Necrotizing ulcerative enterocolitis. Necrotizing enterocolitis: causes, symptoms, diagnosis and treatment Get treatment in Korea, Israel, Germany, USA
Ulcerative-necrotizing enterocolitis (UNEC) is an intrauterine pathological condition of the intestine, which is caused by hypoxic-ischemic damage, which continues in the postnatal period with the development of a local ischemic-hypoperfusion process, necrosis and ulcer formation.
The incidence of necrotizing ulcerative enterocolitis is 4-28% of all newborns hospitalized in the intensive care unit. In the United States of America (USA), during approximately 4 million births each year, between 1,200 and 9,600 newborns develop necrotizing ulcerative enterocolitis. The lowest prevalence of I PEC is in Japan and the Scandinavian countries, where it is 10-20 times lower than in the USA.
Risk factors for necrotizing ulcerative enterocolitis
Antenatal factors:
Chronic placental insufficiency,
Chronic intrauterine fetal hypoxia;
Intrauterine growth retardation.
Postnatal factors:
Birth weight below 1500 g;
Gestational age less than 32 weeks;
Enteral feeding with milk formulas;
The need for artificial ventilation;
Respiratory distress syndrome.
The likelihood of the risk of developing the disease due to the interaction of factors such as chronic intrauterine hypoxia, gestational age less than 32 weeks and enteral feeding with infant formula is 12.3 times higher.
Stages of ulcerative necrotizing enterocolitis
Stage 1 includes newborns with suspected disease. These children have mild systemic and gastrointestinal disorders. X-ray examination reveals moderate dilatation of intestinal loops, but most patients have normal X-ray findings. Malnutrition and refusal to eat are observed, especially in newborns with low body weight.
In stage 2, the diagnosis of necrotizing ulcerative enterocolitis is confirmed by the presence of intestinal pneumatosis during an X-ray examination of the abdomen. Moderate pain on palpation of the anterior abdominal wall in stage 2A becomes more pronounced in stage 2B. The children's condition worsens, signs of metabolic acidosis appear, and laboratory blood tests show thrombocytopenia. The appearance of the anterior abdominal wall, strengthening of the subcutaneous venous network in the umbilical area and along the umbilical vein indicate developing peritonitis.
More severe or progressive disease is classified as stage 3, which is characterized by clinical instability with progressive deterioration of vital organ function, respiratory failure, disseminated intravascular coagulation (DIC), and shock. In stage 3A the intestine is intact, while in stage 3B there is perforation of the intestine.
Diagnosis of necrotizing ulcerative enterocolitis
X-ray examination is an integral part of a comprehensive examination of a newborn with necrotizing ulcerative enterocolitis.
Distension of the intestine and swelling of the intestinal wall manifests itself in the form of multiple gas-filled, overdistended loops of intestine with fluid levels.
Pneumatosis intestinalis is defined as a pathological process characterized by swelling of the intestinal wall due to the formation of gas bubbles in it.
The presence of gas in the portal vein is the accumulation of gas in the direction of the portal vein in the form of linear formations, which spreads from the intestine along the mesenteric veins,
Pneumoperitoneum - free gas in the abdominal cavity indicates intestinal perforation.
Fixed and dilated intestinal loops in any part of the abdominal cavity on a series of radiographs over 24-36 hours are a sign of developing intestinal necrosis.
Treatment of ulcerative necrotizing enterocolitis
Conservative treatment of necrotizing ulcerative enterocolitis
If ulcerative necrotizing enterocolitis is suspected or in the initial stages of its manifestation, the treatment regimen can be presented as follows:
Cancellation of enteral feeding
Decompression of the gastrointestinal tract
Infusion therapy
Parenteral nutrition
Rational antibiotic therapy
Selective gut decontamination
Immunostimulating therapy
Desensitization therapy
Surgical treatment of necrotizing ulcerative enterocolitis
Clinical deterioration of the child’s condition is determined by instability of vital functions and can manifest itself as systemic arterial hypotension, oliguria, lethargy and adynamia, respiratory arrest, and increasing metabolic acidosis. The presence of these symptoms, despite intensive therapy, is an indication for surgical treatment;
Hyperemia and swelling of the anterior abdominal wall, a strong constant on palpation of the abdomen, are signs of peritonitis and an absolute indication for surgical treatment;
Pneumoperitoneum is a classic criterion that determines indications for or;
The radiographic sign of the presence of gas in the portal venous system has high specificity and a positive predictive value for intestinal necrosis;
Reduced gas filling of the intestine and the presence of fluid in the abdominal cavity are considered as signs of hidden intestinal perforation and developing peritonitis;
Fixed dilated intestinal loops, determined on a series of x-ray examinations within 24 hours, serve as an indication for surgery in only 57% of patients. Clinically stable patients with this symptom recover with intensive care;
A positive result of laparocentesis is assessed by the presence of free inflammatory fluid in the abdominal cavity and serves as evidence of intestinal necrosis. The diagnostic sensitivity of the test was the highest (87%) compared with the previously listed criteria;
Laboratory blood tests, including assessment of the number of leukocytes, platelets, determination of the ratio of the number of young neutrophil granulocytes to the total number of segmented leukocytes, have a fairly high diagnostic sensitivity (64%) and specificity (100%) and, therefore, can determine indications for surgical treatment. The diagnostic value of the listed criteria increases with their combination. Tests are considered positive when the number of leukocytes is less than 9000 mm / platelets less than 200,000 mm3, and the ratio of metamyelocytes to the total number of segmented leukocytes is more than 5.
The article was prepared and edited by: surgeonMany gastrointestinal diseases in the neonatal period can lead to necrotizing ulcerative enterocolitis (NUEC).
YNEK risk group
This disease is more common in very low birth weight infants, with 90% of JNEC cases occurring in premature infants. JNEC can also develop in 10% of children hospitalized in neonatal intensive care units. Mortality rates range from 10 to 50%. The age at which JNEC begins depends on birth weight and gestational age. The more premature and immature the baby (less than 26 weeks of gestation), the more susceptible he is to the long-term risk of developing JNEC and its early onset.
Causes of ulcerative necrotizing enterocolitis
The etiology of JNEC is not completely established. Apparently, many factors (including hypoxia, acidosis, hypotension) can lead to ischemic damage to the small intestinal mucosal barrier. Secondarily, bacterial invasion of the altered mucous membrane of the small intestine may be involved in the pathogenesis. Therefore, a change in the intestinal biocenosis, consisting in an increase in the number of opportunistic microbes with a simultaneous decrease in bifidobacteria and lactobacilli, indicates the risk of developing JNEC. Many conditions can contribute to the development of JNEC, including congenital, hypoplastic left heart, coarctation of the aorta, polycythemia, the presence of an umbilical catheter, transfusions, perinatal asphyxia, and maternal preeclampsia.
Children with patent ductus arteriosus are also at high risk of developing JNEC. In this case, oxygenated blood is shunted from the intestines. Inflammatory mediators, platelet-stimulating factor, and free oxygen radicals are also important. A risk factor for JNEC may be early initiation of enteral nutrition, since the feeding process requires changes in blood flow and oxygen. JNEC is rare in children who have not received enteral nutrition. With artificial feeding, the hyperosmolar formula of the mixture promotes the development of JNEC.
Also, very premature, immature children have insufficient production of hydrochloric acid, intestinal motility, and enzyme production. Immaturity of the mucous membrane leads to insufficient mucus production, and immaturity of the local immune system leads to a sharp decrease in secretory IgA. The possible role of oral immunoglobulin for the prevention of JNEC is of interest.
Symptoms of JNEC
The clinical picture of the disease is presented very broadly and is often determined by the degree of maturity of the organism. Bloating, enlargement of the abdomen is usually one of the early and most significant clinical symptoms. The general condition of the child also changes, attacks of apnea, hypothermia, microcirculation disorders, and regurgitation appear. Blood in the stool, bradycardia, drowsiness, and shock are often detected.
Laboratory tests sometimes detect thrombocytopenia, neutropenia, and metabolic acid doses. However, not every patient has all the listed symptoms, and the clinical picture can be very varied.
The diagnosis is made using x-ray examination, which is characterized by the detection of intestinal pneumatosis. Nonspecific radiological signs: thickening of the intestinal wall, dilatation of intestinal loops, ascites. Reduced stools due to carbohydrate malabsorption may be an early manifestation of JNEC. A reliable method for assessing the severity of the pathological process in the intestine and the prognosis of the disease is to determine the content of secretory IgA in coprofiltrates.
Treatment of ulcerative necrotizing enterocolitis
If JNEC is suspected, enteral feeding should be stopped for an extended period of time. Intravenous access should provide the patient with fluid, electrolytes, and nutrients. Antibacterial treatment should be started. prescribed intravenously, taking into account the sensitivity of the intestinal microflora to them. The duration of weaning from enteral feeding depends on the clinical condition of the patients. So, if abdominal bloating and intestinal pneumatosis are pronounced, the duration of parenteral nutrition is up to 2 weeks, with minor clinical and radiological changes - 48-72 hours. Dynamic radiological monitoring of the abdominal organs is necessary to detect intestinal perforation. The sudden appearance of apnea, bradycardia, change in color of the abdominal wall, its swelling or an increase in abdominal circumference should lead to suspicion of intestinal perforation. If intestinal perforation is present, surgery should be performed immediately.
Laboratory tests include a complete blood test, which most often reveals neutropenia and thrombocytopenia. Such children require large volumes of fluid, electrolytes, and blood products to maintain blood circulation and blood pressure. Children with severe metabolic acidosis develop secondary circulatory failure and may require mechanical ventilation.
Children undergoing surgery are at risk of developing short bowel syndrome and various complications associated with total parenteral nutrition.
In some children, inflammation of the mucous membrane leads to transmural necrosis and, in the absence of perforation, to fibroblastic transformation of granulation tissue and strictures. Strictures in the distal parts of the small and large intestine are common complications of JNEC. If symptoms of partial obstruction and malnutrition develop, an X-ray contrast study is necessary to clarify the diagnosis.
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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, most 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 and blood are 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 treatment is accompanied by microbiological monitoring for the purpose of timely targeted correction.
Decontamination is especially important in 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 in case of ineffectiveness, 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 tip of the enema, foreign bodies, and also due to trauma to the perineum is also possible, although such cases are rarely observed 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.
Enterocolitis is a nonspecific inflammatory disease of the large and small intestines of various origins, accompanied by painful sensations in the abdomen 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 upon palpation, 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 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, the patient's 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 substances containing alcohol;
- 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 the 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.
Necrotizing enterocolitis of newborns (NEC) is a nonspecific inflammatory disease that is caused by infectious agents against the background of damage to the intestinal mucosa or its functional immaturity. Symptoms include somatic reactions and abdominal manifestations. With a long course, signs of intestinal perforation and clinical peritonitis are observed. Diagnosis of NEC involves physical examination, symptom assessment using the Walsh and Kliegman scale, and radiography. Treatment depends on the stage of the disease and can be either conservative or surgical.
General information
Most complications of necrotizing enterocolitis in newborns, as a rule, develop after surgical treatment. Most often, after surgery, intestinal fistula, short bowel syndrome, chronic diarrhea, dumping syndrome, dehydration, malabsorption syndrome, colon stricture, abscess, and delayed physical development occur. Also, with NEC, pathological conditions caused by total parenteral nutrition may occur: vitamin D deficiency (rickets), liver damage (hepatitis) and bones (demineralization).
Diagnosis of NEC in newborns
Diagnosis of necrotizing enterocolitis in newborns includes anamnesis, clinical, laboratory and instrumental examination. Anamnestic data can help the pediatrician and pediatric surgeon establish a possible etiology and monitor the dynamics of the disease. An objective examination reveals the currently present clinical symptoms - abdominal, somatic and generalized manifestations. There are no specific laboratory tests to confirm NEC. The following data obtained during laboratory tests are informative: leukocytosis with a shift of the formula to the left, leukopenia and thrombocytopenia in the CBC, acidosis and hypoxemia when determining the blood gas composition, hyperkalemia and hyponatremia in the electrolyte spectrum, dysproteinemia and detection of C-reactive protein in the protein spectrum, detection of blood in stool using Gregersen's test. In order to identify the infectious pathogen, bacterial culture, ELISA and PCR are performed.
The leading role in the diagnosis of necrotizing enterocolitis in newborns is played by instrumental methods: radiography, ultrasound, CT and MRI. They make it possible to visualize swelling of the walls of the intestinal tract, plus tissue, the presence of air in the abdominal cavity, in the lumen of the portal or hepatic veins, as well as the absence of peristalsis on a series of sequential images. In pediatrics, the Walsh and Kliegman scale is used to confirm the diagnosis of necrotizing enterocolitis of newborns and determine the stage of the disease. When using this scale, the somatic symptoms present in the child, manifestations from the gastrointestinal tract and radiological signs are taken into account. Depending on the number and severity of manifestations, suspected NEC (grades 1a and 2a), obvious NEC (grades 2a and 2b), and progressive NEC (stages 3a and 3b) are distinguished. This is essential when choosing treatment tactics.
Differential diagnosis of necrotizing enterocolitis in newborns is carried out with such pathologies as neonatal sepsis, pneumonia, pneumoperitoneum, intestinal obstruction of various origins, neonatal appendicitis, bacterial peritonitis and spontaneous intestinal perforation.
Treatment of NEC in newborns
Treatment tactics for necrotizing enterocolitis in newborns depend on the severity of the child’s condition and the stage of the disease. Conservative therapy is indicated for children with stages 1a, 1b and 2a. From the moment of diagnosis, enteral nutrition is canceled and a naso- or orogastric tube is placed for the purpose of decompression. The child is placed on total parenteral nutrition (TPN) according to clinical protocols. In parallel, antibacterial drugs from the groups of penicillins (ampicillin) and second generation aminoglycosides (gentamicin) are prescribed in combination with medications that act on anaerobic microflora (metronidazole). If the selected antibiotic therapy is ineffective, III-IV generation cephalosporins (ceftriaxone) are used in combination with III generation aminoglycosides (amikacin). For such children, probiotics and eubiotics are recommended to normalize the intestinal microflora. Microwave therapy is also carried out, immunomodulators and gamma globulins are administered.
Children with stages 2b, 3a and 3b are indicated for surgical intervention. The extent of the operation depends on the extent of intestinal damage. As a rule, economical resection of the affected area is performed to form an enterostomy or colostomy. In local forms of NEC, it is possible to perform an end-to-end anastomosis. After surgery, infusion therapy and drug treatment are prescribed, similar to earlier stages.
Prognosis and prevention of NEC in newborns
The outcome of NEC depends on the severity of the child’s general condition and the stage of the disease. Since these indicators are almost always unstable, the prognosis is considered questionable even with full treatment. Prevention of necrotizing enterocolitis in newborns includes antenatal health care of the fetus, rational management of pregnancy, and breastfeeding in physiological quantities. According to some studies, the risk of developing the disease is reduced with the use of eubiotics, probiotics and IgA in children at risk. If there is a high risk of preterm birth, glucocorticosteroids are used to prevent RDS.
