Acute and

chronic digestive
disorders.
Syndrome
of regurgitation and
vomiting




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Vomiting
Physiological gag occurs when stimulation of the
gastric mucosa (Irritation of the gastric mucosa)
(intolerance substance or overflow of the
stomach).
In pathological conditions, the gag reflex occurs
during stimulation of the labyrinth of the brain,
stomach, brain, and as a result of circulating
toxins and metabolites (metabolic products).


:
(5-30 ) 30-60
.
:


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,
(50-100 ,
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( ):

50 , 30
; .

Regurgitation in infants: the dropping of small

amounts of food (5-30 ml) usually 30-60 minutes after
feeding. Syndrome of regurgitation
Atonic vomiting: sluggish leakage of food or weak
eruption is characteristic for dysfunction of the
esophagus and gastric atony.
Profuse vomiting (flow): gastric emptying under
considerable pressure, a large amount of vomit (50100 ml in infants and in older ages, even more). This
is the most common form of vomiting (copious
vomiting).
Spastic vomiting (vomiting, high jet fountain):
stomach content flows under considerable pressure
as a fountain in the distance up to 50 cm, usually 30
minutes after feeding or later, is typical of pyloric
stenosis (pyloristenosis).

 .

,
.

.



,
,
.

SIGHT AND SMELL OF VOMIT

The sour smell and acid reaction to litmus indicate
ejection from the stomach, not from esophagus.
Admixture of bile characteristic masses of the middle
portion of the duodenum. At high impurity located
bowel stenosis of bile indicates narrowing below the
confluence of the common bile duct. Greater stenosis,
including pyloric stenosis, prevents bile in vomit.
Higher stenosis, including pyloric stenosis, prevents
the penetration of bile in the vomit.


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.
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.

 Admixture of mucus - a sign of gastritis

or severe bronchitis (ingestion of sputum).
Admixture of feces and fecal odor - a
sign of bowel obstruction with lowmounted bowel stenosis. Rancid smell of
vomit can point to processes of decay.
Blood in the vomit (hematemesis) is
caused by many reasons. Color of the
blood in this case a light-red or brownishblack when hemoglobin under the
influence of gastric juice is converted to
hematin.


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(
)

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( 50% ).


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.

Diseases of the esophagus

Gastroesophageal reflux, chalasia cardia
(esophageal cardiac insufficiency) cardiac failure
of the esophagus - the most common pathology
of the esophagus in infants, most often occurs in
children during the first months of life (50% of
cases).
Gastroesophageal reflux is regarded as an
immature gastrointestinal motility. Characteristic
of children with signs of morphological and
functional immaturity, prematurity.

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).

Patogenesis
Inappropriate relaxation of the lower
esophageal sphincter associated with
failure or underdevelopment of intramural
sympathetic ganglion cells.
Contributes to improving the appearance
of gastric reflux and intra-abdominal
pressure (flatulence, constipation, obesity,
spasm of the pylorus). Occurrence of
reflux contributes to increased intragastric
and intra-abdominal pressure (for
flatulence, constipation, obesity, spasm of
the pylorus).

,

(
)

Other factors

delayed gastric emptying

changes in esophageal peristalsis
gastric dilatation
weakening of the mechanical factors that
support anti-reflux barrier (crus of the
diaphragm and cardio-easophageal angle)
short esophagus




.
,




.
,

.
,
, .

Clinical signs
Regurgitation - the most common
symptom in infants - it is stress-free and
painless. Regurgitation occurs soon after few
hours of meal in the form of multiple episodes
of leakage from the mouth in small
amounts of milk curds. There is
reflux of stomach contents, especially with a
deep breath and low position of the upper
torso.
Vomiting - usually without any admixture
of bile flow or leakage of food.

. Complications

:
- (
,
,


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).

Complications
Reflux esophagitis
(manifested by
irritability, strong cry, refusal of
food within a few minutes after
the feeding of infants, pain,
localized behind the
sternum and the
epigastrium, in older children).
bleeding from esophageal

 :

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(
)
(

)

Systems complications:
- delay in physical
development (malnutrition)
- anemia (due to blood loss and iron
deficiency)
- hypoproteinemia (protein loss due
to damage in the esophageal
mucosa)

 :

, ,

,
.

Respiratory complications:
- aspiration with the development
of nocturnal cough, bronchospasm,
microaspiration syndrome, recurrent
pneumonia
- episodes of apnea and
bradycardia due
to laryngospasm, reflections from
the vagusnerve.

:

. -
.
,

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( )
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Diagnostics
- X-ray study of the gastrointestinal
tract with barium. The water-siphon test in
the positionTrandelenburg.
It can be seen as a radiopaque
substance numb from the stomach into
the lower esophagus.
Oesophageal angle (the angle
of His) larger (normally hot).

- Fibrogastroscopy

 (chalasia)
-
The water-siphon test

.
10 , 2

20-30

.

.

. ,
10% .

Treatment
Diet.
- Frequent feeding of up to 10 times a
day, every 2 hours.
- After feeding for 20-30 minutes, keep
the baby upright for the elimination of the
consequences aerofagii.
- When chalasia long to keep upright.
antireflux FRISOVOM mixture. If not, then a
teaspoon of cream of 10% in cereal before
feeding.


, - 60
.


.
-:

- Exalted position of the head end

of the bed, with chalasia to 60
degrees.
- Drug therapy is used mainly for
complications.
Reflux oesophagitis:
bleeding epsilonaminocaprotic acid internal
ly
- Almagel or Fosfolyugel.


-
,
.


,


.

Pilorospasm
Pilorospasm - inconstant pyloric obstruction
due to spasm.
The reason is a violation
of pylorospasm regulatory functions of the
central nervous system and
its autonomic division, which is more
common in children with birth injury of the
central nervous system, and
after intrauterine hypoxia.

.


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.

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Main clinical signs

The main clinical
signs are regurgitation and vomiting. The
disease usually manifests itself at
birth. Vomit are curds.
Characteristic symptoms
of perinatal central nervous
system syndrome of hyperexcitability,
vegetative-visceral disorders, intracranial
hypertension.

.

-

:
,
,

Complications
Hypotrophy (malnutrition)
reflux esophagitis,
bronchopulmonary disease:
microaspiration syndrome,
recurrent pneumonia,
bronchial obstruction

(10 , 2
).
.

,
.

20-30 .
30-45
.

.

Treatment
- Frequent feeding (10 times a day,every 2
hours).
- Anti-reflux mixture. You can alternate with
breastfeeding
- Drinking a fraction, considering the water
needs of a spoon.
- After feeding a baby to hold in an upright
position for 20-30 minutes.
raise the head end of bed to 30-45 degrees.
- Watch the baby to prevent aspiration of vomit.

:
2,5% (),
1.5 //. 3
.
0,25%
3 20-30
+
,

:

To reduce muscle
spasm pyloric neurons vegetoblockard
remedy:
2,5% solution of diprazina (Pipolphenum),
a daily dose of 1,5 mg / kg / day. 3 times a
day intramuscularly.
0,25% solution of
novocaine to teaspoon 3 times a day for
20-30 minutes before meals
+ Treatment of
existing syndromes, perinatal encephalopa
thy, as the main causes of pilorospasm:


,


.
- 2 - 3
, 7
.
,
.
.

Congenital pylorostenosis
This is a congenital malformation, manifested
in the narrowing of the pyloric canal due to
thickening of the walls of the pylorus.
Pyloric stenosis - a disease the first 2 3 months of life, the boys affected 7
times more often.
This disease has a definite tendency,
as observed in familial cases. The disease is
inherited in an autosomal recessive trait

 .

3-, 4- .
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.
,
.

The clinical picture

The first signs of the disease often in the 3rd, 4th week of life.
Vomiting - abundant, a
fountain, with a strong jet.
Number of vomit - more of a meal.
Vomit have an unpleasant,
sour odor.


Symptom hourglass

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3. .
4.
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5.


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6.

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- There is rapid loss of weight due exsicosis.

- stool rare (hungry constipation), or with a

mixture of sparse vegetation (empty stool).
- The number of voids rare.
- Increased segmental motility of the
stomach, seen on the abdominal surface in
the form of an hourglass.
- Palpable thickening of
the pylorus during deep palpation through the
abdominal wall in uptight formation of the
size of a plum pit.
- Severity of symptoms depends on the
degree of stenosis of the pylorus and
the duration of the disease (late diagnosis)



:
,
,

-
.

Diagnosis
In the presence of three
clinical symptoms: vomiting a
fountain, visible peristalsis of the
stomach, pylorus probing packed
-leaves no doubt about the
diagnosis.

()

Diagnosis can
be virtually errorfree at endoscopy
(fibrogastroscopy) or X-ray
examination of the
gastrointestinal tract
with barium


30


12


:

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The differential diagnosis

Most often differentiated from:
- pylorospasm
- Adrenogenetic
syndrome(AGS), solteryayuscha
ya form (pseudo-pylorostenosis)
- Chalaza cardiac
- Intestinal infection (repeated
vomiting, dehydration

,


, ,

,


,

The differential diagnosis of pyloric

stenosis and AGS
pyloristenosis
AGS
Vomiting fountain
Vomiting fountain
volume of more than
volume of less than
of food eaten
of food eaten
Exsicosis,
Exsicosis, diarrhea
constipation,
empty chair
palpated
not palpable
porter
porter

 metabolic
alkalosis
hypokalemia
hyponatremia
The delay in
the barium
stomach more than 9
hours
No symptoms
viralization

metabolic
acidosis
hyperkalemia
hyponatremia
No delay in barium

symptoms
viralization
expressed
ECG changes


-,


.

2
10 ,
4 10 2 10
.

.

Surgical treatment of pyloric

stenosis
The operation to Fred-Ramshted, which
consists of dissection of pyloric circular
muscle fibers perpendicular to
the mucosal layer.
After the operation, start to drink in 2
hours of 10 ml, the feeding of the child
beginning at 4 hours and 10 ml every
2 hours, 10 times a day. All other
required water and mineral needs are
provided by infusion therapy

Pilorotomy Fredet-Weber-Bamstedt
The operation involves the dissection of seromuscular layer of pyloric stomach.
Upper, mid-right ad rectal cut 3-5 cm layers
reveal the abdominal cavity. Liver blunt hook
is pulled up and right and extract the
gatekeeper.
Fixing his fingers of his left hand, cut
longitudinally and serous and muscle pylorus.
After that, the grooved director peeled lining
up to its bulging into the wound.

:
2 - 20 2
3 30 2
4 40 2
5 50 2
6 60-70 2.5 8

10
.

Nutrition after operation

Use female expressed milk:
on day 2 - 20 ml after 2 hours
on day 3 - 30 mL in 2 hours
on day 4 - 40 mL in 2 hours
on day 5 - 50 ml after 2 hours
on day 6 for 60-70 ml after 2.5h, 8
times a day
and by the 10th day translate into a
physiological rhythm of food.

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Chronic diarrhea
They are:
intolerance to lactose (milk sugar),
intolerance to cow's milk proteins,
intolerance of disaccharidases,
exudative enteropathy,
celiac disease (gluten enteropathy)
cystic fibrosis (intestinal form).

 .
,
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.
,
3.8-5.0.
,
0.5%

Intolerance to lactose
Reduced activity of lactase, which is most
often secondary.
No part of metabolized carbohydrates enters
the large intestine and undergoes
fermentation.
Hence - flatulence, intestinal colic
Reduced fecal pH to 3.8-5.0.
Hence - a frequent sour, watery stools
In feces carbohydrates more than 0.5%


(
0.5%)
,

( .ALL 110),
(, ,
- )

Treatment
Preparations of lactase (lower level of
carbohydrates in feces is less than 0.5%)
If there is no effect, part of the breast
milk is replaced by a mixture of Low
Lactose(bebilak ALL 110), based on soy
protein (Humana, Humana SL, Nutri-soya,
etc)
Domestic milk mixture


.





( )

(
)

Intolerance of cow's
milk proteins
Develops in the appointment of artificial mixtures
based on cow's milk
Involve all sections of the intestine
Rapidly developing malnutrition (protein deficiency)
Unstable stool mixed with blood and
mucus (differentiated from intestinal infection)
Is the main cause of atopic dermatitis in infants
Often - Iron deficiency anemia


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.

Treatment
Pregestimil, Alfare (Nestle Company) and
others.
As foods are used:
porridge with water (rice, buckwheat)
potatoes, cabbage puree.
As a source of protein in the form of puree:
lean pork, turkey, rabbit, horse
meat (best tolerability)
As a source of fat:
vegetable oils.


.

-

,

Intolerance of disaccharidases.
Hereditary disease
Deficiency of sucrase-isomaltase
Appears when you turn on the
diet products containing sucrose
With chronic diarrhea
Moderate malnutrition

 .
,

(,
,
).

Exudative enteropathy
Often develops secondarily, for
any damage of oesophageal epithelium
(infection,intolerance to cow's milk
protein, disaccharidase deficiency).
Severe diarrhea with great loss of
protein
Hence - the hypoproteinemia
Often associated with malabsorption of
carbohydrates



(, ,
.)

:
5-8%



(, ,
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Treatment
Parenteral nutrition
(aminoacids, intralipid,protein hydrolysates,
etc.)
Diet against total parenteral
nutrition gradually, rice water, or 5-8% of rice
porridge with added fructose
Vegetable oil droplets
Individually selected type of meat
Carbohydrates are introduced to fruits and
vegetables (zucchini, pumpkin, potatoes,
cabbage, bananas)

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)

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)
(
) (

).

Celiac disease (gluten

enteropathy)
Developed for inclusion in the diet
of foods containing gluten (wheat,
rye, barley, oats)
Sometimes the primary (with the
introduction of complementary
foods groats) and secondary
(after an intestinal infection).


-

(,
, ),

Pathogenesis
Gluten protein causes atrophy of
the intestinal mucosa in violation of
the intestinal
absorption (proteins, fats,
carbohydrates) and micronutrients
In the biopsy of the intestine show
a shortening of the villi,
increased crypt
develop hypoproteinemia


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(
200-300 )


, ,





, .

 There
is a profuse diarrhea, greasy, frothy, foulsmelling stool (feces daily volume may
reach 200-300 g)
developing malnutrition
Very often this is combined with rickets,
vitamin deficiencies, anemia
Marked growth retardation
Clinical and morphological characteristics of
the disease disappear against the
background of a gluten-free diet
and resumed after eating foods
containing gluten.



, ,
,

, ,
( )

 Exclude all ready meals with

wheat and oat flour, biscuits,
crackers made from wheatand
rye, pasta
Assign rice, buckwheat,
corn (tolerate well)
Low Lactose is transferred
to food
Pancreatic enzymes




. 1:2000
.
-.

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,

(, ).

Cystic fibrosis (CF)

Is the most common hereditary disease with a
fatal outcome. The frequency
of 1:2000births. Type of autosomal
recessive inheritance.
In cystic fibrosis disturbed function of
exocrine glands (pancreas, sweat, bronchial,
and others). As a consequence, increase the
viscosity of the secretions of these glands,
and the relative lack of them at the site
of action (gut, bronchi).



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),

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),

(

),
.


, (
)


,

 lack of exocrine pancreatic function (hence the impaired

function of the digestion of fats mostly)
Airway obstruction (violation mucokinesis associated
with thickening of bronchial secretions)
recurrent pneumonia with bronchiectasis in
the outcome (low drainage capacity of bronchial
secretions and secondary infection)
cirrhosis of the liver.
Prolonged diarrhea with the release of foulsmelling, greasy stools (hard to wash off with a diaper)
Wasting
Meconium ileus in newborns, older - low intestinal obstruction
Formed with the development of cirrhosis, liver failure

 (CF)

 2 (2 degrees of malnutrition)




.

.

,
( 60 \

Diagnosis
The main method available
to diagnose cystic fibrosis sweat test
with a pilokarpinom. To
stimulate sweating electrophoresed with
pilocarpine.
Next, the concentration
of sodium chloride and allocated per unit
of time (greater than 60mEq \ L pathology

(,
.)
,

Treatment
Pancreatin, Creon in
the individually selected dose
Special mixtures
of infants (Pregestimil, ,
Portagen)
The complex vitamins, calcium