Necrotizing ulcerative enterocolitis (Necrotizing enterocolitis). Ulcerative necrotizing enterocolitis Ulcerative necrotizing enterocolitis in children
Ulcerative enterocolitis is a pathological nonspecific inflammatory process that often occurs in utero against the background of ischemic changes in the intestine and is manifested by the appearance of multiple ulcers and areas of necrosis.
Etiology
The exact cause of the disease still remains unknown. It is known that approximately 75-80% of cases of the disease occur in newborns, primarily premature infants.
Risk factors for the development of ulcerative enterocolitis
- Intrauterine causes:
- long-term fetal hypoxia or asphyxia with amniotic fluid that occurs against the background of rupture of the membranes;
- insufficiency of fetoplacental blood flow in the fetus;
- sudden thrombosis of the vessels of the small intestine with the appearance of areas of ischemia and necrosis;
- varying degrees of disruption of normal fetal development;
- the presence of severe intrauterine infection, in which massive proliferation of bacterial flora occurs;
- congenital malformations of the gastrointestinal tract and heart.
- Extrauterine causes:
- premature birth of a baby with insufficient or critical body weight (less than 1500 g);
- disruption of respiratory processes, including immaturity of the pulmonary component, requiring transfer of the newborn to artificial ventilation;
- enteral method of feeding a newborn with hypertonic mixtures;
- transfusion of blood or its components through the vessels of the umbilical cord;
- traumatic effects on the brain or spinal cord during childbirth;
- septic conditions of an infant of another etiology.
Pathogenesis
An important pathogenetic link in the development of ulcerative enterocolitis is thrombosis of intestinal vessels and the addition of infectious agents. The inflammatory-necrotic process that arises in the mucous membrane very quickly spreads to the entire thickness of the intestinal loops.
Pathological thinning of the wall leads to perforation and release of intestinal contents into the abdominal cavity. The free gas is directed by the bloodstream into the portal vein system. Peritonitis begins to develop and a severe septic condition occurs with a fatal outcome in 30% of cases.
Clinical manifestations, symptoms of ulcerative enterocolitis
- Manifestations of gastrointestinal tract damage:
- frequent attacks of regurgitation or profuse vomiting of bile, blood or mixture residues;
- swollen and sharply painful intestines;
- an increase in the size of the abdomen with a rigid abdominal wall;
- swelling of the abdominal wall, the doctor can clearly palpate dense masses, which indicates the onset of peritonitis;
- bloody loose stools or the occurrence of complete intestinal obstruction at different stages.
- Systemic manifestations of the disease arise as a result of a sharp inhibition of central nervous system functions:
- sudden cessation of breathing, requiring immediate transfer of the newborn to mechanical ventilation;
- decrease in normal blood pressure numbers, up to severe hypotension and shock;
- disturbance of peripheral blood flow and the development of irreversible consequences;
- lack of appetite, the baby refuses to eat naturally;
- urine output decreases, severe oliguria occurs;
- all metabolic processes in the body are disrupted, acidosis occurs;
- completed bleeding from different parts of the intestine.
According to the duration and nature of the course of ulcerative enterocolitis, there are:
- fulminant course, as a rule, is characteristic of a full-term baby who, for one reason or another, suffered asphyxia during delivery, central nervous system injury, blood transfusion, or has severe developmental defects;
- subacute course - typical for premature infants with very low birth weight, occurs gradually and appears from the 3rd week of birth;
- acute course - occurs in infants weighing less than 1500 g and manifests itself already in the 2nd week of the child’s life.
Stages
Clinicians usually distinguish several stages of the disease, depending on the severity of symptoms and characteristic changes on the radiograph:
- Stage I - diagnosed in infants in whom there is a suspicion of ulcerative enterocolitis. Such children refuse to eat; there may be slight swelling of the intestinal loops, which quickly passes. According to the radiograph of the abdominal organs, dilated loops are visualized or no pathology is detected.
- Stage II A - is assigned on the basis of the moderate severity of the clinical manifestations of the disease, confirmed by the presence of a pneumatic component on an x-ray.
- Stage II B - characterized by deterioration of the baby’s condition and increased pain on palpation of the intestines.
- Stage III A - characterized by disruption and inhibition of all vital functions of organs and systems of the body, the intestines become completely inactive.
- Stage III B - accompanied by a perforation process with gas and contents entering the abdominal cavity and the portal vein system; during auscultation, bowel sounds are completely absent.
Diagnostics
- The severity of clinical manifestations is assessed: the child’s refusal to eat, frequent regurgitation or repeated vomiting, swollen intestinal loops, the appearance of bloody impurities in the stool, etc.
- An objective examination of newborns reveals a rigid abdominal wall, normal bowel sounds are not heard on auscultation, dense masses are palpated, etc.
- There are pronounced changes in blood tests: leukocytosis or leukopenia, thrombocytopenia, increased ESR and C-reactive protein, electrolyte disturbances.
- Examination of feces for occult blood is a diagnostic screening for ulcerative enterocolitis.
- Instrumental examination: detection of increased gas formation in intestinal loops, the presence of free gas in the abdominal cavity and in the portal vein system - according to the results of ultrasound, radiography or CT.
Treatment of ulcerative enterocolitis
Premature babies, especially those born with critically low birth weight, are closely monitored in intensive care units. Newborns are under constant monitoring with repeated ultrasound and x-rays, as well as blood testing with its acid-base component. However, the mortality rate in such children is very high.
Conservative therapy
It is a rational treatment option at the onset of the disease.
If ulcerative enterocolitis is suspected, feeding the baby is stopped completely and the intestinal contents are suctioned using a probe. Such children are transferred only to parenteral nutrition.
It is necessary to carry out the necessary infusion and systemic antibiotic therapy, and replenish blood volume by administering fresh frozen plasma. Immunity-stimulating drugs and complex vitamins are also widely used.
Surgical treatment
Indicated in cases of clinical deterioration of the child’s well-being and the onset of peritonitis based on the results of an objective and instrumental examination.
Such patients undergo abdominal surgery with removal of necrotic intestinal tissue. In addition, strictures in the lumen of the intestinal loops are excised. The abdominal cavity must be drained and washed with antiseptic solutions and antibiotics.
Preventive measures
Carefully monitor pregnant women at risk of preterm birth or intrauterine infection. Delivery tactics play an important role in infants at high risk of hypoxia and asphyxia during childbirth. If necessary, the child is promptly transferred to mechanical ventilation.
Enterocolitis is a nonspecific inflammatory disease of the large and small intestines of various origins, accompanied by painful sensations in the abdominal area and dyspeptic symptoms.
As a result, inflammation forms in the wall of the small intestine (enteritis), large intestine (colitis), or both parts (enterocolitis). The stomach and other organs may be involved in the process, resulting in various symptoms.
It is important to know that during the disease the intestines cannot fully perform their function, so the patient may experience other signs of pathology.
Enterocolitis can occur in two main forms
- Spicy. Characterized by inflammation of the superficial layers of the intestine. Most often provoked by aggressive irritants (burn, injury, etc.).
- Chronic. This form is justified if more than 6 months have passed since the onset of the disease. In this case, the structure of the mucous membrane completely changes and the inflammatory process moves to the deeper layers. The villi are less pronounced, the activity of enzyme complexes is disrupted, as a result of which parietal digestion and absorption are reduced.
Five reasons that provoke enterocolitis
It should be noted that not everyone develops enterocolitis, since certain conditions must be created:
- decrease in general immunity (IgA concentration, number of macrophages and other protective factors);
- genetic predisposition (more often in women);
- concomitant gastrointestinal diseases (for example, atrophic gastritis).
Depending on the type of damage, various forms of enterocolitis may occur: catarrhal, ulcerative, ulcerative-necrotic and others.
Symptoms
It is difficult to identify signs that would accurately indicate that the patient has enterocolitis. All symptoms are not specific and reflect only the severity of this pathology.
Main symptoms
- Abdominal pain is a key symptom of gastrointestinal pathology. The pain intensifies when palpated, is paroxysmal in nature and is localized in the navel area and along the flanks.
- Diarrhea or constipation. In the chronic form, these conditions can replace each other.
- General manifestations. We are talking about fever, weakness, muscle pain.
- Flatulence. Patients complain of bloating and gases. This is due to disruption of digestive processes.
- Scatological changes. Feces may change in color and consistency, and fatty patches, streaks of blood, and mucus may appear. All this may confuse the patient, and he will consult a doctor.
Diagnostics
To make a diagnosis of enterocolitis, signs of the disease and epidemiological data (with whom and when the patient had contact, what food he took, etc.) play an important role. Additional analyzes and instrumental methods are also shown:
- complete blood count and liver tests;
- bacteriological and scatological examinations of feces;
- barium radiography;
- if necessary, CT;
- sigmoidoscopy.
Effectively treating enterocolitis: eight key steps
A comprehensive approach to the treatment of enterocolitis should include influence on all parts of the pathological process and symptoms. Treatment of acute forms of this disease is carried out strictly under the supervision of a doctor in an infectious diseases hospital. Chronic enterocolitis in adults can be treated at home. And pediatricians and pediatric surgeons are fighting the necrotic variant (which is more typical for newborns).
Treatment includes the following:
- Diet. With the exception of foods that irritate the intestines, fatty foods, and dairy products. The diet lasts about 1.5 months.
- Taking antibiotics or antifungals. This is etiotropic (directed at the very cause of the disease) treatment.
- Enzymes – eliminate the symptoms of the disease.
- Multivitamins. In any case, the absorption of nutrients and vitamins in the intestine is impaired.
- Probiotics. Improves intestinal motility. And lactobacilli (normalize microflora).
- Sorbents. To improve the removal of toxins from the gastrointestinal tract resulting from indigestion.
- Herbal preparations.
- Steroid treatment (15-30 mg per day with Prednisolone).
Diet for enterocolitis
In the hospital, patients with enterocolitis are always prescribed diet No. 4. In addition, such a diet should be followed for at least 1.5 months until the intestines are completely restored.
Nutritional features of adult patients with enterocolitis
- the basis of the diet is soups made from finely chopped seasonal vegetables, porridge with water (except pearl barley and semolina);
- the diet provides for fractional meals, in small portions, 4-5 times a day, overeating is prohibited;
- dishes should be steamed (in a double boiler, multicooker) with limited addition of fat;
- do not consume foods that increase putrefaction (indole formation) in the intestines;
- for diarrhea - frequent and fractional drinks in the form of strong tea, decoctions of dried fruits;
- Despite the presence of exception products, patients' diet should consist of foods rich in vitamins.
It is also important to remember about foods that should be excluded from the diet during treatment for both acute and chronic enterocolitis:
- the diet excludes dairy products (milk, butter, cheese);
- fatty meat and fatty fish (including soups with fatty meat);
- any hard-to-digest carbohydrates;
- sweets (except honey, it can be eaten 2 weeks after the disappearance of clinical manifestations of the disease);
- alcohol and other alcohol-containing substances;
- hot spices and seasonings.
It is advisable to introduce fruits into the diet of patients who have suffered acute enterocolitis two weeks after stopping antibiotics, gradually, starting with apples and bananas.
Drug treatment
Treatment of acute enterocolitis in adults, as a rule, begins with gastric lavage, laxatives or cleansing enemas. For the first couple of days, such patients are prescribed bed rest, detoxification therapy (infusions of solutions and oral hydration), and sorbents.
Treatment for chronic enterocolitis
- broad-spectrum antibacterial drugs (for example, Fthalazol 1-2 g every four to six hours in the first 1-3 days, then half the dose, Furazolidone 0.1-0.15 g four times a day);
- lactobacilli and probiotics to eliminate the symptoms of dysbiosis (Linex two capsules three times a day, Bifikol);
- sorbents (Enterosgel, Polysorb 1.2 g dissolved in water, taken 3-4 times a day before meals);
- disturbances in water-electrolyte balance are corrected by intravenous administration of saline solution of sodium chloride, calcium gluconate, panangin (20 ml three times a day);
- herbal preparations (Australian Ectis from plant extracts).
Depending on what symptoms are observed in the patient, more points may be added to this treatment. Any correction of therapy is made by the attending physician.
Traditional methods of treating enterocolitis
Enterocolitis is a disease that people have encountered for a long time before the advent of pharmacology as such. Then it was necessary to be treated with herbal remedies, and the most effective methods were passed down from generation to generation until the present day.
Popular means
- for constipation in adults, it is recommended to use laxative tea made from cilantro, licorice root and buckthorn bark before bed (10 g of cilantro seeds and licorice root, plus 80 g of buckthorn bark, pour a glass of hot water and boil for 10 minutes, strain before use);
- in case of diarrhea, freshly squeezed carrot juice on an empty stomach, 1/3 cup three times a day, will help (not only will it stop diarrhea, but will also help replenish vitamin A deficiency);
- An infusion of nutmeg, 50 ml three times a day before meals, has an analgesic effect (1 g of nutmeg is crushed into powder, poured with a glass of boiling water, left for 60 minutes;
- To normalize intestinal function, use a couple of drops of myrtle essential oil 4-6 times a day.
Enterocolitis is a disease that requires long-term and complex therapy. To recover, patients must modify their diet, take medications, and take multivitamins regularly. Some patients with enterocolitis (for example, necrotizing) even require surgical treatment.
is an inflammatory bowel disease in newborns, which is characterized by necrosis of the intestinal wall and the development of accompanying symptoms. It manifests itself as signs of intestinal obstruction and peritonitis, intoxication up to a septic state, as well as the development of disseminated intravascular coagulation syndrome. The course is cyclical, symptoms may reappear. Diagnostics are clinical and radiological; a complex of laboratory tests is also carried out. Treatment is pathogenetic and symptomatic, aimed at eliminating intestinal obstruction, correcting electrolyte disturbances, disseminated intravascular coagulation syndrome and other manifestations. If necessary, surgical interventions are performed.
ICD-10
P77 Necrotizing enterocolitis in the fetus and newborn
General information
Reasons
The etiology of the disease currently continues to be studied by specialists in the field of pediatrics. The genetic aspect plays a certain role, that is, the frequency of necrotizing ulcerative enterocolitis among relatives is significantly higher. Artificial feeding with formulas with high osmolarity increases the risk of developing the disease. The connection between the pathology and pathogenic microorganisms has been proven, but there is no data on a specific pathogen. E. coli, Klebsiella, staphylococcus and clostridia are often detected during the disease. Opportunistic microflora can also contribute to the development of symptoms of necrotizing ulcerative enterocolitis. Microorganisms not only directly damage the villi of the intestinal epithelium, but also increase its permeability.
Pathogenesis
In the pathogenesis of the disease, great importance is attached to a decrease in intestinal barrier function. This is partly due to the high concentration of pathogenic microflora; the gestational age at the time of the baby’s birth also plays a role. Necrotizing ulcerative enterocolitis in most cases develops in premature infants. In addition, any hypoxic damage causes a redistribution of blood in the child’s body with predominant blood supply to vital organs. Intestinal ischemia leads to necrosis of its wall, which is also one of the main links in pathogenesis. As for hypoxia, its causes may be intrauterine infection, pathologies of the placenta and umbilical cord, malformations of the cardiovascular system, etc.
Symptoms
Necrotizing ulcerative enterocolitis develops in stages. First, symptoms of indigestion of food appear in the form of regurgitation and visual enlargement of the abdomen due to overstretching of the stomach and intestines. Possible vomiting mixed with bile, respiratory disorders, including attacks of apnea. The child becomes lethargic and the temperature may rise slightly. Next comes the symptoms of intestinal obstruction. Vomiting becomes more frequent, and an admixture of scarlet blood appears in the stool. The abdomen is significantly distended, the temperature is elevated. Apnea attacks also become more frequent, and saturation (oxygen saturation in the blood) decreases significantly.
If left untreated or rapidly progressing, ulcerative necrotizing enterocolitis manifests itself with symptoms of peritonitis, as intestinal perforation occurs, which is usually found in the terminal ileum. Pneumoperitoneum and signs of sepsis are detected in the form of intoxication, a critical drop in blood pressure, etc. The inflammatory reaction in ulcerative necrotizing enterocolitis is systemic in nature, so signs of multiple organ failure are observed. The disease is characterized by a cyclical course, that is, after normalization of the condition, repeated attacks are possible.
Diagnostics
The first signs of the disease are nonspecific and are characteristic of many nosologies, in particular Hirschsprung's disease and other anomalies of intestinal development. In addition, prematurity itself often manifests itself as difficulties with enteral nutrition due to underdevelopment of the secretory and motor functions of the gastrointestinal tract. A pediatrician may suspect ulcerative-necrotizing enterocolitis in the initial stages if the child was born premature, or hypoxia occurred during intrauterine development or childbirth.
A stool test for occult blood is also carried out, since veins of scarlet blood are not yet visually detectable, but cellular elements are already present due to microdamage to the intestinal wall. Once signs of intestinal obstruction develop, the diagnosis becomes more obvious:
- An x-ray of the abdominal organs reveals dilated intestinal loops and pneumatosis of the intestinal wall. X-ray confirms the development of peritonitis, which can be suspected by severe bloating in the absence of gas filling of the intestinal loops.
- Blood is detected in the stool, although stool may be absent due to intestinal paresis and obstruction.
- An ultrasound of the abdominal organs can detect gas or liquid in the abdominal cavity and detect echogenic points (areas of necrosis of the intestinal wall). This sign is one of the first to diagnose necrotizing ulcerative enterocolitis in the early stages.
- A general blood test reveals signs of inflammation in the form of leukocytosis with a shift to the left. The level of C-reactive protein increases significantly; it is this indicator that is usually monitored over time in order to monitor the effectiveness of treatment. Ulcerative-necrotizing enterocolitis is characterized by severe electrolyte disturbances in the form of hyponatremia and metabolic acidosis, as well as disturbances in blood clotting processes up to DIC syndrome. Often a specific infectious agent is identified, which does not always play a key role in the development of the clinical picture of the disease, but serves as an important point for choosing therapeutic tactics.
Treatment of ulcerative necrotizing enterocolitis
Conservative therapy
Treatment of the disease should begin at the stage of the first suspicion of necrotizing ulcerative enterocolitis. Enteral nutrition is immediately discontinued, and decompression of the stomach and intestines is performed. Preventive administration of broad-spectrum antibiotics is possible. The child needs respiratory support. A couve mode is required in the intensive care unit, mechanical ventilation is carried out according to indications. Syndromic treatment of necrotizing ulcerative enterocolitis involves the correction of electrolyte disturbances and exicosis, which is inevitable with intestinal obstruction. Prevention of DIC syndrome is necessary. In most cases, timely initiation of therapy allows one to limit oneself to conservative methods.
Surgical treatment
Surgical treatment of necrotizing ulcerative enterocolitis is indicated if clinical and radiological signs of peritonitis are detected as a result of perforation of the intestinal wall. The necrotic area of the intestine must be removed. The operation is also indicated when the therapeutic measures are ineffective, that is, when clinical symptoms persist, signs of shock appear, and there is no positive trend in blood tests. The issue of time to return to enteral nutrition is decided individually.
Prognosis and prevention
The prognosis of the disease is doubtful. As a rule, the patient’s condition normalizes after timely diagnosis and treatment. However, a rapid course of necrotizing ulcerative enterocolitis is possible, especially in the presence of predisposing factors or extreme prematurity of the child. Mortality, according to various sources, ranges from 10 to 40%. In addition, if an operation was performed and the resected area was quite extensive, “short bowel” syndrome develops. Statistics show that it is ulcerative necrotizing enterocolitis in most cases that is the cause of this postoperative complication, which significantly reduces the child’s quality of life, and often its duration, since food absorption is significantly and irreversibly deteriorated.
Description:
Necrotizing newborns is a nonspecific inflammatory disease caused by infectious agents against the background of immaturity of local defense mechanisms and/or hypoxic-ischemic damage to the intestinal mucosa, prone to generalization with the development of a systemic inflammatory response. According to the definition of D. Cloherty (2002), NEC is an acute necrotizing intestinal syndrome of unknown etiology.
The intensive development of neonatology and resuscitation has made it possible to survive children born very prematurely, who suffered hypoxia during childbirth and had signs of intrauterine or intrapartum infection, as well as those born with severe congenital malformations of the gastrointestinal tract and/or cardiovascular system. The vast majority of these babies (90%) are preterm, weighing less than 1500 g, which is why NEC is called the “disease of surviving prematurity.”
During the neonatal period, NEC occurs in 2–16% of cases, depending on gestational age, about 80% of which occur in premature infants with low birth weight. In premature infants, NEC occurs in 10–25% of cases. The incidence of NEC in newborns, according to various authors, ranges from 0.3 to 3 per 1000 children. The mortality rate is significantly higher in the group of premature newborns, among children with intrauterine growth retardation syndrome and ranges from 28 to 54%, and after surgical interventions - 60%, despite the intensive joint efforts of neonatologists, pediatric surgeons, anesthesiologists and resuscitators, as well as development of modern technologies for the care and treatment of newborns. In countries where the rate of premature births is low (Japan, Switzerland), NEC is less common - with a frequency of 2.1% among all children admitted to neonatal intensive care units.
Symptoms:
Clinical signs of NEC can be divided into systemic, abdominal and generalized.
Systemic symptoms include: respiratory distress, apnea, lethargy, thermolability, excitability, poor nutrition, hypotension (shock), decreased peripheral perfusion, acidosis, oliguria, bleeding.
Abdominal - bloating and hyperesthesia of the abdomen, gastric aspirates (food debris), (bile, blood), intestinal obstruction (weakening or disappearance of bowel sounds), erythema or, constant localized mass in the abdomen, bloody stools.
The fulminant course of NEC is typical for full-term newborns who have suffered asphyxia, trauma to the brain and/or spinal cord, hemolytic disease, and gastrointestinal defects during childbirth. Apnea and the need for respiratory support are typical, and impaired tissue perfusion or acute cardiovascular failure are possible. Regurgitation or large residual volume appears in the stomach before feeding. Gregersen's reaction is positive. Sometimes there is a significant amount of blood in the stool.
The acute course of NEC is typical for premature newborns with a birth weight of less than 1500 g. The disease begins at 2–4 weeks of life with pronounced abdominal symptoms: regurgitation and vomiting, refusal to eat, bloating, impaired intestinal passage . Soon general somatic symptoms appear, indicating dysfunction of vital organs and systems.
Subacute NEC is common in premature infants with extremely low body weight. Symptoms develop gradually from the 3rd week of life. Early symptoms are the appearance of intolerance to enteral nutrition and changes in stool character. Common, but the abdomen is often soft to palpation, abdominal wall muscle rigidity may be absent, and peristaltic sounds may be detected on auscultation. Such patients require immediate initiation of therapy and examination (frequent radiographs and stool testing for occult blood). If untreated, this form of NEC manifests with severe systemic and radiological symptoms, usually within 24–36 hours.
Among the above diagnostic tests, the most constant and informative are changes in the hemogram (leukocytosis /, shift of the leukoformula to the left), increased C-reactive protein, acidosis, electrolyte imbalance, interstitial pneumatosis and gas in the portal venous system according to ultrasound and x-ray examinations of the abdominal organs .
To determine the stages of NEC, in addition to the criteria described above, the Bell criteria as modified by Walsh and Kleigman are used.
Generalized symptoms resemble a septic process and include lethargy, hypotension, pallor, respiratory distress, oliguria, persistent cyanosis, and bleeding. The more pronounced the listed generalized signs are, the greater the severity of the disease.
Early symptoms of the disease are nonspecific and variable - from signs of intolerance to enteral nutrition to a catastrophic course with a clinical picture, shock, etc. CNS depression syndrome, apnea and signs of impaired tissue perfusion predominate - a positive “white spot” symptom, peripheral cyanosis, acidosis, temperature instability. Flatulence, delayed evacuation of gastric contents, and bloody stools are common.
The progressive process is manifested by erythema and swelling of the abdominal wall, increasing tension of the abdominal muscles. The detection of dense masses during deep palpation of the abdomen indicates a covered intestinal perforation or widespread peritonitis. On auscultation there are no peristaltic sounds, but physical data are very scarce.
Causes:
NEC is multifactorial. It is believed that NEC is a heterogeneous disease and its main components are ischemia suffered in the perinatal period, abnormal colonization of the newborn intestine and inadequate nutrition of the child in the early postnatal period.
Risk factors for the development of NEC: perinatal (decreased blood supply to the intestines due to increased blood supply to the brain and heart), catheterization of the umbilical artery (vasospasm and thromboembolism), (decreased blood flow in the intestinal vessels), (decreased blood flow in the intestines), immaturity of the immune system, nutritional mixtures ( are a substrate for the growth of microorganisms, with enteral nutrition NEC develops more often), direct bacterial invasion, use of hypertonic solutions, direct damage to the intestinal mucosa), allergy to milk, lack of IgA in milk (Gomella, 1998). The following factors play a role in the occurrence of NEC: prematurity, hypoxia in the ante- and intrapartum period, infectious causes, nutritional problems, the presence of congenital and hereditary pathology, mainly of the gastrointestinal tract.
Treatment:
For treatment the following is prescribed:
First of all, if respiratory function is impaired, additional oxygen or oxygen is provided. If hemodynamics are impaired, blood circulation is supported - replenishment of blood volume. For this purpose, fresh frozen plasma is used at a rate of 10 ml/kg body weight, since it is the only donor of antithrombin-III and a source of other blood coagulation factors. To normalize renal and intraorgan blood flow, low doses of dopamine (2–5 mcg/kg/min) are used. If acid-base homeostasis is disturbed, it may be necessary to administer sodium bicarbonate.
An essential point in the management of newborns with this pathology, which largely determines the outcome and prognosis of the disease, is the cessation of all types of enteral feeding, including the administration of medications per os, correctly administered complete (TPF) through a peripheral vein.
The transition from TPN to breastfeeding is a long, multi-stage process that is directly dependent on the severity and stage of NEC. Enteral nutrition is resumed 3–5 days after normalization of the evacuation function of the stomach, the x-ray picture and the disappearance of clinical symptoms of gastrointestinal dysfunction, which usually occurs by 10–12 days from the onset of the disease. Starting with distilled water or glucose solution, you should gradually switch to mixtures diluted 4 times. When the volume of the enterally administered mixture reaches 50% of the total volume of liquid, one should switch to a dilution of 1: 2, and then 3: 4 to the full volume. Thus, a child with NEC goes through the following stages of nutrition: total parenteral nutrition, combined parenteral nutrition and artificial enteral nutrition (EIP), complete EIP, additional EIP and breastfeeding, and is finally transferred to breastfeeding.
Taking into account the requirements for mixtures used as enteral artificial nutrition, as well as the fact that, against the background of long-term antibacterial therapy, severe dysbiosis and secondary failure often develop, especially after severe reconstructive operations, it is recommended to use lactose-free and hypolactose mixtures such as “Nutrimigen” as the first mixture ", "Nutrisoya", "Alprem", "Alfare", "Pregestimil", "Nenatal", etc. This allows you to significantly reduce fermentation processes in the intestines, improve the digestion and absorption of ingredients.
Vitamins, electrolytes (except potassium), microelements are included in the TPN regimen from the first day.
Broad-spectrum antibiotics are a mandatory component of therapy. Preference is given to third generation cephalosporins in combination with aminoglycosides. An alternative is imipenem with metronidazole.
7.12.4. Necrotizing enterocolitis
One of the most common causes of postnatal perforated peritonitis (60% of all perforations) is hemorrhagic or septic infarction, which develops as a result of circulatory disorders in the wall of the gastrointestinal tract.
Among children during the adaptation period, necrotizing enterocolitis occurs in 0.25%, and among children requiring intensive care in the neonatal period - in 4%.
Necrotizing enterocolitis is a polyetiological disease. In the early neonatal period, the disease develops in children who have suffered severe neonatal hypoxia and asphyxia; it can also be a complication of infusion therapy and replacement blood transfusion administered through the umbilical vein; it can develop with decompensation of severe congenital heart disease and the decompensated form of Hirschsprung's disease.
Irrational use of antibiotics also contributes to the development of enterocolitis. Along with the direct damaging effect of some antibiotics (ampicillin, tetracycline) on the intestinal mucosa, the suppression of colonization resistance of saprophytic flora with the development of severe dysbiosis is essential.
Despite the variety of etiological factors, the pathogenesis of necrotizing enterocolitis involves severe microcirculatory disorders in the wall of the gastrointestinal tract.
Centralization of blood circulation occurs with spasm of mesenteric vessels (up to complete cessation of blood circulation), which is resolved by intestinal paresis with hemorrhages. Morphologically, large or small infarctions of the intestinal wall are identified. More frequent damage to premature babies is explained by the low resistance of their capillaries to pressure changes in the vascular bed.
Predominantly, damage occurs to the distal ileum and the angles of the colon (ileocecal, hepatic, splenic, sigmoid). The process begins with necrosis of the mucous membrane, and then spreads to the submucosal, muscular and serous layers, ending with perforation (Fig. 7-18). 
Clinical picture and diagnosis
In the clinical picture of necrotizing enterocolitis in children who have suffered chronic perinatal hypoxia and infection, a clear staged course of the disease is noted.
Stage I
Stage I can be regarded as prodromal. The condition of children at risk who have suffered perinatal hypoxia and infection is closer to severe due to neurological disorders, respiratory impairment and cardiovascular activity. From the gastrointestinal tract, symptoms of dyskinesia are detected. Sluggish intermittent sucking, regurgitation during and after feeding with milk, occasionally bile, malnutrition, aerophagia, bloating, restlessness of the child while stroking the abdomen in the absence of symptoms of peritoneal irritation, delayed passage of meconium stool, and rapid loss of body weight are clearly expressed.
X-rays show increased uniform gas filling of all parts of the gastrointestinal tract with slight thickening of the intestinal walls.
Stage II
Stage II is characterized by clinical manifestations of necrotizing enterocolitis. In newborns on the 5-9th day of life, the condition worsens, the symptoms of dynamic intestinal obstruction increase, the body weight deficit is 10-15% due to dehydration. The child sucks poorly, regurgitates with an admixture of bile, abdominal bloating increases, and local pain appears, often in the right iliac region. The passage of feces is frequent, occurs in meager portions, with an admixture of mucus and greens. The color of the stool is determined by the nature of the pathological intestinal microflora. Thus, staphylococcal dysbacteriosis is characterized by pronounced general toxicosis, and in liquid, foamy stool there is mucus and greens. A gram-negative infection is more characterized by severe dehydration, scanty, porous, pale yellow stool with mucus and a large water spot.
A plain X-ray of the abdominal organs shows increased uneven gas filling of the gastrointestinal tract with a shadowing zone corresponding to the area of maximum intestinal damage. The stomach is distended, with fluid levels. Characteristic thickening
shadows of the intestinal walls due to their edema, inflammation and interloop effusion. The rigidity of the intestinal walls leads to straightening of their contours. Submucosal cystic pneumatosis of the intestinal wall appears (Fig. 7-19). In severe cases, gas is detected in the portal system of the liver (Fig. 7-20).
Rice. 7-19. Macropreparation. Submucosal pneumatosis of the colon wall.
Progressive dehydration and loss of body weight further disrupt the microcirculation of the intestinal wall and contribute to the progression of the necrotic process. Violations of the barrier function of the intestinal wall are accompanied by severe infectious toxicosis.
StageIII
In stage III (pre-perforation) intestinal paresis is pronounced. The duration of the stage is no more than 12-24 hours. The condition is very serious, symptoms of toxicosis and exicosis are pronounced, characterized by persistent vomiting of bile and “feces”, severe bloating, pain and tension throughout the abdomen. Peristalsis is sluggish, but audible. Feces and gases do not pass. The anus is closed. During a rectal examination (finger, probe), scarlet blood is released.
Radiologically, due to hydroperitoneum, shading of the abdominal cavity increases, the external contours of the intestinal loops lose their clear outline (Fig. 7-21).
Stage IV
Stage IV (general perforated peritonitis) is characterized by symptoms of peritoneal shock and intestinal paralysis. The peculiarity of perforated peritonitis in necrotizing enterocolitis is a significant area of intestinal damage, the severity of the adhesive-inflammatory process in the abdominal cavity, and moderate pneumoperitoneum (Fig. 7-22).
A more favorable complication of necrotizing enterocolitis is limited peritonitis, observed in a third of cases during treatment. In a child with clinical symptoms of enterocolitis, a dense infiltrate with clear contours, moderately painful, appears in the abdominal cavity (usually in the iliac region). Against the background of conservative therapy, both complete resorption of the infiltrate and its abscess formation are possible.
There is an intestinal fistula on the anterior abdominal wall. When carrying out differential diagnosis, great difficulties arise, since the clinical manifestations are similar to acute appendicitis.
Hemorrhagic intestinal infarction
Hemorrhagic intestinal infarction is the most severe form of necrotizing enterocolitis, developing, as a rule, after severe asphyxia during childbirth or the introduction of drugs into the vessels of the umbilical cord. It occurs in 15% of cases of all enterocolitis.
Clinical picture. The condition of children after birth is very serious due to symptoms of central nervous system depression, brain disorders
798 F Surgical diseases of childhood F Section II
blood circulation, severe respiratory and heart failure. From birth, abdominal bloating and delayed passage of meconium are noted. On the 2-3rd day, vomiting with an admixture of bile appears, bloating, tension and pain in the abdomen increase, intestinal motility is absent, stool and gases do not pass, mucus with blood is released from the rectum.
Diagnostics. On a plain radiograph of the abdominal organs, shadowing of the abdominal cavity due to hydroperitoneum is noted. In case of intestinal perforation, free air is visible under the dome of the diaphragm.
Treatment
Treatment of necrotizing enterocolitis in stage I is usually conservative, syndromic. It is necessary to reduce the volume of enteral feeding, compensate for water and electrolyte disturbances with infusion therapy, and correct the manifestations of dyskinesia by prescribing promethazine, drotaverine, neostigmine methyl sulfate. When symptoms of infectious toxicosis appear, rational antibacterial therapy and intestinal decontamination are prescribed. Timely therapy prevents further development of the pathological process.
In stages II and III, intensive conservative therapy should include the following points.
Decompression of the gastrointestinal tract (at stage II, a pause for 6-12 hours, at stage III - complete exclusion of fluid intake by mouth for 12-24 hours with constant aspiration of stagnant contents through a probe). You can start giving your child water only if passage through the intestines is completely restored and there is no stagnation in the stomach. A day after this, they begin to feed the baby with expressed breast milk, 5-10 ml every 2 hours.
Infusion therapy aimed at rehydration, restoration of microcirculation, elimination of disturbances in homeostasis and acid-base status.
Antibacterial therapy is carried out according to the principle of de-escalation therapy.
♦ Systemic antibiotics are selected taking into account previous therapy, with parenteral use of the latest generation cephalosporins or carbapenem antibiotics. Le-
The reading is accompanied by microbiological monitoring for the purpose of timely targeted correction.
Decontamination is especially important in case of necrotizing enterocolitis, since in conditions of impaired intestinal barrier function, oral administration of antibiotics reduces the massive translocation of microbes into the internal environment of the body. An effective decontamination regimen is oral administration of polymyxin M 10 mg/kg/day in 3 divided doses or amikacin 20 mg/kg/day in 3 divided doses (to influence gram-negative flora), in combination with fusidic acid 60 mg/kg /day or rifampicin 10 mg/kg/day in 3 divided doses (to suppress multi-resistant staphylococci and streptococci). To suppress anaerobes, metronidazole 15 mg/kg/day, nystatin or fluconazole are prescribed to prevent fungal superinfection.
Treatment with antimicrobial drugs is monitored microbiologically every 4-5 days, and if ineffective, therapy is adjusted. When a positive effect is achieved, antibiotics are promptly discontinued, avoiding “overtreatment” of the patient and the development of superinfection. To consolidate the effect at the stage of restoration of the biocenosis, it is recommended to prescribe biological products (bactisubtil, hilak forte, lactobacilli acidophilus), enzyme preparations (rennet enzymes, Aspergillus oryzae drug, etc.).
Stimulating and symptomatic therapy, including transfusions of hyperimmune plasma, administration of immunoglobulins, vitamins. After studying the immune status indicators, immunocorrective therapy is prescribed.
In the first three stages, conservative treatment of necrotizing enterocolitis is possible. The mortality rate is 17-34%, mainly in very premature infants.
Surgical treatment is indicated at stage IV in case of perforated peritonitis and at stage III of pre-perforation, if there is no positive dynamics in the gastrointestinal tract within the next 6-12 hours of intensive therapy.
The operation of choice is the exclusion of the affected part of the intestine by applying a colostomy to the healthy overlying part. After recovery, reconstructive surgery is performed after 1-2 months. Despite intensive therapy, the mortality rate for diffuse peritonitis of this etiology is 80-90%.
Paraproctitis - inflammation of the tissue around the rectum of the anus - can be acute and chronic. In childhood, it usually occurs during the newborn period and in the first months of life. When pus is cultured, an association of E. coli with staphylococcus or streptococcus is most often found. The infection usually occurs from the rectal mucosa. This is evidenced by the long-term non-healing of fistulas after opening the abscess and often found holes in the Morgani crypts communicating with the perirectal tissue.
Predisposing factors in children include microtrauma of the rectal mucosa and skin diseases in the perineum and anus (maceration, fissures), as well as the presence of congenital pararectal fistulas and long sac-like crypts.
Microtraumas of the rectal mucosa often occur with constipation, diarrhea and some digestive disorders. Particles of feces and pieces of undigested food stagnate in the Morgani crypts, injuring the mucous membrane. In diarrhea, especially with frequent tenesmus, denser stool particles also cause microtrauma of the Morganian crypts. Finally, significant stretching of the rectum by feces can lead to microtears. An aggravating factor is increased tone of the anal sphincter, when favorable conditions arise for prolonged retention of dense intestinal contents and increased rectal intraintestinal pressure.
Damage to the mucous membrane by the enema tip, foreign bodies, and also due to trauma to the perineum is also possible, although such cases are rare in children.
In some cases, acute paraproctitis develops due to a congenital pararectal fistula, when secretions accumulate in the fistulous tract, followed by suppuration and involvement of surrounding tissue in the process. Congenital fistulas are characterized by a recurrent course of the disease.
Boys are more likely to suffer from paraproctitis. The lower propensity for the disease in girls can be explained by the greater elasticity and pliability of the pelvic floor, which reduces pressure in the rectum.
