. In recent years, mortality has dropped to 36% (Girvan, Stephens, 1974), 30% (Stefan, 1977) and even less. This is due, of course, to the presence of concomitant defects and malformations, to the maturity of the child, or to aspiration broncho-pneumonia.
Clinical picture The disease is associated with the location of the septum. Above papilla Vateri it is rare. But if it is located here, then the symptoms do not differ from gastric atresia. These include, in particular, vomiting that appears immediately after childbirth, and there is no bile in the vomit. If the abdomen is swollen, then the swelling relates only to the epigastric region and may not be very noticeable if the child, due to persistent vomiting, has emptied digestive tract above the obstacle. Plain radiograph of the abdomen in vertical position shows a distended stomach on the right in front of the spine and next to it a bladder corresponding to the duodenum, possibly with a level: this is an image of two hydroaeric pockets corresponding to a distended stomach and duodenum. In the remaining parts of the intestine there is not the slightest trace of the presence of air.
With atresia located below p. Vateri, the most striking symptom is the ejection of a light yellow fluid, which appears soon after childbirth.
If vomiting appears only after 48 hours, then this is not atresia, but stenosis (see p. 78). The vomit is actually noticeably green. Zachary writes: "This is the lightest green you will ever see." In this case, meconium usually passes normally, and macroscopically there are no deviations from density, color and quantity during the first two days after birth. If the disease drags on, the amount of meconium quickly and noticeably decreases.
The general condition of the child depends on the duration of the illness. If it is recognized before 48 hours, then general state good and no signs of more significant dehydration. If recognition is late - after 4 or more days - the child’s general condition is usually poor with noticeable weight loss and signs of dehydration.
Establishing a diagnosis of duodenal atresia should not be difficult.
Regarding the meaning of polyhydramnios (polyhydramnios), see p. 15. To date, there are still no exact criteria for its diagnosis. A volume of about 2000 ml is considered a sufficient amount of amniotic fluid to establish the diagnosis of polyhydramnios, and at any stage of pregnancy. Raj (1973) states that the upper limit is 1700 ml at 30 - 37 weeks, while after the 43rd week a volume exceeding 1000 ml is pathological. Ultrasound has proven itself well in the diagnosis of polyhydramnios (Kirkinen, Jouppila, 1978).
Put correct diagnosis congenital atresia of the duodenum using ultrasound was still possible intrauterine Garret, 1975, Kobayashi, 1977, Kuryak, 1975). The most important aid is again a survey radiograph of the abdomen in a vertical (hanging) position, which shows, as noted above, an image of two hydroaeric pockets, of which the larger pocket corresponds to the stomach, and the smaller pocket corresponds to the duodenum. If, however, the child vomits immediately before the shooting, then this image of two levels covered with gas bubbles may not be so bright. In this case, it is advisable to introduce about 40 ml of air into the stomach through a tube. Air negative contrast often produces a much better image than barium suspension or verography. Below the level of the stomach and duodenum there is no air at all.
From such an x-ray, of course, it is impossible to decide with complete certainty whether in this case we are dealing with duodenal atresia, malrotation of the intestine (compression of the duodenum by the cecum that has not turned, congenital volvulus of the midgut, Ladd syndrome) or annular pancreas gland (Fig. 19, 20). If small and few gas bubbles are visible below the level of the duodenum, then we can talk about duodenal stenosis, malrotation of the intestine or annular pancreas. Fortunately, except for a wrong turn, these conditions are treated in much the same way.
Treatment: Preoperative preparation. If the disease is recognized in a timely manner, i.e., up to a maximum of 48 hours after birth, then the child usually does not need correction water-salt balance, nor disturbed mineral balance. But in principle there is no need to operate until correction is achieved possible deviation from the norm.

Rice. 20. Congenital infrapapillary atresia of the duodenum.

Rice. 19. Congenital suprapapillary atresia of the duodenum in the anteroposterior projection.
When to operate? If we know for sure that in this case the child suffers from duodenal atresia (the same applies to duodenal stenosis and annular pancreas), then the operation could be postponed (if the child was admitted to the hospital at night) until the next day, when the conditions for the operation are usually much more suitable. But it is often very difficult, even impossible, to distinguish atresia from congenital volvulus, in which infarction may appear after a few hours. Therefore, in the case of congenital duodenal atresia, surgery should be performed immediately - on the day the child is admitted to the hospital.

The most suitable is the transverse approach: the abdominal cavity is opened with a transverse incision, cutting the right rectus abdominis muscle, as well as the right oblique abdominal muscles. The height of the incision is chosen approximately at the level of the Xth rib, i.e. slightly above the navel. The incision is pulled a little past midline to the left, as a result of which it is not difficult to find the umbilical vein, which can, if necessary, be used for intravenous fluids or for blood transfusions.
The amount of parenterally administered fluid is usually small and blood is often not prescribed, but it should always be available to the surgeon.
After opening the abdominal cavity, it is necessary to remember: if the colon and, in particular, the cecum are located normally with the simultaneous absence of congenital intestinal volvulus, then the diagnosis of duodenal atresia is confirmed; You just need to carefully check whether it is accompanied by an annular pancreas.
On the duodenum there is a double type of atresia:
a) membranous, usually called the duodenal septum,
b) atresia of a type in which the duodenum narrows extremely to an imperceptible diameter, and the septum and membrane are not found.
a) Obstruction caused by the septum - the membrane - is most often located in the third part of the duodenum. The duodenum ends conically above the obstruction, and it is noticeably stretched. The remaining part of the duodenum is noticeably narrowed and the jejunum to the same extent. The conical shape of the duodenum is caused by the septum, which is firmly attached to it at the periphery, and pressure on the septum swells, protrudes and stretches it middle part, resulting in the described conical shape. This type of duodenal obstruction is one of the simplest, which is very easy to treat. surgical correction: The duodenal wall is incised longitudinally just above the level of the septum. Having hooked a thin hook into the middle of the septum, it is brought into the distended section of the duodenum. The septum is then excised circularly with scissors, leaving only a very narrow border of this septum to avoid possible damage to the duodenal wall. In principle, this is enough. But according to Zachary’s experience, patency is not restored quickly after this intervention. Therefore, it is very advisable to make a longitudinal incision of the duodenum through its conical section, bringing it up to its narrowed section and to the jejunum. The wound is then sutured transversely in only one layer. Thus, a wide anastomosis with the jejunum is formed.
It is always advisable to supplement excision of the septum with the plastic surgery described above: it is known that after surgery for duodenal atresia, children usually vomit for many days, even weeks, until sufficient evacuation capacity of the stomach and duodenum is created. If excision alone is performed, the surgeon may feel that it is not enough, as a result of which the child is unnecessarily re-operated.
b) Actually (typical) duodenal atresia in the absence of a septum. At this type atresia, the duodenum narrows at the site of atresia into an extremely narrow lumen. Most often this occurs in the second section of the duodenum, close to its lower section. The most convenient access to this area is obtained by moving the colon to the side or, if necessary, dissecting it downwards and to the left. The distended area of ​​the duodenum is then clearly visible.
Previously, duodenojejunostomy or even gastroenteroanastomosis was performed. Despite the fact that some (Sigur, Esk) believe that the child has virtually no risk of developing peptic ulcer, exclusion of the peripheral part of the duodenum, but at least, not physiological. It is recommended, therefore, to form a duodenoduodenoanastomosis, without leaving, if possible, a blind, dead-end loop. If both atretic segments - above and below the septum - are located close to each other, then the anastomosis is relatively easy provided there is sufficient mobilization of the duodenum (in principle we're talking about about the method and method of mobilization according to K ocher). But even if both segments are located relatively far from each other, duodenoduodenoanastomosis seems possible; only it is necessary to mobilize the duodenum below the site of atresia (best behind the upper mesenteric vessels), moving it along with the duodenojejunal flexure towards the right; In this way, it seems possible to perform an anastomosis without creating tension in both sections of the intestine: both sections of the intestine are brought closer to each other, the back layer of sutures is applied, both sections are opened and an anastomosis is formed.
In the postoperative period, prolonged, protracted vomiting often occurs, or bile-stained contents have to be sucked out for many days. This is why Ehrenpreis and Sandblom (1949) and Glover and Barry (1949) began more than thirty years ago to use a transanastomotic probe, inserted intraoperatively at least 10 cm distally below the anastomosis. The modification according to Waterston also justified itself: a thin catheter made of plastic material is inserted into a rubber catheter, which is cut longitudinally on one side. Both catheters are inserted into each other and then inserted through the nose into the stomach. During the operation, the surgeon easily finds a thicker rubber catheter by touch and withdraws it through the pylorus into the duodenum, and further through the anastomosis into the jejunum. The outer, cut rubber catheter is then easily removed through the nose, leaving the thin catheter in place. It must again be emphasized that the plastic catheter must be inserted a minimum of 10 cm into the jejunum (Zachary), since otherwise there is a danger that when injecting milk it will protrude back due to a reactive effect.
c) For atresias located in the area of ​​the duodenojejunal flexure, unless, of course, you are dealing with the membranous type, when the method described in point a) is used - duodenojejunostomy is applied.
d) In case of supravateric atresia, gastroenteroanastomosis is performed, which in other cases it is advisable to avoid; Marshall's (1953) work on gastrojejunal ulcers in children very convincingly shows this danger (in contrast to Esk).
e) Children suffering from duodenal atresia behave as if their distended duodenum has lost - at least temporarily - all its strength and ability to contract. Gastric emptying occurs - according to Wilkinson, no earlier than the 8th day, and according to Aubrespy et al., no earlier than the 10th day. This problem can be solved, in principle, in two ways: either by exclusively parenteral feeding of the child for the required period of 8-10 days (without pointlessly operating on him again!), or by narrowing the distended proximal part of the duodenum - the sac - cul-de-sac-, “recalibrating”, thus, the duodenum on the recommendation of pediatric surgeons from Marseille (Aubrespy, Derlon, Seriat-Gautier, 1975, 1978).

1. A two-stage operation is recommended by Rehbein and Ochoa (1963): first, the distended duodenum is dissected just in its blind area, and its lumen is closed. The distal section is resected approximately 12 cm in length, a soft, thin rubber drain is inserted there and this section of the intestine is brought out in the upper third of the abdominal cavity. A drip infusion of 5% glucose solution is then poured into this aboral section, followed by breast milk. At the same time, gastroduodenal juice is injected and sucked out. The lumen of the jejunum quickly increases, as a result of which it is easier to apply an anastomosis - after 8-9 days. We ourselves have no experience in this method, and we had no need to resort to it; It remains questionable whether two operations do not increase the therapeutic risk.

Before completing the operation by suturing the abdominal wall, it is always necessary to make sure that there are no other anomalies in the abdominal cavity. Anomalies associated with duodenal atresia primarily include:
a) congenital volvulus of the midgut due to malrotation;
b) multiple atresias in the subsequent section of the intestine.
Postoperative treatment. Postoperative obstruction is often very protracted and the disruption of the humoral environment due to loss of gastric and duodenal juices can actually be very significant (Wilkinson, Hughes, Stevens, 1965); that is why it is advisable to introduce a transanastomotic probe, which allows you to soon start feeding the baby with milk.
There is no doubt, however, that despite all the advantages of the transanastomotic probe, there are also some negative aspects: a) insertion of the probe, even using the Waterston method, may encounter difficulties when passing through the pylorus, the upper part of the duodenum and the duodenojejunal flexure; b) as a result, the operation may take a long time and, moreover, may cause injury to the child; c) the literature describes cases of perforation with such a probe, in particular in premature infants. Rickham does not use a probe and, with impeccable parenteral therapy, did not notice the more significant metabolic disorders described by Wilkinson et al.
According to Rickham, gastrostomy has proven itself, especially in premature infants. Through gastrostomy, the stomach is easily relaxed, as a result of which postoperative vomiting - so dangerous, in particular for immature newborns - usually completely disappears. As soon as the sucked contents are no longer stained with bile, feeding can begin using a gastrostomy tube catheter. This is especially beneficial in immature children who do not have a sufficiently developed sucking reflex. Becker and Schneider (1963) performed a gastrostomy and simultaneously inserted a transanastomotic tube through the gastrostomy in parallel with the gastrostomy catheter, or used a double-lumen tube.
We believe that the transanastomotic probe inserted during surgery has a certain positive value. After all, an extended period during which it is necessary to constantly suck out the bile-colored contents - even if this is caused either by edema at the site of the anastomosis, or rather by impaired peristalsis of the distended part of the duodenum above the initial obstacle - can significantly complicate the successful course of postoperative nursing. Moreover, the position may be adversely affected by gastritis caused by the contents of the duodenum, which constantly returns through the wide open pylorus into the stomach, severely irritating the mucous membrane of the latter. Sometimes it helps to place the child on his right side or bring him to sitting position. Rickham, on the contrary, claims that the position of lying on his tummy has paid off for him; we have no such experience.
Forecast very different depending on what the child is like. In a full-term newborn without an additional combined defect, without another disease (for example, aspiration bronchopneumonia), it is very good; with a timely and properly performed operation, as well as with proper pre- and postoperative care, more than 90% of patients survive. Relatively good prognosis also applies to immature children who do not have other combined defects or diseases. Unfortunately, it is precisely in duodenal atresia that we are faced with serious concomitant malformations, and not as an exception, but quite regularly. In these cases, the prognosis is much more serious. Moreover, the prognosis for children with Mongolism is more serious, even if they do not suffer from other defects or diseases. Their increased mortality is likely due to increased susceptibility to both infection and injury. Rickham believes that the fact that children with Mongolism are often not provided (on purpose) with the same care and concern as those provided to healthy children may also play a significant role. Most common cause Mortality in Down's disease is bronchopneumonia, atelectasis, while sepsis, inflammation of the peritoneum, adhesive narrowing, heart failure (in children with congenital heart disease) or kidney failure (renal malformations) occupy only the second place among the causes of death.
The prognosis can be made more favorable by timely recognition and use of appropriate surgical techniques (refusal of gastrojejunostomy, use of the Aubrespy approach), as well as through the use of a transanastomotic tube or gastrostomy, as a result of which you can quickly move on to normal feeding of the child.

Atresia (fusion, obliteration) of the intestine is congenital pathology development of gastrointestinal intestinal tract child, consisting in the absence of a lumen in one of its areas.

Depending on the location of the pathology, several types of atresia are distinguished:

• pyloric – located directly after the stomach;
• duodenal atresia - located at the very beginning small intestine;
• jejunal atresia - the area is located between the upper and bottom small intestine;
• ileal atresia;
• colonic atresia - diagnosed in the area of ​​the rectum and anus.

Duodenal atresia

Duodenal atresia develops in the second or third gestational month. The pathology is characterized by complete closure of the lumen of the intestinal tube. In this case, a significant expansion of its proximal end occurs, capable of reaching the size of the stomach in its volume. In this case, the distally located intestinal loops have a small diameter and are welded together.

The following signs may indicate atresia:

• regurgitation amniotic fluid;
• after feeding, the child develops vomiting with bile impurities. This is explained by the fact that the intestinal fusion is located below the papilla of Vater;
• The abdomen is painless and soft on palpation, visually retracted;
• with obliteration of the duodenum, the passage of original feces is observed, but then the stool stops completely;
• In the first - two days after birth, the baby remains calm - the general condition of the child is normal. Later, he develops signs of toxicosis and exhaustion: the fat layer disappears, facial features become sharper, the skin becomes dry;
• aspiration pneumonia develops.

If left untreated, the child dies within 1.5 weeks from exhaustion and progressive pneumonia.

Diagnosis and treatment

To clarify the preliminary diagnosis, radiography is used. The image will clearly show gas bubbles located in the stomach and duodenum. In this case, the intestinal loops remain free. To obtain a more accurate image, a contrast technique is used.

On x-ray the absence of a section of the duodenum is quite clearly visible

Additionally carried out differential diagnosis with other congenital anomalies, in particular, annular pancreas. Treatment of pathology involves immediate surgical intervention. Its type depends on the location of the atresia relative to the papilla of Vater.

If the gastrointestinal tract is obliterated, a duodenojejunostomy is performed; if the obliteration is located higher, a gastrojejunostomy is performed. After the operation, the child may experience signs of duodenal dysfunction for quite a long time - regurgitation and vomiting.

Pathology of the small intestine

Atresia thin section intestines in newborns is most often diagnosed in lower section ileum. Slightly less common in the upper gastrointestinal tract. In some cases, the cause of obstruction of the intestinal tube is the presence of a membranous septum.

With atresia small intestine the newborn develops a fairly characteristic clinical picture:

• the child develops uncontrollable vomiting with impurities of blood and bile, and later impurities appear feces;
• no passage of meconium is observed;
• after feeding, intestinal motility increases significantly, clearly visible through the abdominal wall;
• bloating occurs against the background of a decrease in urine output, up to the complete cessation of its passage;
• vomiting causes the development of toxicosis and rapid weight loss, despite a good appetite.

Symptoms of small intestinal atresia appear on the first day of a baby’s life

A sharp retraction of the abdominal wall indicates an intestinal rupture. The newborn's condition deteriorates sharply, skin acquire a characteristic gray-green color.

The main method for diagnosing pathology is x-ray examination. If, in addition to the characteristic gas bubble, several more bubbles with a level are distinguished, then the location of the atresia is upper sections Gastrointestinal tract.

Numerous air bubbles with fluid levels become a sign of atresia, localized in the lower ileum or the very beginning of the large intestine. The use of barium porridge during radiology is strictly prohibited. orally.

The drug causes significant distension of the intestines, increasing the risk of perforation, and also increases the urge to vomit.

The disease has a poor prognosis, but in full-term children with early surgery and a small number of atresias, it improves. Surgery is recommended immediately after identifying pathology.

Rectal atresia

Rectal atresia is a congenital pathology characterized by underdevelopment anus(anus). Most often, the anomaly is diagnosed in boys. The disease requires emergency surgical correction performed within the first 24 hours after birth.

The pathology develops in the early antenatal period (from 12 to 29 gestational weeks) and is caused by fetal developmental disorders. The condition is characterized by the absence of an opening at the proctodeum (the depression at the posterior end of the fetal body that then becomes the anus) and the failure of the cloaca to separate.

Classification

Rectal atresia is usually divided into:

• to high (supralevator);
• average;
• low (sublevator).

The second classification of pathology divides rectal atresia into total (complete closure of the lumen of the intestinal tube occurs, without a fistula), occurring only in 10% of all diagnosed cases, and fistula format, which occurs in the remaining 90%.

The fistulous form of rectal atresia is of the following types:

• the pathological channel is discharged into the organs of the urinary system;
• fistulas come out into reproductive system;
• directly into the perineum.

Symptoms

First Clinical signs pathologies form 12 hours after the birth of a child - he becomes restless, sleeps poorly, refuses to latch on to the breast and almost constantly pushes. By the end of the first day of life, symptoms of intestinal obstruction appear: absence of meconium; the child begins to swell - observed severe bloating belly.

Vomiting begins, which contains bile and feces, and signs of intoxication and dehydration appear. If the baby does not receive qualified training in the near future medical care, he will die from intestinal perforation and subsequent peritonitis.

With low rectal atresia, instead of the anus, the child has a small funnel-shaped depression. Sometimes it is completely absent.

In some cases, the anomaly manifests itself as an overgrowth of the intestine, and then the anus is simply blocked by a film through which the accumulated meconium is clearly visible. A sign of this form of pathology is bulging of the anus during tension, the so-called “push” syndrome. With high supralevator atresia, it is absent.

After birth, all children, without exception, are tested for congenital anomalies. The anal area is also subject to mandatory inspection. In case of pathology, instead of the anus, the child will have a small depression.

It is important for doctors to determine the severity of the pathology. If the baby is missing only the anus, and the intestine itself is fully developed, then when the child cries, a protrusion is observed in the area of ​​the anus.

Fistulas extending into the urinary system are diagnosed in most cases in male infants. In girls, this type of atresia is much less common. A sign of pathology is the presence of meconium particles in the urine, and when straining, urethra gases come out.

Entry of intestinal contents into urinary tract causes the development of cystitis, pyelonephritis, and urosepsis.

A sign of a fistula of the colon, which has an outlet into the vagina, is the release of original feces through the genital opening. Acute intestinal obstruction does not develop in this format of atresia, but the release of feces in a similar way leads to the formation of vulvitis and various inflammations of the urinary system.

Another option for opening a fistula is the perineal area. Most often, an anomalous channel is formed near anus, scrotum or at the base of the penis. It is also impossible to perform a normal act of defecation, so in the next few hours the baby will develop symptoms of intestinal obstruction.

Diagnosis and treatment

To diagnose atresia, an X-ray examination is prescribed to the infant. In some cases, palpating the rectum is sufficient, during which the doctor encounters an obstacle.

Treatment of rectal atresia is only possible surgically. Children with sublevator (low) rectal atresia undergo perineal plastic surgery. For moderate and high forms of pathology, use surgical intervention an end colostomy is formed (removal of part of the colon or sigmoid colon on left side abdomen) with subsequent correction.

An infant operated on for intestinal atresia with a removed colostomy

After surgical treatment With moderate and high atresia, children often develop fecal incontinence. The prognosis in the absence of adequate therapy is unfavorable: the death of the child occurs on the fifth or sixth day after birth. But timely surgery does not guarantee a complete recovery. The intestines begin to function fully only in 30% of operated infants.

Colon atresia

Colonic atresia is characterized by complete obstruction of this section of the intestine. The pathology is extremely rare and accounts for only 2% of all diagnosed cases of intestinal atresia. The cause of the formation of the anomaly is considered to be intrauterine necrotization of a section of the colon as a result of pathological conditions, in particular, volvulus.

Signs of colon atresia appear in an infant on the second or third day. This is indomitable vomiting containing meconium impurities, bloating. Upon visual examination, you can notice stretched loops of intestine protruding through the abdominal wall.

Diagnosis includes mandatory radiography. The image clearly shows numerous gas bubbles with horizontal liquid levels. The intestinal loops are stretched, and the non-functioning section of the intestine itself looks like a thin cord.

An atretic area can be diagnosed in any part of the colon

Treatment of the pathology is surgical and consists of removing the atretic portion of the intestine, followed by the application of a colonic anastomy. In case of intestinal rupture and peritonitis, a proximal colostomy may be installed.

Intestinal atresia is one of the most complex anomalies in the formation of the intestinal tract. After the pathology is diagnosed, the baby needs emergency surgical intervention. Otherwise, the disease has an extremely unfavorable prognosis.

The main diagnostic method for suspected high intestinal obstruction is an X-ray examination, which begins with survey radiographs in a vertical position in two projections. A typical radiological symptom of “complete” high CI (duodenal atresia) is the presence of two gas bubbles with fluid levels (double bubble sign) and the absence of gas in the underlying intestine (Fig. 6). This X-ray picture absolutely reliably confirms the diagnosis of high CI, and therefore no additional methods studies (including the use of contrast agents) are not required.

Rice. 6. Atresia of the 12th duodenum. There are 2 gas bubbles with fluid levels and no gas in the underlying bowel.

With duodenal stenosis or a membrane with a hole (partial duodenal obstruction), radiographs sometimes show a small amount of gas distal to the duodenum, while the characteristic radiological sign of duodenal obstruction (double bubble sign) may be absent. A similar radiological picture is observed with partial intestinal obstruction caused by an annular pancreas (Fig. 7).

Rice. 7 Ring-shaped pancreas. There are 2 gas bubbles and poor gas filling of the distal intestine.

In this case, it is necessary to perform a contrast study and, first of all, to exclude malrotation syndrome, which radiographically and clinically may resemble partial duodenal obstruction. However, with malrotation (as opposed to malformations of the duodenum itself), life-threatening complications caused by midgut volvulus can develop if the diagnosis is not timely. Therefore, after survey radiographs, irrigography is performed in a direct projection to determine the position of the colon in the abdominal cavity. For irrigography in newborns, we use a 25-30% solution of verografin, which we prepare immediately before the examination by diluting 2.5-3 times with a 76% solution contrast agent. To fill the entire colon in full-term newborns (the first days of life), 45-60 ml of contrast agent is sufficient, in premature infants - 25-30 ml (at the rate of approximately 15-20 ml per kg of body weight).

If the colon is positioned correctly in the abdominal cavity (horseshoe-shaped), the diagnosis of malrotation syndrome with midgut volvulus can be excluded. In this case, to clarify the diagnosis, it is necessary to conduct a study of the passage of the contrast agent through the gastrointestinal tract. For this purpose, after washing the barium suspension from the colon, 15-20 ml of iodolipol or barium sulfate is injected into the child’s stomach. The delay in evacuation of the contrast agent from the stomach for 2 hours and the appearance on radiographs taken in a vertical position of two levels in the projection of the stomach and the initial part of the duodenum confirms the diagnosis of duodenal obstruction.

Almost all patients with high CI need preoperative preparation, which can last as long as the child’s condition requires, since this pathology usually does not cause life-threatening complications requiring emergency surgical care. Needs to be normalized biochemical composition blood (electrolytes, bilirubin, sugar, etc.), CBS, completely eliminate the symptoms of exicosis. Calculation of liquid volume for infusion therapy and the qualitative composition of the infusate is produced in the same way as in children with pyloric stenosis (see above).

The operation of choice in children with high CI with duodenal atresia and annular pancreas is duodenoduodenoanastomosis, and with duodenal membrane - membranectomy. If the obstruction in the duodenum is located near the ligament of Treitz, then a duodenojejunostomy is performed, since creating a duodenoduodenoanastomosis in this situation is impossible.

The choice of surgical correction method is determined by the need to maximize the restoration of the normal anatomy of the affected area, which is especially important for a growing organism. Therefore, with high CI in newborns and small children, an operation that is often performed in adult patients, namely gastrojejunostomy, should not be performed, despite the fact that this intervention is technically simpler than duodenoduodenoanastomosis or duodenojejunostomy. No matter how well the gastrojejunostomy is applied, the “left” blindly ending loop of the duodenum quickly increases in size as the child grows, which can be the cause of severe dyspeptic disorders (heaviness in the abdomen, frequent belching, periodic vomiting of stagnant contents, etc.) .

With any type of surgical intervention in newborns, we try to immediately during the operation provide ways for early initiation of enteral nutrition, especially in connection with our very modest capabilities for long-term balanced parenteral nutrition. To do this, during surgery for duodenal obstruction, we insert two probes: one into the stomach for decompression, the other into the jejunum (beyond the anastomosis area) for insertion nutritional mixture. We leave the gastric tube open to constantly remove stagnant contents from the stomach, and through an intestinal tube on the 3rd day of the postoperative period we begin the introduction of a nutritional mixture (adapted milk formula, breast milk) micro-stream at a low speed (2 ml/hour). As the patient's condition improves, we increase the speed of micro-jet administration. When the passage through the intestines is restored (as indicated by the cessation of “stagnation” in the stomach and the appearance of colored stools), we begin feeding into the stomach, while simultaneously reducing the volume of milk introduced into the intestine. Duodenoduodenoanastomosis begins to function, as a rule, on the 6th – 7th day of the postoperative period. By 8–10 days, it is usually possible to transfer the patient to full enteral feeding through the mouth and remove the intestinal tube.

Duodenal agenesis- an extremely rare congenital defect. We observed it in acardia in combination with aplasia of the liver and pancreas. TTP - before the 4th week of intrauterine life of the fetus. Atresia and stenosis of the duodenum. The population frequency of atresia of this localization is approximately 1 case per 10,000, stenosis - the first case and 27,000. The proportion of patients with this defect among those who died under the age of 1 month is 1%.

Among the occlusions of the distal part of the duodenum, stenosis predominates, and that of the proximal part - atresis; in the middle section the distribution of these defects is approximately equal. The most common type of atresia is membranous; as a rule, the membranes are devoid of muscle fibers; types II and III occur in 22.9 and 17.9% of cases, respectively. The work of other authors and experience show that the cord-like form of duodenal atresia is rare; the majority of malformed areas that have a strand VD, histologically represent a pronounced stenosis. Localization - most often near the major papilla of the duodenum, often in the area of ​​the duodenum-jejunal flexure.

Atresia at the level of the major duodenal papilla may be accompanied by dilatation of the common bile duct and are called T-shaped. Among suprapapillary forms, atresia in the form of free isolated blind ends predominates; below the major duodenal papilla, the membranous form is more often observed.

Stenoses are a perforated membrane or a hypoplastic area of ​​the duodenum, sometimes with a sharp violation differentiation of its wall.

A significant part of the anomalies of the duodenum is accompanied by a vicious formation of the head of the pancreas and bile ducts in the form of atresia and bifurcation of the common bile duct, anomalies of the cystic duct, and additional bile ducts.

Clinically atresia duodenum are manifested by a picture of high intestinal obstruction. At x-ray examination a sharp expansion of the duodenum is revealed, the volume of which is sometimes equal to the stomach, and two horizontal levels of fluid.

Cases of prenatal detection of duodenal atresia have been described.

Diagnostic criterion for ultrasound examination is the presence of contours of a sharply dilated stomach.

Atresia and stenosis must be differentiated from other causes of duodenal obstruction, mainly from its compression due to various disorders of duodenal rotation.

Treatment surgical - application of duodeno- or gastrojejunal anastomosis.

Most authors associate the occurrence of atresias and stenoses of the duodenum with the persistence of epithelial occlusions. TTP - before the 8-10th week of intrauterine life. However, it cannot be excluded that developmental anomalies, accompanied by the vicious formation of the entire duodeno-pancreatobiliary complex, arise earlier - during the period of initial organogenesis. In such cases, TTP - before the 5th week of intrauterine life.

Duodenal atresia accompanied by polyhydramnios, half is part of a complex of multiple congenital defects; in 32.4: ±5.8% of cases of multiple defects, including duodenal atresia, trisomy 21 is noted; 5.9±2.9% are a manifestation of syndromes with autosomy-recessive inheritance - Smith-Leml-Opntz, McKusick-Kaufman.

Atresia or stenosis of the duodenum has been described in trisomy 13, partial trisomy lq, Zp, partial monosomin 20p, monogenic Saldino-Noonan syndrome, and Dicker's lissencephaly. Duodenal atresia in combination with focal skin defects are signs of a recently identified autosomal recessive syndrome. Two related families are known, each of which had membranous atresia of the upper part of the duodenum. The type of inheritance, according to the authors, is autosomal recessive. Most cases of atresia and stenosis of the duodenum are of multifactorial origin; the RNC for siblings is 2.3±0.6%. Duplication of the duodenum accounts for 4-12% of all doublings of the gastrointestinal tract. Duplicatures of the duodenum are more common in boys; can be located submucosal, intramural and retroperitoneal. The dimensions of the duplicated part range from 2 to 25 cm. In 89% of cases, the duplication is located in the upper or descending part of the duodenum, rarely in the area of ​​the major duodenal papilla. Duodeiogastric duplications are known. In half of the cases, the lining of the duplications is similar to the mucous membrane of the duodenum, in other cases it is represented by the mucous membrane of the stomach, small intestine, or primitive intestinal epithelium.

Duplication of the duodenum penetrating into the chest cavity, in 12 of 13 described cases were observed in boys; usually they are combined with various vertebral anomalies. Of other congenital defects, duodenal duplications are most often combined with a reverse arrangement internal organs, duplication of the gallbladder and intestinal rotation disorders.

Clinically manifest themselves in 40% of cases in the neonatal period with symptoms of intestinal obstruction, jaundice and pancreatitis. In case of ulceration of the mucous membrane with subsequent perforation of the wall of the duplication, bloody vomiting is observed and peritonitis develops.

Treatment operational.