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Congenital high and low
intestinal obstruction in children
Lecture for 5th year students
of the medical faculty
Urgenic branch of TMA
Department of Pediatric Surgery
The purpose of the lesson:
 To acquaint with the etiology,
pathogenesis, clinic, diagnosis,
principles of treatment of congenital
intestinal obstruction in children.
Lesson objective:
 Deepening the integration of knowledge and skills
gained during previous training in topics related to
congenital intestinal obstruction. To train a general
practitioner in self-diagnosis, to carry out differential
diagnostics of patients with intestinal obstruction in
primary health care with other types of intestinal
obstruction, liver and biliary tract diseases, etc. To
train students in the application of practical skills in
the diagnosis and differential diagnosis of intestinal
obstruction at all stages of the activity of a general
practitioner.
Theoretical part.
The concept - intestinal obstruction or "ileus" is a
violation of the passage of its contents due to
obstruction, compression or dysfunction of the
intestine. According to etiology, congenital and
acquired are distinguished, according to the
mechanism - mechanical (strangulation, obturation
and intussusception) and dynamic (spastic, paralytic).
Congenital intestinal obstruction
Organogenesis begins at 3-4 weeks of intrauterine development.The
"solid" stage passes when the proliferating epithelium completely closes
the intestinal lumen.Then - vacuolization and restoration of the lumen of
the intestinal tube.
Bowel Rotation Process
consists in returning the
"middle" intestine to a
sufficiently grown abdominal
cavity, the intestine
continues to rotate
counterclockwise by
another 90 °.If rotation is
delayed at this stage, the
baby is born with
incomplete bowel rotation.
Stage of physiological umbilical hernia
In this case, the "middle" intestine remains fixed at one point at the origin of the
superior mesenteric artery. The cecum, located in the epigastric region, is fixed
by embryonic strands that squeeze the duodenum and cause its obstruction
The loops of the small
intestine are located in
the right half of the
abdominal cavity, the
blind loops are located in
the epigastric region, and
the large intestine is
located on the left. With
such fixation, there are
conditions for the
development of volvulus
around the mesentery
root and for the
development of acute
strangulated intestinal
obstruction.
Rotation around the mesenteric artery
Congenital intestinal obstruction
Acute (in newborns)
Highlow
Recurrent (Malformations of the
intestines, mesentery and other
abdominal organs)
High congenital bowel
obstruction
Acute congenital bowel obstruction
 malformations of the intestinal tube itself (atresia
and stenosis of the intestine).compression of a
normally formed intestinal tube ("external type" of
obstruction): - incorrectly located mesenteric
vessels (more often the duodenum is compressed by
the superior mesenteric artery); adhesions of the
peritoneum; a tumor or cyst in the abdomen; the
annular pancreas, which encloses the duodenum in
the descending part;impaired rotation of the midgut
in the embryo (isolated volvulus and Ladd
syndrome).obturation of the intestinal lumen with
viscous meconium (meconium ileus - cystic
fibrosis);
Types of intestinal atresia. a, b - two blindly ending sections of the intestinal tube are connected by a fibrous
cord, the latter may have a narrow lumen (b); c - multiple intestinal atresia; d - complete break of the intestinal
tube throughout; e, f - membranous (membranous) form of atresia, the membrane can be solid or have a narrow
opening (f).
Duodenal obstruction caused by compression by an abnormally located
vessel (a) and an annular pancreas (b).
The combination of compression of the
duodenum with volvulus of the "midgut" is
regarded as Ledd's syndrome.
Malrotation syndrome
Duodenal atresia below the nipple of Vater
Variants of duodenal atresia below the Vater papilla
Variant of duodenal atresia below the nipple of Vater
Duodenal atresia 12 below the nipple of VaterWebbed
form
Duodenal atresia 12 above the nipple of Vater
Variants of duodenal valves
Types of membranes
Variants of the location of the annular pancreas
Variants of the location of the annular pancreas
Variants of the location of the annular pancreas
Diagram of intestinal rotation disorders
The clinical picture. Vomit.
 manifests itself from the first day of life, and
sometimes in the first hours after birth.The most
persistent and early symptom is vomiting.With
obstruction of the duodenum above the Vater's
nipple, vomiting occurs soon after birth, the amount
of vomit is large, there is no admixture of bile, which
enters the intestines entirely.With obstruction of the
duodenum below the nipple of Vater, the vomit is
colored with bile. After latching the newborn to the
mother's breast, vomiting becomes repeated and
profuse, exceeding the amount of milk swallowed by
the baby.With partially compensated stenoses,
vomiting occurs on the 2-4th day of the child's life
and usually not immediately after feeding, but after
20-40 minutes, sometimes with a "fountain".
The clinical picture. Meconium.
 As a rule, there is a discharge of meconium. If the
obstruction is located above the Vater's nipple, then
the amount and color of meconium is almost normal,
its discharge is observed up to 3-4 days.With a lower
obstruction, the amount of meconium is small, its
consistency is more viscous than that of a healthy
child, and its color is grayish.With atresia and
subtotal stenosis, there is usually a single excretion
of meconium or it is excreted in small portions
several times within 1-2 days, and subsequently
absent.Neonates with multiple intestinal atresia do
not pass meconium. With congenital volvulus,
meconium leaves, but in a meager amount.
The clinical picture. Child behavior.
 on the first day the usual. Sometimes
lethargy attracts attention. At first, he
actively sucks, but as the general
condition worsens, he refuses to
breast. Characterized by progressive
loss of body weight (0.2-0.25 kg /
day). Already from 2 days, the
phenomena of dehydration are clearly
expressed.
The clinical picture. Locally.
 The abdomen is swollen in the upper sections,
especially in the epigastric region, due to the
distended stomach and duodenum. In the early
days, you can see the waves of peristalsis. After
profuse vomiting, the swelling in the epigastric
region decreases, sometimes completely
disappears. There is some retraction of the lower
abdomen.On palpation, the abdomen in all parts
is soft, painless; if the obstruction is caused by a
tumor or cyst, then usually these formations are
quite easily felt through the thin and somewhat
flabby abdominal wall. In some cases, in
children with congenital volvulus, it is possible to
palpate a conglomerate with indistinct outlines in
the abdominal cavity.
Laboratory indicators
 Due to prolonged vomiting, hypochloremia
develops, in which the ratio changes and the
amount of K + and Na + ions decreases.
Against the background of exsicosis, there is
a thickening of the blood: an increase in the
hematocrit number, hemoglobin content, an
increase in the number of erythrocytes and
leukocytes.
X-ray examination (with an upright
position of the child.)
 two gas bubbles with horizontal liquid levels are visible, which
corresponds to a distended stomach and duodenum. The size
of the gas bubbles varies. With a complete interruption of
patency in the lower parts of the intestine, gas is not
detected. Sometimes it is also absent in the stomach, and
then X-ray reveals a "dumb" stomach.For children with this
type of obstruction, it is recommended to carry out
irrigography (40-60 ml of a water-soluble contrast agent) to
clarify the position of the colon: If the colon is partially
filled with a contrast agent, it is located on the left, one
should think about the presence of a midgut volvulus in the
newborn. This clarification of the anatomical cause of the
obstruction is necessary for the correct calculation of the
preoperative preparation time.
Plain X-ray of the abdominal cavityin frontal and lateral projection
(two levels of liquid are visualized)
Passage through the gastrointestinal tract (the delay of the contrast
agent in the stomach for more than 8 hours). The picture is typical for
duodenal stenosis
After 8 hours Also in lateral projection
Differential diagnosis
 Pylorospasm manifests itself in the first days after birth
by vomiting, which is unstable and less abundant in
quantity than with congenital intestinal obstruction. In
addition, there is no admixture of bile in the vomit with
pylorospasm. Plain radiographs usually help clarify the
diagnosis.
 Pyloric stenosis is suspected in children with congenital
subcompensated stenosis, in which there is a partial
intestinal obstruction. However, constant staining of
vomit with bile can completely exclude pyloric stenosis.
The diagnosis is confirmed by X-ray examination: with
pyloric stenosis, there is one large gas bubble
corresponding to an enlarged stomach, in the remaining
parts of the intestine, a uniform distribution of gas is
visible. The study with contrasting according to Yu.R.
Levin helps to clarify the diagnosis.
Differential diagnosis
 Congenital diaphragmatic hernia is sometimes
accompanied by vomiting, which gives rise to
differential diagnosis with high congenital obstruction.
Unlike obstruction in congenital diaphragmatic hernia
in a newborn, dysfunctions of the respiratory and
cardiovascular systems come to the fore. X-ray
examination reveals the displacement of the intestine
into the chest cavity.
 Birth trauma to the brain is often accompanied by
vomiting with an admixture of bile. However, the
passage of meconium is normal. With a brain injury,
symptoms of damage to the central nervous system
are revealed. The diagnosis is clarified by X-ray
examination.
Low congenital intestinal
obstruction
The clinical picture of congenital low
intestinal obstruction
 lack of meconium.
 Vomiting appears relatively late, by the end
of the 2nd - on the 3rd day of life, and is
usually not associated with food intake.very
soon motor restlessness appears, twisting
with legs, refuses to breast or sucks very
sluggishly, does not sleep.
 The general condition is rapidly deteriorating,
intoxication phenomena are increasing, the
child becomes lethargic, adynamic, the skin
is gray-earthy, there may be an elevated
body temperature (37.5-38 ° C).
The clinical picture of low congenital
intestinal obstruction
 Already on the first day, uniform bloating is detected,
which progresses rapidly. The size of the abdomen after
vomiting does not decrease.Intestinal loops stretched
by meconium and gas are contoured through the
anterior abdominal wall. Often, their peristalsis is
visible, which is not traced in later periods, since
intestinal paresis occurs.
 Percussion is determined by tympanitis in all parts of
the abdomen. Auscultation reveals rare deaf sounds of
intestinal peristalsis. Palpation of the abdomen is
painful, accompanied by anxiety and a cry of the child.
Newborn with ICH
X-ray examination
 swollen bowel loops with multiple irregular
horizontal levels (obstruction of the distal
ileum and colon) or several large gas bubbles
with wide levels (obstruction of the jejunum
or ileum, meconium obstruction) are
determined.
 Perforation of the dilated bowel above the
site of the obstruction is usually
radiographically detected by the presence of
free gas in the abdominal cavity.
Congenital low intestinal obstruction (X-ray examination).
Multiple horizontal levels in bowel loops
Small bowel obstruction: wide, numerous, centrally located
Kloyber bowls, even levels, Kerkring folds, arcades (swollen
intestinal loops)
Ileal atresia
Differential diagnosis
Paralytic obstruction occurs relatively gradually against
the background of a severe general illness (peritonitis,
pneumonia, sepsis, enterocolitis, etc.), usually 5-10 days
after the birth of the child. The phenomena of obstruction
in intestinal paresis are not expressed clearly enough,
less constantly. From the anamnesis it turns out that the
child's meconium departs normally, and on examination,
there is usually a chair (after a gas tube or
enema).Hirschsprung's disease (acute form) can be
relatively easily achieved by conservative methods
(abdominal massage, introduction of a gas tube, enema).
The decisive factor in the diagnosis is X-ray examination
with contrast, in which the enlargement of the lumen of
the colon with the presence of a narrowed zone of
agangliosis, characteristic of Hirschsprung's disease, is
revealed.
Treatment
 The prognosis of the disease depends mainly
on timely diagnosis, correct surgical
correction of the defect, rational preoperative
preparation and postoperative management.
 Preoperative preparation is carried out
strictly individually. In newborns with high
intestinal obstruction, the duration and
quality of preoperative preparation depend
on the severity of the condition, the time of
admission to the hospital and the presence
of complications.
Surgical treatment.
-Operational access is paramedian.
-- Revision of the abdominal cavity.
-- elimination of obstruction:duodenojejunostomy with carrying
out the jejunum behind the transverse colon (in rare cases, it is
possible to impose a duodenoduodenostomy).
-enterotomy and membrane excisionlongitudinal dissection of
the area of stenosis followed by oblique transverse suturing of
the woundDissection of adhesions
-Operation Ladd"Unloading" Y-shaped anastomosisdirect end-
to-side anastomosis.ileocolostomy ("end to side").
-Mikulich's operation.
-Removal of a compressed cyst or tumor
Multiple atresia of the small intestine
Meconium ileus (cystic fibrosis)
The imposition of an anastomosis between the duodenum and the jejunum, and -
the transverse colon is retracted upward, the mesentery is bluntly stratified; the
initial part of the jejunum is enlarged according to the Wangensteen method; b -
the jejunum is sewn to the duodenum, the lumen is opened, the second row of
sutures is applied to the back
Excision of the membrane from the duodenum. a - cut line of the
intestine; b - excision of the membrane; c - stitching up the
wound of the intestine.
Operation Ladd. a - congenital volvulus of the "midgut"; b - elimination of bloat; c -
the intersection of the strands of the peritoneum, fixing the cecum; d - the cecum
is transferred to the left half of the abdominal cavity.
"Unloading" Y-shaped anastomosis
End-to-side ileocolostomy.
Double ileostomy according to Mikulich
Postoperative treatment of AIO includes the
following mandatory areas:
 Reimbursement of BCC, correction of the electrolyte
and protein composition of the blood;
 Treatment of endotoxicosis, including mandatory
antibiotic therapy;
 Restoration of the motor, secretory and absorption
functions of the intestine, that is, the treatment of
enteral insufficiency.
Postoperative complications
 peritonitis resulting from insufficient
anastomotic sutures.
 Aspiration pneumonia
 Adhesive obstruction.
 Divergence of the edges of the
postoperative wound and intestinal
eventration
Recurrent intestinal
obstruction
Recurrent Congenital Intestinal
Obstruction
 Most often it occurs in connection with congenital
circular stenosis of the ileum and colon, disruption of
the normal rotation of the midgut in the embryo,
entrapment of an intraperitoneal hernia and
compression of the intestinal lumen by cystic formation.
 All types of this disease are characterized by
inconsistent symptoms, but the common thing is the
intermittent nature of the obstruction. It is not always
possible to establish the cause of congenital recurrent
obstruction before the operation.
 The first signs of the disease usually appear months or
years after birth due to a weakening of the
compensatory capabilities of the body and a change in
the nature of the child's diet.
Internal abdominal hernia, a - a true hernia; b - false
hernia.
Clinical picture
 The child has periodic bouts of anxiety, bloating,
vomiting. The chair is rare, but independent, gases go
away. The attacks are short-lived, occur several times a
day, sometimes much less frequently. The child does
not take the breast well, the body weight increases a
little.
 Gradually, the attacks of pain become more intense,
stool retention appears, the general condition
worsens.When examining the patient, attention is
drawn to bloating and some asymmetry of the
abdomen. Visible peristalsis is usually determined.
Intestinal noises are heard, percussion - tympanitis.
The abdomen is slightly painful, muscle tension is not
detected.
 There is no stool, gases do not go away. After a
hypertensive enema, a temporary improvement may
occur, gases may pass away.
X-ray examination
 Plain radiographs show many horizontal
levels in the upper abdomen and gas-
distended loops of the small intestine.
 Study with contrasting is possible only in the
"light" interval. A liquid suspension of barium
sulfate given through the mouth during mass
production of radiographs (every 2 hours)
can be detected due to a long retention of
the mass above the narrowing point. In
acute cases, such a study is unacceptable.
Treatment
 In the period of recurrence of
obstruction, an emergency operation is
indicated.
 Midline laparotomy, revision and
elimination of the cause of obstruction.
Congenital pyloric stenosis in
children
Congenital pyloric stenosis
severe malformation, has an autosomal recessive
inheritance.
The disease is based on a congenital disorder of
the morphological structures of the pyloric gastric
pulp as a result of the proliferation of the circular
muscle layer and interstitial tissue, leading to
pyloric stenosis and impaired patency in this
section of the gastrointestinal tract.
Morphologically, pyloric stenosis is manifested by a
thickening of the pyloric canal wall up to 3-7 mm
(norm 1-2 mm).
In the structure of malformations, congenital pyloric
stenosis occurs quite often, second only to
malformations of the musculoskeletal system and
the cardiovascular system. The population
frequency is 4: 1000. The male to female sex ratio is
5: 1.
The severity and time of onset
of symptoms of pyloric stenosis
are determined by the degree of
narrowing of the pylorus and the
compensatory capabilities of the
child's body.
All manifestations of the disease
intensify over time. Usually, until the
3-4th week of a child's life, parents do
not consult a doctor, since the
symptoms of the disease are
indistinct. Previously, the diagnosis
was made at a later date, when the
symptoms of the disease became most
pronounced, so the clinical
characteristics are fairly well described
in older children.
The leading symptom of the disease is vomiting, which
appears most often on the 13-21st day of a child's life and
has a persistent character. However, in the early days,
regurgitation and infrequent vomiting are noted. Vomit in
the early stages can sometimes contain an admixture of
bile, but over time, the degree of narrowing of the
gatekeeper increases, and there is no bile in the vomit, then
vomiting appears in a fountain. The volume of vomit
exceeds the volume of the last feeding.
Dystrophy with a typical clinical picture
appears and steadily progresses. There is a
deficiency of trace elements (iron, calcium,
phosphorus) and multivitamins, the child also
loses chlorine and hydrochloric acid. Anemia
develops, there is a violation of water-
electrolyte metabolism, which is manifested by
blood thickening. Alkalosis is characteristic of
this disease.
Particular attention in pyloric stenosis is paid to
the examination of the abdomen, while it is
possible to detect an increase in the epigastric
region in comparison with the sunken lower
parts, to reveal the characteristic symptom of an
"hourglass" caused by the visible peristalsis of
a distended stomach. Sometimes in children
with severe malnutrition, it is possible to
palpate the gatekeeper
Hourglass symptom
The stool is scanty, dark green in color due to the low milk
content and the predominance of bile and secretions of the
intestinal glands. The amount of urine excreted and the
frequency of urination are reduced. Concentrated urine,
intensively stains the diapers.
EFGDS - endoscopic imaging pyloric
Diagnostics
Endoscopic imaging with pyloric
stenosis
Fine
Plain X-ray of the abdominal cavity
Contrast examination of the stomach
To the Trendelenburg position
The enlarged stomach is contrasted
Contrast study after 2 hours - evacuationabsent
through the stomach
After 4 hours, gastric emptying 20%
After 24 hours, the presence of contrast in the stomach
Treatment - operation pyloromyotomy according to
Frede-Ramshdett
Operation Frede-Ramschdett (incision site)
lateral projection Direct projection
Hirschsprung's disease
Hirschsprung's disease
 Hirschsprung's disease is a malformation of the distal
colon, congenital agangliosis. According to the latest
data, the incidence rate is 1: 5000 newborns.
 Hereditary pathology, the main clinical manifestations of
which are constipation and bloating. The reason is
underdevelopment (hypogangliosis) or complete absence
(agangliosis) of ganglionic cells of the intermuscular
(Auerbach) and submucosal (Meissner) plexus.
 The aganglionic zone is most often (80-90% of cases)
localized in the rectum (in adults), on a larger or smaller
section of the sigmoid colon, or in another section of the
colon (in children).
Hirschsprung's disease
 The part of the intestine, devoid of ganglia, is in a
state of spastic contraction, as a result of which the
higher parts of the intestine are hypertrophied.
 Constipation is persistent and appears from the
moment a child is born or in early childhood.
 The duration of constipation is from several days to
several months. The bloating of the intestines that
accompanies constipation and complements the
clinical symptoms does not disappear even after a
cleansing enema, which patients usually resort to
independently and often.
Anatomical forms of Hirschsprung's
disease
%
Hirschsprung's disease - total form,
acute course
Clinical stages of the course
 Compensated stage
 Subcompensated stage
 Decompensated stage
The clinical stage and severity of the
course of Hirschsprung's disease are in
direct proportion to its anatomical
shape, the length of the aganglionic
zone, the degree of suprastenotic
expansion of the intestine and the age
of the child.
Clinic and diagnostics
 The earliest and main symptom of
Hirschsprung's disease is the absence of
independent stool (chronic constipation).
 In most cases, this symptom is observed from
the neonatal period or appears somewhat later.
In the first days and weeks of life, stool
retention is observed in 90–95% of patients, at
the age of 1 to 6 months - in 3–5%, from 6
months to 1 year - in approximately 1%, and
after a year - in less than 0, 5% of patients.
 With a short aganglionic segment, the retention
of meconium and then feces in newborns is
limited to one or two days and is easily resolved
with a cleansing enema.
Clinic and diagnostics
 With a long lesion zone, the picture of intestinal
obstruction is growing, which requires more
vigorous measures.
 A constant symptom of Hirschsprung's disease is
flatulence, which, like constipation, is observed
from the first days and weeks of a patient's life.
Chronic retention of feces and gases leads to the
expansion of the sigmoid colon, and sometimes
the superior colon.
 The older the child or the worse the care for
him, the more pronounced are the secondary
changes arising from chronic fecal intoxication.
So, many children are diagnosed with anemia
and hypotrophy.
With the duration of the disease 3-4
years or more, deep changes in the
intestinal wall lead to sclerosis and
become irreversible, the degree of
structural changes in the intestinal wall
is in direct proportion to the duration
and clinical stage of the disease.
Diagnostics
 1. Detailed history taking
 2. General analysis of blood, urine, scatology
 3. Irrigography
 4. Colonoscopy
 5. Profilometry of intraintestinal pressure
 6. Sphincterometry
 7. Tissue biopsy according to Svenson and
determination of AChE activity
 8. Additional research methods: ultrasound, ECG,
immunological status
General view of a child
sufferingHirschsprung's disease
View of a patient with Hirschsprung's disease
Hirschsprung's disease. Irrigography
The main diagnostic method is contrast
irrigography:
Possible ultrasound diagnosis of Hirschsprung's
disease
Echogram normalstraight
and
sigmoidintestines
after filling
Echograms for
Hirschsprung's disease
Echogram of the rectum
and sigmoid colon in
Hirschsprung's disease
Echogram of the sigmoid colon in
Hirschsprung's disease
Echogram of the rectum and sigmoid
colon in Hirschsprung's disease
Colonoscopic picture
 Catarrhal colitis Erosive colitis
Tactics and optimal terms of treatment
 In the acute form of Hirschsprung's disease and in young
children (up to 3 years), it is recommended to impose a
terminal left-sided colostomy with the removal of the
transition zone on the skin.
 At the age of over 3 years, the decompensated stage of the
course of the disease and if it is impossible to carry out an
effective debridement of the colon, a right-sided colostomy
according to Girdaladze is preferable.
 One-stage radical correction of Hirschsprung's disease in
children should be carried out in a clinically compensated and
subcompensated stage of the course of the disease with
effective sanitation and reduction of the suprastenotically
enlarged sections of the colon to 1-2 degrees; in the
decompensated stage, preliminary colostomy is advisable.
 The optimal age for radical surgery in children with
Hirschsprung's disease is 1-3 years.
The main tasks of preoperative
preparation
 - elimination of chronic
coprostasis and
endotoxemia,
 - elimination or reduction of
megacolon syndrome.
Preoperative preparation program
1-siphon and healing enemas - traditional treatment,
2-percutaneous pulse magnetotherapy using
electroactivated saline solutions - optimized local
treatment,
3-detoxification, infusion, substitution and
immunomodulating therapy.
Svenson-Hiat-Isakov operation scheme
Operation Duhamel-Bairov
Operation on Soave-Lenyushkin (diagram)
The nature of early postoperative
complications
Соаве
%
Clinical evaluation of long-term results of surgical
treatment of Hirschsprung's disease
 - good - regular independent stool,
no signs of colitis and dysbiosis;
 - satisfactory - recurrent
constipation, kalomazaniya,
flatulence, catarrhal colitis, dysbiosis;
 - unsatisfactory - persistent
constipation, stool only after an
enema, fecal incontinence, erosive
and ulcerative colitis, phase III
dysbiosis.
Reasons for unsatisfactory results of radical
correction of Hirschsprung's disease
1. Coccyx agenesis
2. Injury to the internal sphincter
3. Annular cicatricial narrowing .
4. Incomplete excision of aganglionic
zones
5. Resistance of the mucous membrane
reduced intestines
Thank you for
attention

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Congenital intestinal obstruction in children lecture

  • 1. Congenital high and low intestinal obstruction in children Lecture for 5th year students of the medical faculty Urgenic branch of TMA Department of Pediatric Surgery
  • 2. The purpose of the lesson:  To acquaint with the etiology, pathogenesis, clinic, diagnosis, principles of treatment of congenital intestinal obstruction in children.
  • 3. Lesson objective:  Deepening the integration of knowledge and skills gained during previous training in topics related to congenital intestinal obstruction. To train a general practitioner in self-diagnosis, to carry out differential diagnostics of patients with intestinal obstruction in primary health care with other types of intestinal obstruction, liver and biliary tract diseases, etc. To train students in the application of practical skills in the diagnosis and differential diagnosis of intestinal obstruction at all stages of the activity of a general practitioner.
  • 4. Theoretical part. The concept - intestinal obstruction or "ileus" is a violation of the passage of its contents due to obstruction, compression or dysfunction of the intestine. According to etiology, congenital and acquired are distinguished, according to the mechanism - mechanical (strangulation, obturation and intussusception) and dynamic (spastic, paralytic).
  • 6. Organogenesis begins at 3-4 weeks of intrauterine development.The "solid" stage passes when the proliferating epithelium completely closes the intestinal lumen.Then - vacuolization and restoration of the lumen of the intestinal tube.
  • 7. Bowel Rotation Process consists in returning the "middle" intestine to a sufficiently grown abdominal cavity, the intestine continues to rotate counterclockwise by another 90 °.If rotation is delayed at this stage, the baby is born with incomplete bowel rotation.
  • 8. Stage of physiological umbilical hernia
  • 9. In this case, the "middle" intestine remains fixed at one point at the origin of the superior mesenteric artery. The cecum, located in the epigastric region, is fixed by embryonic strands that squeeze the duodenum and cause its obstruction
  • 10. The loops of the small intestine are located in the right half of the abdominal cavity, the blind loops are located in the epigastric region, and the large intestine is located on the left. With such fixation, there are conditions for the development of volvulus around the mesentery root and for the development of acute strangulated intestinal obstruction.
  • 11. Rotation around the mesenteric artery
  • 12. Congenital intestinal obstruction Acute (in newborns) Highlow Recurrent (Malformations of the intestines, mesentery and other abdominal organs)
  • 14. Acute congenital bowel obstruction  malformations of the intestinal tube itself (atresia and stenosis of the intestine).compression of a normally formed intestinal tube ("external type" of obstruction): - incorrectly located mesenteric vessels (more often the duodenum is compressed by the superior mesenteric artery); adhesions of the peritoneum; a tumor or cyst in the abdomen; the annular pancreas, which encloses the duodenum in the descending part;impaired rotation of the midgut in the embryo (isolated volvulus and Ladd syndrome).obturation of the intestinal lumen with viscous meconium (meconium ileus - cystic fibrosis);
  • 15. Types of intestinal atresia. a, b - two blindly ending sections of the intestinal tube are connected by a fibrous cord, the latter may have a narrow lumen (b); c - multiple intestinal atresia; d - complete break of the intestinal tube throughout; e, f - membranous (membranous) form of atresia, the membrane can be solid or have a narrow opening (f).
  • 16. Duodenal obstruction caused by compression by an abnormally located vessel (a) and an annular pancreas (b).
  • 17. The combination of compression of the duodenum with volvulus of the "midgut" is regarded as Ledd's syndrome.
  • 19. Duodenal atresia below the nipple of Vater
  • 20. Variants of duodenal atresia below the Vater papilla
  • 21. Variant of duodenal atresia below the nipple of Vater
  • 22. Duodenal atresia 12 below the nipple of VaterWebbed form
  • 23. Duodenal atresia 12 above the nipple of Vater
  • 26. Variants of the location of the annular pancreas
  • 27. Variants of the location of the annular pancreas
  • 28. Variants of the location of the annular pancreas
  • 29. Diagram of intestinal rotation disorders
  • 30. The clinical picture. Vomit.  manifests itself from the first day of life, and sometimes in the first hours after birth.The most persistent and early symptom is vomiting.With obstruction of the duodenum above the Vater's nipple, vomiting occurs soon after birth, the amount of vomit is large, there is no admixture of bile, which enters the intestines entirely.With obstruction of the duodenum below the nipple of Vater, the vomit is colored with bile. After latching the newborn to the mother's breast, vomiting becomes repeated and profuse, exceeding the amount of milk swallowed by the baby.With partially compensated stenoses, vomiting occurs on the 2-4th day of the child's life and usually not immediately after feeding, but after 20-40 minutes, sometimes with a "fountain".
  • 31. The clinical picture. Meconium.  As a rule, there is a discharge of meconium. If the obstruction is located above the Vater's nipple, then the amount and color of meconium is almost normal, its discharge is observed up to 3-4 days.With a lower obstruction, the amount of meconium is small, its consistency is more viscous than that of a healthy child, and its color is grayish.With atresia and subtotal stenosis, there is usually a single excretion of meconium or it is excreted in small portions several times within 1-2 days, and subsequently absent.Neonates with multiple intestinal atresia do not pass meconium. With congenital volvulus, meconium leaves, but in a meager amount.
  • 32. The clinical picture. Child behavior.  on the first day the usual. Sometimes lethargy attracts attention. At first, he actively sucks, but as the general condition worsens, he refuses to breast. Characterized by progressive loss of body weight (0.2-0.25 kg / day). Already from 2 days, the phenomena of dehydration are clearly expressed.
  • 33. The clinical picture. Locally.  The abdomen is swollen in the upper sections, especially in the epigastric region, due to the distended stomach and duodenum. In the early days, you can see the waves of peristalsis. After profuse vomiting, the swelling in the epigastric region decreases, sometimes completely disappears. There is some retraction of the lower abdomen.On palpation, the abdomen in all parts is soft, painless; if the obstruction is caused by a tumor or cyst, then usually these formations are quite easily felt through the thin and somewhat flabby abdominal wall. In some cases, in children with congenital volvulus, it is possible to palpate a conglomerate with indistinct outlines in the abdominal cavity.
  • 34. Laboratory indicators  Due to prolonged vomiting, hypochloremia develops, in which the ratio changes and the amount of K + and Na + ions decreases. Against the background of exsicosis, there is a thickening of the blood: an increase in the hematocrit number, hemoglobin content, an increase in the number of erythrocytes and leukocytes.
  • 35. X-ray examination (with an upright position of the child.)  two gas bubbles with horizontal liquid levels are visible, which corresponds to a distended stomach and duodenum. The size of the gas bubbles varies. With a complete interruption of patency in the lower parts of the intestine, gas is not detected. Sometimes it is also absent in the stomach, and then X-ray reveals a "dumb" stomach.For children with this type of obstruction, it is recommended to carry out irrigography (40-60 ml of a water-soluble contrast agent) to clarify the position of the colon: If the colon is partially filled with a contrast agent, it is located on the left, one should think about the presence of a midgut volvulus in the newborn. This clarification of the anatomical cause of the obstruction is necessary for the correct calculation of the preoperative preparation time.
  • 36. Plain X-ray of the abdominal cavityin frontal and lateral projection (two levels of liquid are visualized)
  • 37. Passage through the gastrointestinal tract (the delay of the contrast agent in the stomach for more than 8 hours). The picture is typical for duodenal stenosis After 8 hours Also in lateral projection
  • 38. Differential diagnosis  Pylorospasm manifests itself in the first days after birth by vomiting, which is unstable and less abundant in quantity than with congenital intestinal obstruction. In addition, there is no admixture of bile in the vomit with pylorospasm. Plain radiographs usually help clarify the diagnosis.  Pyloric stenosis is suspected in children with congenital subcompensated stenosis, in which there is a partial intestinal obstruction. However, constant staining of vomit with bile can completely exclude pyloric stenosis. The diagnosis is confirmed by X-ray examination: with pyloric stenosis, there is one large gas bubble corresponding to an enlarged stomach, in the remaining parts of the intestine, a uniform distribution of gas is visible. The study with contrasting according to Yu.R. Levin helps to clarify the diagnosis.
  • 39. Differential diagnosis  Congenital diaphragmatic hernia is sometimes accompanied by vomiting, which gives rise to differential diagnosis with high congenital obstruction. Unlike obstruction in congenital diaphragmatic hernia in a newborn, dysfunctions of the respiratory and cardiovascular systems come to the fore. X-ray examination reveals the displacement of the intestine into the chest cavity.  Birth trauma to the brain is often accompanied by vomiting with an admixture of bile. However, the passage of meconium is normal. With a brain injury, symptoms of damage to the central nervous system are revealed. The diagnosis is clarified by X-ray examination.
  • 41. The clinical picture of congenital low intestinal obstruction  lack of meconium.  Vomiting appears relatively late, by the end of the 2nd - on the 3rd day of life, and is usually not associated with food intake.very soon motor restlessness appears, twisting with legs, refuses to breast or sucks very sluggishly, does not sleep.  The general condition is rapidly deteriorating, intoxication phenomena are increasing, the child becomes lethargic, adynamic, the skin is gray-earthy, there may be an elevated body temperature (37.5-38 ° C).
  • 42. The clinical picture of low congenital intestinal obstruction  Already on the first day, uniform bloating is detected, which progresses rapidly. The size of the abdomen after vomiting does not decrease.Intestinal loops stretched by meconium and gas are contoured through the anterior abdominal wall. Often, their peristalsis is visible, which is not traced in later periods, since intestinal paresis occurs.  Percussion is determined by tympanitis in all parts of the abdomen. Auscultation reveals rare deaf sounds of intestinal peristalsis. Palpation of the abdomen is painful, accompanied by anxiety and a cry of the child.
  • 44. X-ray examination  swollen bowel loops with multiple irregular horizontal levels (obstruction of the distal ileum and colon) or several large gas bubbles with wide levels (obstruction of the jejunum or ileum, meconium obstruction) are determined.  Perforation of the dilated bowel above the site of the obstruction is usually radiographically detected by the presence of free gas in the abdominal cavity.
  • 45. Congenital low intestinal obstruction (X-ray examination). Multiple horizontal levels in bowel loops
  • 46. Small bowel obstruction: wide, numerous, centrally located Kloyber bowls, even levels, Kerkring folds, arcades (swollen intestinal loops)
  • 48. Differential diagnosis Paralytic obstruction occurs relatively gradually against the background of a severe general illness (peritonitis, pneumonia, sepsis, enterocolitis, etc.), usually 5-10 days after the birth of the child. The phenomena of obstruction in intestinal paresis are not expressed clearly enough, less constantly. From the anamnesis it turns out that the child's meconium departs normally, and on examination, there is usually a chair (after a gas tube or enema).Hirschsprung's disease (acute form) can be relatively easily achieved by conservative methods (abdominal massage, introduction of a gas tube, enema). The decisive factor in the diagnosis is X-ray examination with contrast, in which the enlargement of the lumen of the colon with the presence of a narrowed zone of agangliosis, characteristic of Hirschsprung's disease, is revealed.
  • 49. Treatment  The prognosis of the disease depends mainly on timely diagnosis, correct surgical correction of the defect, rational preoperative preparation and postoperative management.  Preoperative preparation is carried out strictly individually. In newborns with high intestinal obstruction, the duration and quality of preoperative preparation depend on the severity of the condition, the time of admission to the hospital and the presence of complications.
  • 50. Surgical treatment. -Operational access is paramedian. -- Revision of the abdominal cavity. -- elimination of obstruction:duodenojejunostomy with carrying out the jejunum behind the transverse colon (in rare cases, it is possible to impose a duodenoduodenostomy). -enterotomy and membrane excisionlongitudinal dissection of the area of stenosis followed by oblique transverse suturing of the woundDissection of adhesions -Operation Ladd"Unloading" Y-shaped anastomosisdirect end- to-side anastomosis.ileocolostomy ("end to side"). -Mikulich's operation. -Removal of a compressed cyst or tumor
  • 51. Multiple atresia of the small intestine
  • 53. The imposition of an anastomosis between the duodenum and the jejunum, and - the transverse colon is retracted upward, the mesentery is bluntly stratified; the initial part of the jejunum is enlarged according to the Wangensteen method; b - the jejunum is sewn to the duodenum, the lumen is opened, the second row of sutures is applied to the back
  • 54. Excision of the membrane from the duodenum. a - cut line of the intestine; b - excision of the membrane; c - stitching up the wound of the intestine.
  • 55. Operation Ladd. a - congenital volvulus of the "midgut"; b - elimination of bloat; c - the intersection of the strands of the peritoneum, fixing the cecum; d - the cecum is transferred to the left half of the abdominal cavity.
  • 59. Postoperative treatment of AIO includes the following mandatory areas:  Reimbursement of BCC, correction of the electrolyte and protein composition of the blood;  Treatment of endotoxicosis, including mandatory antibiotic therapy;  Restoration of the motor, secretory and absorption functions of the intestine, that is, the treatment of enteral insufficiency.
  • 60. Postoperative complications  peritonitis resulting from insufficient anastomotic sutures.  Aspiration pneumonia  Adhesive obstruction.  Divergence of the edges of the postoperative wound and intestinal eventration
  • 62. Recurrent Congenital Intestinal Obstruction  Most often it occurs in connection with congenital circular stenosis of the ileum and colon, disruption of the normal rotation of the midgut in the embryo, entrapment of an intraperitoneal hernia and compression of the intestinal lumen by cystic formation.  All types of this disease are characterized by inconsistent symptoms, but the common thing is the intermittent nature of the obstruction. It is not always possible to establish the cause of congenital recurrent obstruction before the operation.  The first signs of the disease usually appear months or years after birth due to a weakening of the compensatory capabilities of the body and a change in the nature of the child's diet.
  • 63. Internal abdominal hernia, a - a true hernia; b - false hernia.
  • 64. Clinical picture  The child has periodic bouts of anxiety, bloating, vomiting. The chair is rare, but independent, gases go away. The attacks are short-lived, occur several times a day, sometimes much less frequently. The child does not take the breast well, the body weight increases a little.  Gradually, the attacks of pain become more intense, stool retention appears, the general condition worsens.When examining the patient, attention is drawn to bloating and some asymmetry of the abdomen. Visible peristalsis is usually determined. Intestinal noises are heard, percussion - tympanitis. The abdomen is slightly painful, muscle tension is not detected.  There is no stool, gases do not go away. After a hypertensive enema, a temporary improvement may occur, gases may pass away.
  • 65. X-ray examination  Plain radiographs show many horizontal levels in the upper abdomen and gas- distended loops of the small intestine.  Study with contrasting is possible only in the "light" interval. A liquid suspension of barium sulfate given through the mouth during mass production of radiographs (every 2 hours) can be detected due to a long retention of the mass above the narrowing point. In acute cases, such a study is unacceptable.
  • 66. Treatment  In the period of recurrence of obstruction, an emergency operation is indicated.  Midline laparotomy, revision and elimination of the cause of obstruction.
  • 68. Congenital pyloric stenosis severe malformation, has an autosomal recessive inheritance. The disease is based on a congenital disorder of the morphological structures of the pyloric gastric pulp as a result of the proliferation of the circular muscle layer and interstitial tissue, leading to pyloric stenosis and impaired patency in this section of the gastrointestinal tract. Morphologically, pyloric stenosis is manifested by a thickening of the pyloric canal wall up to 3-7 mm (norm 1-2 mm).
  • 69. In the structure of malformations, congenital pyloric stenosis occurs quite often, second only to malformations of the musculoskeletal system and the cardiovascular system. The population frequency is 4: 1000. The male to female sex ratio is 5: 1.
  • 70. The severity and time of onset of symptoms of pyloric stenosis are determined by the degree of narrowing of the pylorus and the compensatory capabilities of the child's body.
  • 71. All manifestations of the disease intensify over time. Usually, until the 3-4th week of a child's life, parents do not consult a doctor, since the symptoms of the disease are indistinct. Previously, the diagnosis was made at a later date, when the symptoms of the disease became most pronounced, so the clinical characteristics are fairly well described in older children.
  • 72. The leading symptom of the disease is vomiting, which appears most often on the 13-21st day of a child's life and has a persistent character. However, in the early days, regurgitation and infrequent vomiting are noted. Vomit in the early stages can sometimes contain an admixture of bile, but over time, the degree of narrowing of the gatekeeper increases, and there is no bile in the vomit, then vomiting appears in a fountain. The volume of vomit exceeds the volume of the last feeding.
  • 73. Dystrophy with a typical clinical picture appears and steadily progresses. There is a deficiency of trace elements (iron, calcium, phosphorus) and multivitamins, the child also loses chlorine and hydrochloric acid. Anemia develops, there is a violation of water- electrolyte metabolism, which is manifested by blood thickening. Alkalosis is characteristic of this disease.
  • 74. Particular attention in pyloric stenosis is paid to the examination of the abdomen, while it is possible to detect an increase in the epigastric region in comparison with the sunken lower parts, to reveal the characteristic symptom of an "hourglass" caused by the visible peristalsis of a distended stomach. Sometimes in children with severe malnutrition, it is possible to palpate the gatekeeper
  • 76. The stool is scanty, dark green in color due to the low milk content and the predominance of bile and secretions of the intestinal glands. The amount of urine excreted and the frequency of urination are reduced. Concentrated urine, intensively stains the diapers.
  • 77. EFGDS - endoscopic imaging pyloric Diagnostics
  • 78. Endoscopic imaging with pyloric stenosis Fine
  • 79. Plain X-ray of the abdominal cavity
  • 80. Contrast examination of the stomach
  • 82. The enlarged stomach is contrasted
  • 83. Contrast study after 2 hours - evacuationabsent through the stomach
  • 84. After 4 hours, gastric emptying 20%
  • 85. After 24 hours, the presence of contrast in the stomach
  • 86. Treatment - operation pyloromyotomy according to Frede-Ramshdett
  • 87. Operation Frede-Ramschdett (incision site) lateral projection Direct projection
  • 89. Hirschsprung's disease  Hirschsprung's disease is a malformation of the distal colon, congenital agangliosis. According to the latest data, the incidence rate is 1: 5000 newborns.  Hereditary pathology, the main clinical manifestations of which are constipation and bloating. The reason is underdevelopment (hypogangliosis) or complete absence (agangliosis) of ganglionic cells of the intermuscular (Auerbach) and submucosal (Meissner) plexus.  The aganglionic zone is most often (80-90% of cases) localized in the rectum (in adults), on a larger or smaller section of the sigmoid colon, or in another section of the colon (in children).
  • 90. Hirschsprung's disease  The part of the intestine, devoid of ganglia, is in a state of spastic contraction, as a result of which the higher parts of the intestine are hypertrophied.  Constipation is persistent and appears from the moment a child is born or in early childhood.  The duration of constipation is from several days to several months. The bloating of the intestines that accompanies constipation and complements the clinical symptoms does not disappear even after a cleansing enema, which patients usually resort to independently and often.
  • 91. Anatomical forms of Hirschsprung's disease %
  • 92. Hirschsprung's disease - total form, acute course
  • 93. Clinical stages of the course  Compensated stage  Subcompensated stage  Decompensated stage
  • 94. The clinical stage and severity of the course of Hirschsprung's disease are in direct proportion to its anatomical shape, the length of the aganglionic zone, the degree of suprastenotic expansion of the intestine and the age of the child.
  • 95. Clinic and diagnostics  The earliest and main symptom of Hirschsprung's disease is the absence of independent stool (chronic constipation).  In most cases, this symptom is observed from the neonatal period or appears somewhat later. In the first days and weeks of life, stool retention is observed in 90–95% of patients, at the age of 1 to 6 months - in 3–5%, from 6 months to 1 year - in approximately 1%, and after a year - in less than 0, 5% of patients.  With a short aganglionic segment, the retention of meconium and then feces in newborns is limited to one or two days and is easily resolved with a cleansing enema.
  • 96. Clinic and diagnostics  With a long lesion zone, the picture of intestinal obstruction is growing, which requires more vigorous measures.  A constant symptom of Hirschsprung's disease is flatulence, which, like constipation, is observed from the first days and weeks of a patient's life. Chronic retention of feces and gases leads to the expansion of the sigmoid colon, and sometimes the superior colon.  The older the child or the worse the care for him, the more pronounced are the secondary changes arising from chronic fecal intoxication. So, many children are diagnosed with anemia and hypotrophy.
  • 97. With the duration of the disease 3-4 years or more, deep changes in the intestinal wall lead to sclerosis and become irreversible, the degree of structural changes in the intestinal wall is in direct proportion to the duration and clinical stage of the disease.
  • 98. Diagnostics  1. Detailed history taking  2. General analysis of blood, urine, scatology  3. Irrigography  4. Colonoscopy  5. Profilometry of intraintestinal pressure  6. Sphincterometry  7. Tissue biopsy according to Svenson and determination of AChE activity  8. Additional research methods: ultrasound, ECG, immunological status
  • 99. General view of a child sufferingHirschsprung's disease
  • 100. View of a patient with Hirschsprung's disease
  • 102. The main diagnostic method is contrast irrigography:
  • 103. Possible ultrasound diagnosis of Hirschsprung's disease Echogram normalstraight and sigmoidintestines after filling Echograms for Hirschsprung's disease Echogram of the rectum and sigmoid colon in Hirschsprung's disease Echogram of the sigmoid colon in Hirschsprung's disease Echogram of the rectum and sigmoid colon in Hirschsprung's disease
  • 104. Colonoscopic picture  Catarrhal colitis Erosive colitis
  • 105. Tactics and optimal terms of treatment  In the acute form of Hirschsprung's disease and in young children (up to 3 years), it is recommended to impose a terminal left-sided colostomy with the removal of the transition zone on the skin.  At the age of over 3 years, the decompensated stage of the course of the disease and if it is impossible to carry out an effective debridement of the colon, a right-sided colostomy according to Girdaladze is preferable.  One-stage radical correction of Hirschsprung's disease in children should be carried out in a clinically compensated and subcompensated stage of the course of the disease with effective sanitation and reduction of the suprastenotically enlarged sections of the colon to 1-2 degrees; in the decompensated stage, preliminary colostomy is advisable.  The optimal age for radical surgery in children with Hirschsprung's disease is 1-3 years.
  • 106. The main tasks of preoperative preparation  - elimination of chronic coprostasis and endotoxemia,  - elimination or reduction of megacolon syndrome.
  • 107. Preoperative preparation program 1-siphon and healing enemas - traditional treatment, 2-percutaneous pulse magnetotherapy using electroactivated saline solutions - optimized local treatment, 3-detoxification, infusion, substitution and immunomodulating therapy.
  • 111. The nature of early postoperative complications Соаве %
  • 112. Clinical evaluation of long-term results of surgical treatment of Hirschsprung's disease  - good - regular independent stool, no signs of colitis and dysbiosis;  - satisfactory - recurrent constipation, kalomazaniya, flatulence, catarrhal colitis, dysbiosis;  - unsatisfactory - persistent constipation, stool only after an enema, fecal incontinence, erosive and ulcerative colitis, phase III dysbiosis.
  • 113. Reasons for unsatisfactory results of radical correction of Hirschsprung's disease 1. Coccyx agenesis 2. Injury to the internal sphincter 3. Annular cicatricial narrowing . 4. Incomplete excision of aganglionic zones 5. Resistance of the mucous membrane reduced intestines