Pediatric pseudomembranous colitis

Introduction to pediatric pseudomembranous colitis Pseudomembranous enteritis (PME) is an acute intestinal inflammation. It is named after a layer of pseudomembrane on the surface of the necrotic mucosa of the small intestine or colon. It usually occurs in the small intestine, colon, or both. The disease is prone to major surgery and the application of broad-spectrum antibiotics, so some people call it post-operative enteritis, antibiotic enteritis. The essence of pseudomembranous colitis is the imbalance of the ecological balance of the intestinal flora, so it can also be seen in shock, heart failure, uremia, colonic obstruction, diabetes, leukemia, aplastic anemia, and chronic heart and lung diseases. basic knowledge The proportion of illness: 0.03% Susceptible people: children Mode of infection: non-infectious Complications: shock dehydration peritonitis intestinal obstruction

Causes of pediatric pseudomembranous colitis

(1) Causes of the disease

Pseudomembranous colitis is caused by the production of toxins by two floras.

1. Clostridium difficile

It is an important cause of pseudomembranous colitis associated with antibiotics. In 1935, the elongated and strict anaerobic Gram-positive bacilli were first isolated from the feces of infants by Hall et al. Normal in the intestines.

Among patients who have not received antibiotic treatment, the number of Clostridium difficile accounts for only 2% to 3% of anaerobic bacteria, and the bacteria produce less toxins, even without causing toxins that cause disease to humans.

The detection rate of Clostridium difficile in the population is 5% to 13%. Under normal circumstances, these bacteria are mutually restricted, cannot be multiplied, and will not cause disease. Long-term use of a large number of antibiotics can inhibit various bacteria in the intestine. Growth, non-antibiotic-resistant drug resistance, Clostridium difficile is rapidly multiplying, and Clostridium difficile in stool can be as high as 10% to 20% of anaerobic bacteria, producing a large amount of exotoxin, causing mucosal necrosis Exudative inflammation with pseudomembrane formation, which is almost found in the stool of all pseudomembranous colitis. Clostridium difficile produces at least four substances, namely toxin A (enteric toxin), toxin B. (cytotoxin), a motility-influencing factor and a heat-sensitive toxin, in which toxins A and B have been purified. Toxin A has a molecular weight of 500,000 and toxin B has a molecular weight of 360,000. They are all composed of glycoproteins and acid. Alkali-sensitive, ether-tolerant, heat-resistant, most of the two toxins are destroyed at 50 °C for 30 min, sensitive to trypsin, chymotrypsin and cellular protease, not decomposed by ribonuclease and deoxyribonuclease, pH 4 Under the condition of pH 10, the toxicity of toxin B disappears and the virulence of toxin A is not affected. Toxin A can stimulate the secretion of water and electrolytes by mucosal epithelial cells, causing a large loss of water and electrolytes. Toxin B can cause local allergic reaction to the intestines. Mucosal degeneration and necrosis, cellulose, mucin exudation forms a pseudomembrane. If this toxin is injected into the animal, it can cause enteritis and death. Toxin A can stimulate intestinal mucosal epithelial cells to activate guanosine cyclase at low concentration. Lead to the increase of intracellular G-phosphate guanosine, the role of toxin A and toxin B is synergistic, first toxin A causes intestinal tissue lesions, then toxin B acts on these damaged tissue cells, both toxins It is antigenic and can interact with the corresponding antibody. The antiserum of toxin A cannot neutralize toxin B, while the anti-blood clearance of toxin B can neutralize toxin B and neutralize part of toxin A. In addition, toxin B can be Soxhlet Clostridium antitoxin neutralizes.

The third toxin motility factor is present in the filter sterilizing supernatant of Clostridium difficile culture medium, which can change the electrical activity of rabbit ileum iliac muscle. The fourth toxin is low molecular weight protein, which is sensitive to heat. It is very unstable, and its action is the same as that of Vibrio cholerae and Escherichia coli, which can cause an increase in the secretion of ileal fluid in rabbits, but does not cause tissue damage.

2. Coagulase-positive hemolytic drug-resistant Staphylococcus aureus

When a large number of broad-spectrum antibiotics (such as oxytetracycline, chloramphenicol, tetracycline, ampicillin, cephalosporin, etc.) are used to inhibit various bacterial flora including Escherichia coli in the intestine, resistant Staphylococcus aureus Proliferation produces exotoxin, which leads to the occurrence of pseudomembranous colitis. Gram staining of fecal smears in such patients can be found in piles of cocci. For example, the injection of toxins from this bacterium can also cause pseudomembranous enteritis.

It has been reported that 17% of Staphylococcus aureus is detected in the stool of a group of admitted patients, and the detection rate of Staphylococcus aureus in the stool after admission for 1 week after antibiotic treatment is 38% to 40%. In pseudomembranous colitis, Staphylococcus aureus is only a concomitant bacterium is not a true pathogenic factor. Some people have not found Staphylococcus aureus in tissue culture or stool culture of autopsy material of pseudomembranous colitis. It has been reported that Staphylococcus aureus and its toxins are present in the stool of patients with antibiotic-associated pseudomembranous colitis, but the aforementioned Clostridium difficile and toxin are not seen, and it can be seen that it has been confirmed that it is difficult to identify Clostridium spores. Bacillus is an important cause of antibiotic-associated pseudomembranous colitis, but not all pseudomembranous colitis is caused by Clostridium difficile.

Under normal circumstances, the gastrointestinal tract is a balanced ecosystem. There are a large number of bacteria in the intestine. The bacteria and the number of these bacteria are basically constant. These bacteria help the bacteria itself and the antibodies it produces. Infection, once certain factors cause the system to lose its ecological balance, it will cause disease, and the proportion of antibiotics most likely to produce flora is imbalanced. Therefore, it is one of the important causes of pseudomembranous colitis, and the antibiotics most commonly cause pseudomembranous colitis. In turn, ampicillin, clindamycin and cephalosporins, not often caused by penicillin, erythromycin and sulfamethoxazole, can even cause chloramphenicol, tetracycline, metronidazole and aminoglycosides Drugs, cancer and surgery are important susceptibility factors.

(two) pathogenesis

Pathogenesis

The bacteria in the intestines come from the mouth, and the bacteria that enter the digestive tract from the outside are mostly killed by stomach acid when passing through the stomach. Only a small number of unkilled bacteria enter the duodenum and the upper part of the ileum, duodenum and The surviving bacteria in the jejunum are mainly Gram-positive streptococci, Lactobacillus, Mycobacterium and yeast, with a total number of less than 105/ml. The number of bacteria in the lower and middle ileum begins to increase, and the content is estimated to be 105-106/ml in the ileum. The last part is mainly aerobic Escherichia. After the intestinal contents enter the large intestine, the bacteria are neutral or weakly alkaline in the anoxic environment, and the contents are moved in a slow and vigorous condition. The main one is Anaerobic opportunistic flora, the number of anaerobic bacteria can be as high as 1011 per ml of colon content. In normal human intestinal tract, it is mainly obligate anaerobic bacteria, and facultative aerobic bacteria only account for 1%, in the digestive tract. The normal flora is regularly distributed according to bacterial colonization, and is excreted while excreting, and remains unchanged for life. The results of research on human fecal flora in China are similar to those reported in foreign countries, suggesting that the intestinal flora is anaerobic. Mainly bacteria, 9 species The order of common bacteria is: Bacteroides, Bifidobacterium, True bacillus, Enterobacter, Lactobacillus, Enterococcus, Clostridium, Staphylococcus, Yeast, and the division cycle of bacteria in normal human intestinal tract is 6 to 48 hours, except Gastric acid plays an important role in maintaining the number of bacteria in the jejunum. The gastric and jejunal mucosa also have intrinsic pH-independent inhibition properties. In the stomach and small intestine of patients with gastric acid deficiency or partial gastrectomy, the number of aerobic and anaerobic bacteria can be found. Significantly increased, Escherichia coli and anaerobic Gram-negative bacilli appeared in the proximal small intestine, and the number of streptococcus, lactobacilli and fungi increased. The normal flora promoted the digestion and absorption of nutrients in the body, and participated in cholesterol, steroids and fat in the body. , protein, lipids, amino acids and the absorption and metabolism of certain drugs.

The intestinal flora plays a non-specific immune role through the following mechanisms:

1H2O2 action.

2 bacterial toxins.

3 occupancy protection.

4 the role of organic acids.

5 compete for nutrition, the normal flora can also produce a variety of antigenic substances to stimulate the body to develop an immune response, so that the immune system remains active to prevent a variety of infections, intestinal flora disorder, such as reduced bacterial levels will cause lymphoid tissue dysplasia, Decreased lymphocyte proliferation, decreased white blood cells, decreased gamma globulin content, and decreased lymphocyte secretion capacity will also affect cellular immune response and establishment of delayed type hypersensitivity.

One of the main physiological functions of Escherichia coli is its immunogenicity. Escherichia coli can produce trace amounts of toxins like other normal flora, and it acts as an immunogen to induce immunity to toxins. The intestinal flora is affected by the intestinal peristalsis of the host. The effects of physiological factors such as intestinal digestive pH, intestinal endocrine enzymes, mucus, antibody secretion and function, which vary with intestinal bacterial interactions, food, drugs, climate, and age. Normal intestinal peristalsis is to prevent bacterial overgrowth in the small intestine. The main defense mechanism for growth.

The small intestine relies on strong creep to make the bacteria in the intestines far less than the colon. When the intestinal peristalsis is reduced, the small intestine bacteria will grow densely. The stomach acid kills the upper small intestine bacteria, making the bacteria in this part rare. Once the stomach acid is reduced, it enters the stomach. The number of aerobic and anaerobic bacteria in the small intestine will increase significantly, and E. coli and anaerobic Gram-positive bacteria will appear in the proximal small intestine, and the number of fungi and streptococci will increase accordingly. Under normal circumstances, the human intestine The bacteria in the channel depend on each other and restrict each other to form a natural ecological balance between bacteria and human body.

The bacteria present in the intestine are basically balanced in terms of the species and quantity. The number of bacteria per gram of content in the large intestine is 1010-1011, and the small intestine also contains 108. Under normal ecological balance, these bacteria Bacteria itself and bacteria cause antibodies produced by the body to resist the invasion of pathogenic bacteria. Bacteria do not pose a hazard to humans and can also synthesize certain vitamins. A large number of antibiotics are used, especially by oral administration to change the balance between intestinal bacteria. Relationship, there will be dysbacteriosis of intestinal bacteria, non-pathogenic intestinal bacteria, such as E. coli, etc., which are killed by antibiotics, are relatively resistant to bacteria, such as Staphylococcus aureus, P. aeruginosa Bacillus, some Bacillus capsulatum and fungi, etc., rapidly grow and multiply, secreting exotoxin to cause intestinal lesions.

The immune system and disease resistance of the patient's body decline or some diseases lead to intestinal ischemia, congestion, etc. can cause intestinal flora imbalance, pseudomembranous colitis, pseudomembranous colitis must have intestinal flora disorder, within Derived or exogenous refractory Clostridium or Staphylococcus aureus and the above-mentioned bacteria produce toxins and susceptible organisms, etc., in infants and young children, Clostridium difficile is the normal intestinal flora First, because the toxin receptors on the intestinal mucosa of newborns and infants may not be mature, they will not cause disease.

In the intestines of infants less than 1 month old, Clostridium difficile can account for more than 50% of the total bacteria, and 30% to 90% of infants within 1 year of age carry the bacteria in the intestines, and then grow with age. Gradually reduce to about 3% of intestinal bacteria in adulthood. After the patient uses antibiotics, the intestinal flora is killed or inhibited, resulting in disorder of the normal flora, although the Clostridium difficile is also largely eliminated, but in If the bacteria with antagonism are reduced, they are still prone to mass reproduction. If the patient is not carriers before receiving antibiotics, the aerobic and anaerobic bacteria in the intestines are removed after receiving antibiotics, and the intestinal colonization resistance is reduced, resulting in the original The bacterial receptors on the intestinal mucosal cells occupied by these bacteria are eventually colonized by the externally attached Clostridium difficile.

In addition to the use of antibiotics, other diseases not treated with antibiotics, such as partial gastrectomy or vagus nerve ablation plus pyoplasty, gastrectomy, gastrojejunostomy, duodenum or jejunum diverticulum, surgical blindness (end side anastomosis), intestinal obstruction (stenosis, adhesion, inflammation, cancer) intestinal short circuit and sputum effect, low gastric acid and accompanied by motor dysfunction, intestinal fistula, ileocecal resection, etc. can cause gastrointestinal Changes in motor function, combined with changes in the environment of the intestine, such as ileocecal resection, loss of ileocecal valve plays an important role in regulating the normal distribution of intestinal flora, can not prevent the colonic flora from flowing back into the small intestine, weakening the intestinal tract Antibacterial defense ability such as excessive proliferation of flora.

Others such as leukemia, malignant tumors or receiving radiotherapy, chemotherapy, hormone therapy and infection, chronic wasting diseases can also change the ecological balance of the normal intestinal flora, and the bacterium can also be isolated from the strain of Clostridium difficile. Pseudomembranous colitis.

2. Pathology

Histological studies have shown that typical pseudomembranous colitis has histologically specific lamellar pathological changes, no vasculitis, early lesions, normal mucosa between lesions and lesions, advanced mucosa completely necrotic and only a small number of glands The body survives, covered with a thick layer of inflammatory cells, mucin and cellulose, edema and inflammation continue to develop, extending to the submucosa or even beyond the submucosa is not easy to distinguish from other intestinal inflammation, about 60% of lesions occur In the small intestine, 15% occur in the large intestine, 25% in the large intestine. The pathological changes are mainly confined to the mucosa and submucosa. The affected intestines may have staged distribution of mucosal necrosis, pseudomembrane formation, and mucosal lesions manifest as congestion and edema. Sexual necrotic lesions can fuse with each other.

(1) Gross morphology: The intestinal lumen of pseudomembranous colitis is visible to the naked eye, and a large amount of thick mucus accumulates. The mucosa is covered with spots or patches of yellowish white, yellow, brown or yellow scattered from several millimeters to several centimeters. The green pseudomembrane is severely fused into a piece to completely cover the entire intestine segment with a pseudomembrane. The pseudomembrane is formed by the solidification of cellulose, neutrophils, monocytes, mucin, bacteria and necrotic cells, and the pseudomembranous texture is soft. It is brittle, easy to separate from the mucous membrane, floats in the intestinal fluid and excretes with the stool. After the pseudomembrane falls off, the submucosa is exposed to form an ulcer, the serosa is congested, edematous, thickened, even necrotic and perforated.

(2) Histomorphology: under the microscope, the mucosa of the lesion is congested, and the mucous gland tube contains a lot of thick mucus. After the mucus is discharged, it participates in the composition of the pseudomembrane. When the lesion is heavy, the villi and the top of the mucosa have different degrees of necrosis or disappearance. In the lamina propria, there are neutrophils, plasma cells and lymphocytes infiltration, glandular rupture and necrosis, submucosal telangiectasia, congestion and thrombosis, and vascular wall necrosis can lead to mucosal ischemic necrosis. The lesions are generally limited to the mucosal layer. However, it can also extend to the submucosal layer to affect the entire layer, and even lead to large pieces of necrosis.

Generally can be divided into mild, severe, severe type 3 according to the degree of disease:

1 mild lesions: the initial lesion is the appearance of acute inflammatory cells in the lamina propria of the mucosa, eosinophil infiltration and cellulose exudation, formation of focal necrosis, fibrinogen and polymorphonuclear in necrotic lesions Cell aggregation forms a special apical lesion.

2 severe lesions: the lesion did not invade the submucosa, the mucosal glands were destroyed, the pseudomembrane formed, the destruction of acute inflammatory cells containing mucin and the gland was covered by a typical pseudomembrane, the lamina propria neutral polymorphonuclear cells Infiltration, accompanied by typical volcanic ridge-like necrotic lesions.

3 severe lesions: the mucosa is completely destroyed, the deep layer of the lamina propria is violated, and the lamina propria is covered by a thick and intertwined pseudomembrane.

Prevention of pseudomembranous colitis in children

The prognosis of this disease is often quite serious. The clinical work should prevent the occurrence of this disease as much as possible. First of all, attention should be paid to the use of antibiotics to avoid the abuse of antibiotics to reduce the incidence of pseudomembranous colitis. In particular, the use of broad-spectrum antibiotics should have a clear purpose. After taking the expected effect, the drug should be stopped in time. The medical staff should be introduced to the onset of pseudomembranous colitis to prevent the growth of drug-resistant strains. The exogenous C. difficile may be a cross infection in the hospital. Some people have to detect Clostridium difficile or its spores from the floor of the hospital, the utensils of the bathroom, and the hands and feces of the staff of patients with pseudomembranous colitis. Therefore, it is necessary to take the necessary cases for pseudomembranous colitis. Isolation measures and environmental disinfection prevent cross-infection of the refractory Clostridium by room, skin, and medical devices.

Complications of pediatric pseudomembranous colitis Complications, shock dehydration, peritonitis, intestinal obstruction

Severe cases can be complicated by irreversible shock, rapid dehydration, acidosis; or complicated acute abdomen with toxic megacolon, colon perforation or peritonitis, can also be complicated by acute intestinal obstruction; can be complicated by hypoproteinemia, multiple arthritis.

1. Toxic megacolon:

1 Introduction:

Most occur in patients with explosive or severe ulcerative colitis. At this time, the colonic lesions are extensive and severe, involving the muscular layer and the intestinal nerve, the intestinal wall tension is reduced, the colonic peristalsis disappears, and the intestinal contents and gas accumulate in a large amount, causing acute colonic expansion, generally the most serious in the transverse colon. Often induced by low potassium, barium enema, anticholinergic drugs or opioid preparations.

2. Clinical manifestations:

The condition deteriorated drastically, the toxemia was obvious, there was a disorder of dehydration and electrolyte balance, and there was tenderness in the intestines and abdomen, and the bowel sounds disappeared. Its clinical features are severe symptoms of poisoning and segmental or total colonic dilatation, abdomen with flatulence, and the most obvious dilated site in the transverse colon.

Second, hypoproteinemia:

1 Introduction:

Protein malnutrition is also known as edematous malnutrition or hypoproteinemia.

Protein is the basic component of the body's tissue cells, and all tissue cells in the human body contain proteins. The growth and development of the body, the renewal of aging cells, and the repair of tissue damage are inseparable from protein. Protein is also an indispensable ingredient in enzymes, hormones and antibodies. Since the protein is a zwitterion, it has a buffering effect. Protein is also a determinant of water retention and control of water distribution, and is one of the sources of heat. 1g of protein can produce 16.6 kilojoules of heat in the body. For example, children's protein deficiency is not only affecting their physical development and mental development, but also causes the entire physiology to be in an abnormal state, with low immune function and reduced resistance to infectious diseases.

2. Clinical manifestations:

The patient developed edema on the face and feet due to hypoproteinemia, and even spread throughout the body. White-skinned children have specific skin lesions, starting with erythema, the pressure can subside, followed by small dark purple spots, clear borders, higher than the surrounding skin, the pressure does not fade, the surface is bright, and there is a waxy feeling. It turns into a dry, brown or black spot with cracks. Occurs in the compression parts, such as trochanter, knee, ankle, shoulder, elbow and torso pressure, can also occur in wet areas, such as diaper area, irregularly clothed throughout the body, showing exfoliative dermatitis.

Pediatric pseudomembranous inflammatory symptoms Common symptoms abdominal pain high fever diarrhea abdominal tenderness bloating nausea acute abdomen peritonitis hemorrhagic shock

Some sick children have simple diarrhea on the first day after applying some antibiotics, no other symptoms, and relieve themselves after stopping the drug. This is the temporary intestinal tract sensitivity to antibiotics, causing a transient internal environment change without causing false Membranous enteritis, pseudomembranous colitis occurs in the first 2 to 3 days after the use of antibiotics, at the latest 3 weeks after stopping the antibiotics, generally 4 to 6 days after the administration of the drug, the child suddenly has fever, abdominal distension, a large number of watery stools It is a yellow egg flower or seawater sample, containing a detached pseudomembrane. Due to the sudden loss of fluid, the child rapidly develops dehydration acidosis, abdominal tenderness, muscle tension, heavier toxic shock, and some children with acute abdomen. Symptomatic toxic megacolon, colon perforation or peritonitis as the primary manifestation, and no diarrhea symptoms, stool smear can find Gram-positive cocci increased, Gram-negative bacilli decreased, when the condition allows, colonoscopy can be performed, showing the colon wall Congestion, edema and yellow-white pseudomembrane.

Asymptomatic infection

Most children are asymptomatic, but they are an important source of infection.

2. Simple diarrhea

The child has no systemic symptoms, mainly manifested as loose stools, 3 to 4 times / d, for mucus watery stools, large white blood cells, occult blood test positive, sigmoid colonoscopy showed mild intestinal edema, congestion, no pseudomembrane, Shortly after the broad-spectrum antibiotics are discontinued, the symptoms disappear and no special treatment is required.

3. pseudomembranous colitis type

Diarrhea is heavier, more than 10 times a day, the stool is egg-like soup, there are pseudomembranous and bloody stools, children often have systemic symptoms in addition to diarrhea, manifested as fever, abdominal pain, nausea, anorexia, abdominal pain often relieved after diarrhea, Severe cases can be manifested as dehydration, peripheral white blood cells rise, a large number of white blood cells in the stool, sigmoidoscopy can be seen on the diseased colon and rectal mucosa there are a large number of scattered, plaque-like yellow convex pseudomembrane, diameter 2 ~ 10mm, Known as pseudomembranous nodules.

4. fulminant colitis type

Diarrhea can be more than 20 times a day, the amount is large, strange smell, often bloody stools, pseudomembrane is large or tubular, accompanied by fever, abdominal pain, abdominal distension, vomiting; critically ill can be high fever, wilting, pale, even complicated , renal failure, shock, DIC, intestinal perforation, etc., this type of prognosis is poor, this type of children should try to avoid colonoscopy, so as not to cause intestinal perforation, major surgery.

Examination of pediatric pseudomembranous colitis

Laboratory inspection

1. Fecal routine: Microscopic examination of fecal smear, if Gram-positive bacilli and their spores are found to be helpful for clinical judgment, then staged bacterial culture can be carried out to check for the presence of a large number of Gram-positive bacteria.

2. Bacteriological examination: 90% of the cases can be cultured in the feces of the disease to the bacterium in the stool, in order to reduce contact with the air, must take at least more than the container capacity of fresh feces, together with the container for inspection Inoculate CCFA-specific medium (composed of cycloserine, thiophene methoxycephalosporin, fructose and protein agar) to selectively isolate Clostridium difficile under anaerobic conditions, if the colonies are flat and the edges are not Regular, rough, Gram staining for positive bacilli can be diagnosed.

3. Cytotoxicity toxicity test: diluted stool or bacterial culture filtrate, specific cell pathological effect on tissue culture cells (HELA), this effect can be neutralized by the antitoxin of Clostridium septicum, thus confirming that it is difficult Bacillus licheniformis is a toxigenic strain.

4. Detection of toxin A: Toxin A can be examined by convection immunoelectrophoresis, enzyme-linked immunosorbent assay, latex agglutination assay, monoclonal antibody method, and the like.

Film degree exam

1. Colonoscopy: pseudomembranous colitis invades the colon at the same time, especially the sigmoid colon can be examined by colonoscopy. It has been reported in China that 16 patients with pseudomembranous colitis have been examined by fiberoptic colonoscopy, 14 of which are in the rectum and sigmoid colon. Found lesions, the typical manifestations of mucosal redness and edema, plaque or fusion of the pseudomembrane, biopsy showed acute inflammation of the mucosa, pseudomembrane containing necrotic epithelium, fibrin, inflammatory bacteria, etc., using fiber colonoscopy It is necessary to grasp the stage of the progression of the disease. The enteritis has not formed a pseudomembrane or the local pseudomembrane has fallen off. The pseudomembrane may not be found under the microscope. Therefore, the pseudomembrane is not necessarily the only diagnostic basis. No pseudomembrane is not necessarily excluded. In this disease, pseudomembranous colitis lesions can be skipped. In order to prevent missing small lesions, the scope of microscopic examination must include the whole colon. The lesion tissue should be taken at a representative site, and the biopsy should have a certain depth.

2. Abdominal X-ray film: often thickened in the intestinal mucosa, small intestine flatulence, some patients with intestinal paralysis showed intestinal obstruction, barium enema may be found in the bow of the intestine, brushed, and scattered circular, irregular Shape filling defects, double contrast of gas sputum can provide more diagnostic indicators, but must be carefully operated to prevent the occurrence of intestinal perforation.

3. Ultrasound diagnosis: Ultrasound can detect the local intestinal wall pseudomembrane, mucosal and submucosal edema caused by severe thickening, narrowing or disappearing of the intestinal lumen, careful exploration of the pseudo-renal sign of intestinal tuberculosis or tumor can be found in the right lower abdomen, conditions A good ultrasound diagnostic instrument can more accurately distinguish the level of lesions. In addition, ultrasound diagnosis can find ascites associated with the disease.

4. CT diagnosis: CT performance is not specific, and even a low attenuation of the thickened intestinal wall can be found.

Diagnosis and diagnosis of pediatric pseudomembranous colitis

diagnosis

Long-term use of antibiotics in large quantities, severe chronic diseases or high-risk patients suddenly have fever during the recovery of the disease, diarrhea, discharge of green seawater or egg-like water should first think of the disease, chemotherapy during malignant tumors and large gastrointestinal malignancies The incidence rate after surgery is higher. For example, if the stool smear is used for Gram staining, the number of positive cocci is increased, and the diagnosis of negative bacilli is basically confirmed. The typical case of atypical cases lacks stool, which often causes diagnostic difficulties. Patients who have diarrhea due to surgery or antibiotics should repeat the stool smear examination to observe changes in the proportion of cocci and bacilli, and if necessary, colon endoscopy, if conditions are used to determine stool by the antibiotic toxin method of Clostridium difficile The presence or absence of the refractory Clostridium toxin can help diagnose.

Diagnostic criteria:

1 There is a history of certain antibiotics before diarrhea.

2 typical clinical manifestations such as diarrhea, bloating, fever, increased white blood cell count, severe blood in the stool, toxic intestinal paralysis, intestinal perforation, toxic shock.

3 Fecal bacteriological separation, identified as Clostridium difficile.

4 The fecal filtrate or the filtrate of the isolated strain culture has toxin, has a cytopathological effect in tissue culture, and can be neutralized by Clostridium difficile antitoxin or Bacillus subtilis antitoxin.

Differential diagnosis

Identification of enteritis caused by Salmonella, Shigella, Campylobacter jejuni and Amoeba protozoa by pathogen examination.

Patients with severe abdominal pain should be differentiated from acute abdomen. Chronic diarrhea should be differentiated from inflammatory bowel disease and dyspepsia syndrome.

First, acute abdomen:

1 Introduction:

It is a general term for acute abdominal diseases. Common acute abdomen diseases include: acute appendicitis, acute perforation of ulcer disease, acute intestinal obstruction, acute biliary infection and cholelithiasis, acute pancreatitis, abdominal trauma, urinary calculi and rupture of ectopic pregnancy. In addition, certain systemic or other systemic diseases such as hematoporphyria, hypokalemia, septicemia, spinal trauma or spinal cord disease may also have clinical manifestations similar to acute abdomen.

2. Clinical manifestations:

Sustained severe and dull pain, the patient used the lateral knee flexion position to relieve abdominal pain, cough, deep breathing and loud speech all aggravated the pain, accurate positioning, suggesting that the part of the parietal peritoneal inflammation stimulation - acute peritonitis. Persistent pain is often caused by the expansion of the visceral peritoneum, which is aggravated by abdominal pain, such as paralytic ileus and liver tumors.

Second, dyspepsia syndrome:

1 Introduction:

Dyspepsia is a clinical syndrome that is caused by gastric motility disorders, as well as gastroparesis and esophageal reflux disease with poor gastric motility. Indigestion is mainly divided into functional dyspepsia and organic dyspepsia. Functional dyspepsia belongs to the category of "sputum", "stomach pain" and "noisy" in traditional Chinese medicine. The disease is in the stomach, involving organs such as liver and spleen. It should be treated according to syndrome differentiation, spleen and stomach, liver and qi, digestion. Treatment with lead and other methods.

2. Clinical manifestations:

Symptoms include intermittent upper abdominal discomfort or pain, fullness, heartburn (acid reflux), and hernia. Often due to chest tightness, early satiety, abdominal distension and other discomfort and reluctance to eat or eat as little as possible, it is not easy to sleep at night, often have nightmares after sleep.

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