Neonatal pneumonia

Neonatal pneumonia-About Neonatal pneumonia:

Neonatal pneumonia is a common disease, and the four seasons are prone to winter and spring for more than. Such as the treatment is not complete, easy to recurrent impact child development. The clinical manifestations of pneumonia in children are fever, cough, dyspnea, without fever and cough re-The main cause of children factors like eating sweet, salty, fried food, causing Sushi stagnation while the raw heat, phlegm dampness, the occasional cold lung undeclared, both as cause and effect and pneumonia.

Neonatal pneumonia - the cause of
(A) of neonatal pneumonia - causes
An aspiration pneumonia is usually caused by inhaled meconium, amniotic fluid, breast milk, can also be due to immature swallowing reflex, swallowing incoordination, esophageal reflux, or cleft palate, and other factors that cause milk or secretions caused by the inhalation. Premature child and the brain and sick children swallowing function and lack of coordination, poor or absence of reflection, is prone to vomit, milk aspiration pneumonia.
Infectious pneumonia, infectious pneumonia is divided into intrauterine, intrapartum and postnatal infection infection.
(1) antenatal, intrapartum infection pneumonia: the case of the fetus in utero infection, the infection, mostly the mother spread through the blood line. Production of infectious pneumonia and obstetric factors.
(1) prenatal infection: the mother during pregnancy by the virus (such as cytomegalovirus, herpes simplex virus, rubella virus), bacteria, protozoa (eg, toxoplasmosis), chlamydia and mycoplasma infection, pathogens, blood line through the placenta and amniotic membrane invasion the fetus.
② labor infection: premature rupture of membranes more than 6h, amniotic fluid may be contaminated, if premature rupture of membranes more than 24h, the incidence of infection may reach 30%, or amniotic chorioamnionitis, birth canal, bacteria such as Escherichia coli, Klebsiella, Listeria monocytogenes, B streptococcus, upstream lead to infection, or the fetus in utero inhalation of contaminated amniotic fluid and disease. In addition, radical production, prolonged labor or birth canal is not thoroughly disinfected, etc., fetal pneumonia by inhalation of contaminated secretions in the birth canal during delivery.
(2) after the birth of infectious pneumonia:
① respiratory ways: by contact with newborns suffering from respiratory infections, the pathogens can be transmitted through droplets from infants on respiratory tract is propagated down to the lung; can also be due to the decline of infant resistance (such as cold, etc.), its downstream upper respiratory tract infection caused by pneumonia .
② of hematogenous spread of infection: risk of omphalitis, skin infections, sepsis, pathogens, blood line spread to the lungs and cause pneumonia. Pathogen group B hemolytic streptococcus, Staphylococcus aureus, Escherichia coli and cytomegalovirus, respiratory syncytial virus are common.
(3) iatrogenic spread of infection: iatrogenic infection caused by Pseudomonas aeruginosa, anaerobes, and some of the low virulence of bacteria. Medical equipment such as suction, atomization, oxygen masks, endotracheal intubation, such as disinfection lax incubator humidity is so high that aquatic bacteria is easy to breed, or a ventilator for too long cause pneumonia; wards crowded, disinfection system of strict, health care workers wash their hands do, will bring the pathogens of children with other newborns; broad-spectrum antibiotic used for a long time prone to fungal pneumonia. Late-onset pneumonia is most common in the neonatal care units, neonatal chronic lung disease require long-term intubation.
3 other inappropriate care, cold, etc., is also the occurrence of pneumonia incentives.


(B) of neonatal pneumonia - pathogenesis
Aspiration pneumonia due to lack of oxygen to stimulate fetal breathing leaving the amniotic fluid, meconium, or vaginal secretions, inhaled, causing aspiration pneumonia. Meconium aspiration pneumonia is the most serious, see meconium aspiration syndrome. Milk inhalation is common in swallowing function was incomplete, sucking vomiting, esophageal atresia and cleft lip and palate.
Infectious pneumonia pathological change in the widely intrauterine, birth, alveolar exudate containing multinucleated cells, monocytes and a small amount of red blood cells. Microscopy can be seen in the amniotic fluid sediment, such as keratinized epithelial cells, fetal sebum and pathogens. Infectious pneumonia pathological changes after the birth of bronchial pneumonia and interstitial pneumonia, scattered lesions, affecting leaf or several leaves, sometimes fused into large areas of lesions, atelectasis, and emphysema are more prone to. Microscopic lesions exist at different stages of the inflammatory response. Different etiology, pathological changes are also different

Neonatal pneumonia - SymptomsNeonatal pneumonia and pneumonia in children What are the performance and how to diagnose?(A) light bronchial pneumonia.
A fever: Most higher.
Cough: a frequent irritant dry cough, followed by the throat, sputum, cough, vomiting, choking.
Faster, breathing shallow, nose fan some of the children perioral, mild nail cyanosis.
In addition to respiratory symptoms in children may be associated with listlessness, irritability, loss of appetite, shaking, diarrhea and other systemic symptoms.
(B) severe pneumonia: in addition to the performance of mild pneumonia increased, sustained high fever, symptoms of systemic poisoning is serious and associated with other organ dysfunction.
Respiratory symptoms: superficial breathing, shortness of breath, more than 80 times per minute, nasal flap, there are three depressions, groaning breath, facial and extremities obvious cyanosis, worse pale or greenish-blue. Lungs could be heard and intensive fine wet rales.
2, the symptoms of the circulatory system: infant pneumonia is often accompanied by ventricular dysfunction.
Nervous system symptoms (1) irritability, drowsiness, gaze, strabismus, eye Upward. (2) lethargy and even coma, convulsions. (3) the bulbar conjunctiva edema. (4) pupil change and unresponsive to light or disappear. (5) respiratory rhythm is not the whole. (6) fontanelle expansion meningeal stimulation levy, cerebrospinal fluid in addition to increased pressure were normal as toxic encephalopathy, severe cases, intracranial pressure, herniation can occur.
Digestive symptoms: children with loss of appetite, vomiting, diarrhea, abdominal distension, severe vomit is brown or blood in the stool, bowel sounds disappear in paralytic ileus, and toxic hepatitis.
5, metabolic acidosis, respiratory acidosis, can also be mixed acidosis.
Neonatal pneumonia - CheckNeonatal pneumonia in children with pneumonia should do what?(1) to check white blood cell: cell pneumonia, increased WBC count, about 15 ~ 20 × 109 / L Severe Staphylococcus aureus pneumonia and influenza bacillus pneumonia, and sometimes the total number of leukocytes but reduced. Viral pneumonia, white blood cell count is normal or reduced, increase in the proportion of lymphoid number, the number of neutrophils without increased.
(2) C-reactive protein test in the bacterial infections, sepsis, and this value increased, increased in direct proportion with the severity of the infection. Virus and mycoplasma infection does not increase.
(3) cell pathologic examination.
(4) The viral etiology of inspection.
(5) chest X-ray examination.
Neonatal pneumonia - TreatmentChildren with pneumonia should be treated?
The principle of treatment of pneumonia is the application of anti-inflammatory drugs, and kill the pathogen. Selected according to different pathogens sensitive to the drug, early treatment, the full course of treatment, according to the disease, treatment options should also be given to taking the antipyretic symptomatic treatment such as fever, cough should given Huatanzhike drugs, severe pneumonia should be promptly hospitalization to the hospital.
(A) general care and supportive therapy:
The room temperature should be maintained at about 20 ℃ is appropriate, and 55-65% relative humidity to prevent the respiratory secretions dry, difficult to expectorate. Prevent cross-infection.
2, attention to nutrition and water supply; should try breastfeeding, if artificial feeding according to its digestive function and disease decision milk and concentration, and if diarrhea be given skimmed milk for infants and young children should supply light, easy to digest, rich a variety of vitamins diet, recovering from sick children should be given to nutrient-rich, high-calorie foods. Intravenous fluid replacement for critically ill children can not eat, heat and moisture.
3, to maintain airway patency: nose scab, nasal secretions, and respiratory sputum should be promptly removed. Improve ventilatory function, increased alveolar ventilation to correct hypoxia, reduce CO2 retention. Phlegm and thin, you can repeatedly stand up to shoot back in order to facilitate sputum discharge. Oral expectorant drug ammonium chloride mixture. Thick phlegm difficult to expectorate, suctioning or use of ultrasonic atomizing inhalation.
Antibiotics (b) anti-infectives.An antibiotic of choice.
(1), pulmonary gram-positive bacterial infections: pneumococcal pneumonia, penicillin remains the first choice. Change drops erythromycin allergic to penicillin.
(2), pulmonary gram-negative bacilli infections, generally available ampicillin or aminoglycoside antibiotics. Pseudomonas aeruginosa pneumonia can be used to re-Fortum, ceftriaxone, and so on.
(3) Mycoplasma pneumonia: use of erythromycin for 2 weeks is appropriate.
(4) clear bacterial pneumonia, according to the disease choose broad-spectrum antibiotic combination therapy (one should be emphasis on drugs in Gram-negative bacteria).
Two antiviral drugs.
Interferon and ribavirin.
(C) oxygen therapy:
(D) symptomatic treatment:
1, fever, and calm.
2, expectorant cough and asthma.
(5) important organ damage processing.

Pay attention to weather changes at any time to change clothes, children bedroom Do not smoke, should not be placed or to avoid exposure to fumes, paint, gas, dichlorvos harmful objects and cage. Prevalence during the Eat sweet, salty, spicy greasy Atsumi. The indoor temperature is not too high, not too dry; normally open doors and windows to keep the air fresh.Neonatal pneumonia - to identifyChildren with pneumonia and the diseases easily confused?
Neonatal pneumonia, bronchitis, systemic mild symptoms, usually without symptoms of dyspnea and hypoxia, the lungs could be heard and dry rales in coarse moist rales, not fixed, often with cough or postural change and disappear.2, the abrupt onset of acute miliary tuberculosis in children is often accompanied by fever, chills, body discomfort, shortness of breath, cyanosis and other symptoms of systemic poisoning resembles the bronchitis, but the lungs are often no obvious signs or fine wet rales scattered in the lungs, and found the end of the suction. X-ray findings and bronchial pneumonia are similar. According to the history of exposure to tuberculosis, clinical symptoms, positive tuberculin test, ESR, sputum or washing the gastric juice and check TB and X-ray follow up can be identified.
, Caseous pneumonia lesions mostly in the weak or the lower the resistance of children to X-ray showed a lung segment as well as leaf most of the lungs showed dense consolidation than the vague outline, usually can be seen more translucent liquefaction areas, and even opaque hollow. Combining history, tuberculin test, easy to identify with bronchial pneumonia.
Bronchial foreign body in the history of foreign body aspiration, or choking history. Clinical and light and heavy different disease duration ranging. Prolonged course of secondary infection can be recurrent fever, cough, lungs could be heard and moist rales with pneumonia, and sometimes to auscultation smell and trachea slap sound can be helpful in the diagnosis, but the diagnosis rely on fiber air passenger microscopy.
5, bronchiolitis and acute pneumonia phase 0 seems, but this disease to wheezing. Lungs wheeze and fine moist rales could be heard. Seriously ill children with hypoxia, X-ray only lungs transmittance enhancement, the diaphragm down, emphysema was a change, a small number of sick children have a little blotchy shadow.
Neonatal pneumonia - PreventionNeonatal pneumonia in children with pneumonia should be how to prevent it?Risk of pneumonia among children, parents should be careful, careful attention to the child's body temperature and breathing, to keep indoor air fresh, quiet, and let the child rest well. In the diet, eat digestible, high-calorie and vitamin-rich food, soft food is best, gastrointestinal absorption. Pat on the back of the child's cough is conducive to the discharge of sputum from the bottom up shoot shoot back, the room should not be too dry, children should be appropriate to drinking water, mucus, is conducive to the discharge of phlegm.
Pneumonia recovered, and do not take it lightly, with particular attention to the prevention of upper respiratory tract infection, or prone to repeated infections. Attention to strengthening exercises and proper exercise, according to age. If the child into yao living room doors and windows closed, and the ability to adapt to the outside air backward. Outdoor activities, pay attention to the appropriate increase in clothes. Flu epidemic in the community, do not take their child to public places to The home was suffering from a cold, do not contact with the children.
Prevention: family prevention of pneumonia, the main is to enable children to adhere to exercise and strengthen resistance to disease, while paying attention to climate change, at any time to change clothes to the children, to prevent colds. Reasonable feeding to prevent malnutrition. Education children to develop good health habits, and do not spit, so that infants and young children more than the sun. Continue to enhance the infant's resistance to disease is the key to preventing this disease.
Neonatal pneumonia - complicationsChildren with pneumonia complicated by the diseases?
Neonatal pneumonia and pneumonia in children with timely detection and effective treatment of sick children can be quickly recovered. But severe prone to the following complications if not treated in time, a poor prognosis.① heart failure: the onset of pediatric restless, dyspnea, and cyanosis, rapid heart rate, 180 beats / min, shortness of breath,> 60 beats / min, increased liver, lower extremity edema, should take immediate measures to control its development, the use of tonic, diuretic therapy.
② respiratory failure: Pediatric irritability, dyspnea, and cyanosis, respiratory early to speed up the weight when you slow down, moaning breathing and respiratory rhythm changes. Speed ​​up or slow down the heart rate in critically ill, and can be followed by coma and convulsions.
③ pus pneumothorax: Staphylococcus aureus pneumonia, high incidence of pus pneumothorax. At this point, the persistent high fever or body temperature decreased and then rise again, frequent coughing, shortness of breath, can not do it lying full side of the thorax.
④ hypoxic encephalopathy: pneumonia, difficulty breathing, hypoxia weight, children vomiting, headache, lethargy or irritability, followed by coma and convulsions. More acute encephalopathy, ferocious, dangerous condition, often interlaced with a variety of complications appear, influence each other, so that the disease has become more complex, and high mortality.
⑤ toxic shock, the sudden jump in temperature up to 40 ~ 41 ℃ or plunged, chills, pale gray, irritability, or coma, sweating, skin was marble pattern changes, blood pressure, or could not be determined, and multiple organ function changes The symptoms of danger.
⑥ toxic intestinal paralysis: the performance of a high degree of abdominal distension, vomiting, constipation and anal exhaust (not fart). Abdominal distension and oppression of the heart and lungs, making breathing difficulties more serious. Bread pale gray, abdominal percussion was the drum sound, bowel sounds disappear, the vomit was brown or stool-like material, x-ray examination found that intestinal dilatation, wall thinning of the diaphragm up the intestine, the liquid surface.
In addition, children with pneumonia complicated by atelectasis, emphysema, bullae, bronchiectasis, psychosis, so that both children with pneumonia is a common disease, but also as a dangerous disease, so the parents can not pay no attention to prevention and care.

Undo edits

Iron deficiency anemia in children

Iron deficiency anemia in children-What is iron deficiency anemia in children?

Iron deficiency anemia (iron deficiency ancemia) is a common disease in children, occurs mainly in June to 3-year-old infants. With small cells with low color, serum iron and transferrin saturation decreased, good iron treatment.

Iron deficiency anemia in children - diagnosis
Children with iron deficiency anemia alone symptoms is not easy to make an early diagnosis. Should be asked in detail about the history, with particular attention to the cause of analysis, can be diagnosed early clues, such as birth weight, with or without loss of blood through the placenta, placental abruption, weight growth rate after birth, children with diet, daily fresh milk intake . Older children should pay attention to chronic blood loss and parasitic diseases, girls should pay attention to menstruation. Available iron test treatment is difficult to diagnose.

Iron deficiency anemia in children - treatmentIron supplements and removal of disease, because in principle.
(1) iron treatment
Children with iron deficiency anemia iron is a cure for the treatment of iron deficiency anemia, and its many different types of general oral inorganic salt is the most economical, convenient and effective way. The divalent iron is easily absorbed than ferric iron, so the use of ferrous sulfate, the iron content of 20%; fumarate iron, the iron content of 30%. Easy to take the baby for the multi-dubbed 2.5% ferrous sulfate mixture solution (ferrous sulfate 2.5g, dilute hydrochloric acid 2.9ml, glucose 12.5g, chloroform, water 100ml). The dose calculation shall be contained in the iron, the experiments to 4.5 ~ 6mg/kg · d, at times taking appropriate, ferrous sulfate (equivalent 0.03g/kg / day; fumarate iron 0.02g/kg / days; 2.5% ferrous sulfate mixture 1.2ml/kg · d), this amount can reach the highest limit of absorption, more than this amount of absorption decreased, but increased the stimulation of the gastric mucosa, overdose can produce toxicity. The best medication in between meals, not only to reduce the stimulation of the gastric mucosa, but also conducive to absorption. Should be avoided while taking a lot of milk can affect iron absorption due to higher milk phosphorus.
Vitamin C can make ferric reduced to ferrous iron, it is easy to dissolve, so that the small intestine, the pH increased, and still maintain the iron in the dissolved state. For example, vitamin C60mg added to the rice allows the absorption of iron three times. Therefore, while taking iron, it is best to take vitamin C On the clothes iron four hours before taking vitamin C, whereas no such effect.
For a very small number of strong reaction in children, could be replaced by a small irritant glucose ferrous ferrous gluconate is above iron is reduced to half the amount to be nausea, Ah, diarrhea or stomach upset symptoms, coupled to the amount used. Can not tolerate oral iron, severe diarrhea, anemia and heavier sick children, consider using the iron injection. Iron injection: iron dextran per ml iron 50mg, intramuscular; sugar iron oxide per ml iron 20mg, intravenous injection. Intramuscular injection of iron local produce pain, and urticaria, also visible fever, joint pain, headache or local lymph node enlargement. Intravenous iron can also occur in thrombophlebitis. The treatment effect of injected iron is not faster than the oral, and thus should be used with caution.
Iron therapy are generally required to continue applied to red blood cells and hemoglobin reached normal levels after at least 6 to 8 weeks. Due to iron deficiency anemia, not only the hemoglobin decrease in storage iron is exhausted. As the children continue the growth and development, blood volume expansion continuously, can not meet the needs of the iron in the diet, therapeutic purposes should not only correct the iron deficiency anemia and adequate iron storage, for later use. Vitamin B12, folic acid or liver fine for the treatment of iron deficiency anemia is invalid, not abuse.
(2) go for treatmentThe majority of the causes of the disease is improper diet, it is necessary to improve the diet, reasonable feeding. Some patients with mild alone to improve the diet can be cured. To improve diet, should be based on the age of the children being given the right food. Digestion in children is poor, replace and add a food supplement must be careful. Generally start a few days later, clinical symptoms improved to drug treatment, and gradually add a food supplement, so as not to cause indigestion due to increased food too fast. About 1 year old baby can be added to the eggs, pureed vegetables, liver and minced meat. Infants and children must be corrected to a partial eclipse, give food rich in iron, vitamin C and protein.


Do not drink tea chronic intestinal blood loss caused the result of taking a large number of fresh milk, the amount of milk should be reduced to the following daily 500ml or switch to formula, the evaporation of milk or milk replacer mouth. Intestinal malformations, hookworm anemia corrected line surgery or insecticide.
3 TransfusionThe onset is slow, the body's compensatory ability generally does not require blood transfusion. Management and severe anemia or severe infections or immediate surgery is transfusion indications. Hemoglobin 30g / L or less, for a blood transfusion, but must take a small number of ways, or enter the concentration of red blood cells, every 2 ~ 3ml/kg. Blood transfusion too fast, excessive, can lead to heart failure. If severe heart failure, the available shake-up method, concentrated red blood cells instead of whole blood, treatment generally do not need ocean in yellow.
Treatment after the reaction taking iron from 12 to 24 hours after the cells containing iron enzyme began to recover, first appeared in the spirit of improvement in clinical symptoms, irritability and other symptoms were relieved, appetite increase. 36 to 48 hours later, bone marrow hyperplasia phenomenon of the red blood cell system. Reticulocyte 48 to 72 hours after the medication expenditure reached a peak in long, 4 to 11. At this point, the hemoglobin increased rapidly, generally in 3 to 4 weeks after the treatment of anemia is corrected. The heart murmur is lessened or disappeared after 2 to 3 weeks, spleen gradually reduced. Medication 1 to 3 months, the stored iron to normal.
Iron deficiency anemia in children - etiologyThe most productive in the growth and development in infancy, if the iron stored in the body is exhausted and dietary iron content is not enough, the increase in gastrointestinal iron absorption is insufficient to add volume and red blood cells, anemia can occur. Its causes are mainly the following four aspects.
A primary body iron content and anemia.
Normal neonatal blood volume of approximately 85ml/kg hemoglobin 190g / L. More than 75% of the total iron content of the neonatal period, the body of hemoglobin, about 15% to 20% is stored in the reticuloendothelial system, the amount of the synthetic myoglobin rarely. Iron enzymes, but the number of Hawk. Neonatal body iron content depends on blood volume and hemoglobin concentration. Blood volume and weight is proportional to. Down lift a 3.3kg newborn with a 1.5kg premature infants, and its total body iron content difference between the 120mg.


The wok spinach iron unreliable normal neonatal body iron content of about 70mg/dl in preterm infants and low birth weight, child body's iron content and its weight is proportional to the. Health epigenetic rational hemolytic release of iron stored in the reticuloendothelial cells, coupled with the storage of iron sufficient raw weight growth times of application. Therefore, the more low birth weight, the less the total amount of iron in the body, the greater the likelihood of anemia. In addition, the fetus through the placenta, blood transfusion to a fetus in the mother, or the twin transfusion to another fetus, and delivery of placental rupture of blood vessels and bile with ligation (umbilical cord ligation delay allows newborns have more than 75ml of blood or 40mg iron), may affect neonatal body iron content.
Mother during pregnancy, iron deficiency anemia, there is no positive relationship with infant anemia owed because the placenta may be low iron content of serum maternal iron transported to the serum concentration of fetal body, regardless of the mother, iron deficiency or not, or The quality of the food enter the iron isotope labeling, about 10% of the iron into the fetus. Therefore, at birth, regardless of the mother, with or without anemia, neonatal hemoglobin, serum ferritin and serum iron concentration there is no significant difference between the mother's hemoglobin and disproportionate. Even if the mother is suffering from anemia, or weight Chong infant serum ferritin can still be within the normal range.
Growth rate and anemia.Children with rapid growth, increased blood volume quickly. Normal babies grow up to 5 weight gain. Premature infants to increase faster, increase the 1-year-old six times. If the primary to the blood protein 19g/dl. Dropped to 4.5 to 5 months when the 11g/dl about, only the use of stored iron can maintain, without iron in food. Preterm child is different, its requirements are far more than the normal infants.
Normal infant weight gain, to maintain the hemoglobin at 11g/dl, the body storage of iron is sufficient. So the weight gain times before, if the iron deficiency anemia, generally not due to iron deficiency due to diet, you must look for other reasons.
(3) dietary iron deficiency
Infant to the dairy food, low content of iron in these foods. Breast milk iron content and the maternal diet, generally 1.5 mg / L iron. Cattle 0.5 ~ 1.0mg / L, goat milk less. Iron absorption in the dairy of about 2% to 10%, the rate of absorption of iron in human milk than cow's milk (iron deficiency, iron absorption rate in human milk may be increased to 50%). Do not feed infants under six months are subject to a sufficient amount of breast milk after birth?? Can not breast-feed should be fed formula fortified iron, and timely complementary feeding, or times after the weight gain, storage iron and completion of, namely anemia. Breastfeeding children at 6 months, if not add a food supplement, can also become anemic. According to the investigation of the cause of the Beijing Children's Hospital, 39 patients with small-cell anemia, 65% for artificial feeding, partial breast feeding is neither timely complementary feeding.
The older children each dimensionless poor eating habits, poor feeding, partial eclipse or nutrient supply Erzhi anemia.
(4) long-term small amount of blood loss
Peaches iron ranks of the crown eat of the fruit to help the treatment of iron deficiency anemia of iron stored in the normal human body, 30% of the total iron content of the body, such as acute blood loss does not exceed 1/3 of the total amount of whole blood, though additional iron supplements can also be quickly restored without anemia. Chronic blood loss, blood loss, 4ml, approximately equal to the loss of iron 1.6mg, although the daily blood loss, iron consumption has more than 1 times or more, can cause anemia. Infants less than 1 year of age due to rapid growth, storage of iron are used to add volume expansion, so that a small amount of chronic blood loss can also lead to anemia. Discovered in recent years, to a large number (> 1L) without a cook for the purpose of fresh milk, feeding children, there may be chronic intestinal blood loss, anti-fresh milk is not heat-resistant protein antibodies can be found in the blood of such children. Also suggested that intestinal blood loss and the ingested amount of fresh milk without boiling, 2 to 12 months of age if the daily intake of total fresh milk does not exceed 1L, (preferably not more than 750ml) or evaporation of milk, hemorrhagic phenomena can be reduced.
Common chronic blood loss but also the gastrointestinal tract malformation, diaphragmatic hernia, polyps, ulcer disease, esophageal varices, hookworm, epistaxis, thrombocytopenia purpura, pulmonary hemosiderosis disease and girls menorrhagia and other reasons.
(5) Other reasons for long-term diarrhea and vomiting, colitis, celiac sprue, etc., can affect the absorption of nutrients. Acute and chronic infection, children with loss of appetite, gastrointestinal absorption is not good, can also cause iron deficiency anemia.

Iron deficiency anemia in children - pathogenesisA human body iron distribution and function
The ⑴ synthesis of hemoglobin: hemoglobin iron accounts for about 2/3 of the total body iron content, accounting for 99% of the red blood cell protein hemoglobin. Iron deficiency the shadow hemoglobin synthesis Erzhi anemia.
(2) Synthesis of myoglobin: the synthesis of myoglobin iron accounting for pediatric body iron content of 3%. Myoglobin oxygen affinity compared with hemoglobin, the oxygen storage role play in the striated muscle and myocardium. When the lack of pull it can release oxygen for the much-needed muscle contraction, muscle myoglobin content in the iron deficiency is not fully understood.
⑶ the enzymes necessary to constitute the human body: a very small amount of iron constitute the essential enzymes, such as various cytochrome enzymes, had catalase, peroxidase, and succinate dehydrogenase, xanthine oxidase involved in a variety of cell metabolism in the final stages and the generation of adenosine diphosphate, which is the essential substance of the cell metabolism. Early iron deficiency, it may be before anemia appears, such iron or iron-dependent enzyme function that affected. But 48 to 72 hours after treatment, the spirit and the appetite improved, suggesting that the functional recovery of enzyme, appeared before the anemia was improved.

Potato - to reduce morning sickness reaction (4) storage: about 30% of the iron stored in the form of ferritin and hemosiderin in the bone marrow and reticuloendothelial system, where 1/3 stored in dry liver tissue of the liver (neonatal 1 g, about iron 15mg, 2 years old 2mg), 1/3 is stored in the bone marrow, the other 1/3 is stored in the spleen and other organizations. Ferritin iron can reach the ferritin weight of 20% to 25%. And plasma iron to maintain a state of equilibrium, when the body needs to increase, can easily use. Hemosiderin iron content of 30%, but can not easily be used, such as sick children of pulmonary hemosiderosis disease although a large number of hemosiderin deposition in the lungs, but can not be used for the synthesis of hemoglobin. Its function and ferritin is not yet clear.
⑸ operation: a small amount of iron in the plasma and a β-globulin (transferrin), running in between the organizations. For example, the intestinal absorption of iron or red blood cells in the reticuloendothelial system is free of iron, Fe3 + form of iron transport protein binding, and transported to the bone marrow. Attached to transferrin to reticulocyte membranes in young red blood cells and the network, the initiative to operate within one minute of iron into the cells and hemoglobin synthesis in erythroblast. One molecule of transferrin with two molecules of iron, which carries iron to quickly enter and leave the blood circulation half-life of about 20 to 120 minutes. Under normal circumstances, similar to transferrin in plasma lactoferrin binding. In addition, still similar to the transferrin lactoferrin, it exists in milk, a variety of fluid secretion and neutrophil, it has a strong affinity with iron, through the competition deprived of microbially available iron inhibitory effect, its iron transport function of further study.
Source of iron absorption
The body of iron from food. Food iron highest in the most important black fungus, kelp and liver, etc.; followed by meat, beans, eggs. Levin with a wok, cooking can be a considerable amount of inorganic iron salts. In addition, red blood cell destruction in the body, the decomposition of iron from hemoglobin almost entirely de novo synthesis of hemoglobin or other organizations to provide the needed iron.
Iron absorption, there are two main forms, namely in the form of free iron in the form of heme absorption. Plants in the iron-clad high-speed rail in the form of colloidal hydroxide deposit. Under the action of pepsin and free hydrochloric acid, the non-heme iron in food is released and becomes free of divalent iron. Vitamin C enable divalent iron reduced to ferrous iron, in order to facilitate absorption. In addition, fructose, amino acids (cystine, histidine and lysine) all promote iron absorption. Easy to form phosphoric acid iron salts and oxalic acid iron salts in the alkaline environment of the small intestine, impaired absorption. Tea and coffee will also affect the absorption of iron, tannic acid in tea and iron formation of tannin-iron complexes, to make the iron absorption decreased by 75%.
The absorption of heme and free iron absorption, hemoglobin and myoglobin in the animal food in the role of gastric acid and proteolytic enzymes, the heme and globin separation, can be directly absorbed by the intestinal mucosal cells, intestinal epithelial cells within the separation by the heme enzyme released from the iron.
Iron absorption due to the type of food. Vegetables, rice and other plants in the iron absorption rate is only about 1%, while the form of heme iron in meat, the absorption rate, approximately 10% to 22%.
Fish or other meat and plant food intake, at the same time will enable the increase in iron absorption by plant diet, but milk, eggs and other animal food will not achieve this effect. Poor iron absorption in the egg, but its content is rich, and still man-made supply of infant iron food.


Liver of animals - to avoid the occurrence of iron deficiency anemia iron absorption in the duodenum area, rely on small intestinal regulation. Intestinal cell survival period of 4-6 days, play a role in temporarily stored iron. If the body with too much iron, the iron into the body, mass storage in the form of ferritin in the intestinal mucosa, a small amount into the plasma with the intestinal mucosa off the discharge; in the case of in vivo iron deficiency, iron from a large number of mucosal cells into the bloodstream, and rarely from the intestinal tract. Adjustment mechanism, though not fully understood, but is mainly determined by the nature of the food and the content of iron and body iron stores status, and hematopoietic function. The less iron stored in the body absorb more. In hematopoietic function is strong, iron absorption increases, such as blood loss, iron absorption increased significantly, so the anemia quickly recover; chronic hemolytic diseases such as thalassemia patients, even if the increase in the amount of iron storage in the body, can still cause iron over- more absorption. Normal hematopoietic case, although the change of iron in the diet, but the amount of iron in the body constant.
(3) iron excretion
Under normal circumstances, the day only a very small amount of iron excreted children daily excretion of about 15μg/kg; about 2/3 with the shedding of intestinal mucosal cells, bile and red blood cells from the intestinal tract, the other by the kidneys and The sweat glands discharge, the the excoriation loss of a trace amount of iron.
Iron deficiency anemia in children - clinical manifestationsThe incidence of more than 6 months to 3 years, most of the slow onset, the beginning and more attention for parents, the majority of sick children caused by treatment of moderate anemia. The symptoms of minor depends on the degree of anemia and anemia, the speed of development.

(1) the general performance: Start often irritability or lethargy, do not love the activities, loss of appetite, skin and mucous membranes pale to the lips, oral mucosa, nail bed and the palm is the most obvious. Preschool and school-age children at this time readme fatigue, weakness.
⑵ hematopoietic organ performance: Due to the response of extramedullary hematopoiesis, liver, spleen and lymph nodes often slightly enlarged. The younger, anemia management, the longer course, more obvious hepatosplenomegaly, but enlargement is rarely crossed moderate.
In addition to the changes in the hematopoietic system, iron deficiency has an impact on the metabolic From the cytological point of view, can lead to lack of the cytochrome enzyme system; over oxidation of catalase, glutathione peroxidase, succinate dehydrogenase, monoamine oxidase, aconitase enzyme and α-glycerophosphate dehydrogenase enzyme activity was reduced; and affect DNA synthesis. Can occur due to metabolic disorders, loss of appetite, weight gain slows down, tongue, papillary atrophy, reduce gastric acid secretion and small intestinal function disorders. Pica disorder is more common in adults, rare in children.


Adrenal neuropsychiatric changes gradually pay attention to. Has been found that anemia is not severe, namely, irritability, and are not interested in the surrounding environment. Intelligence tests found that sick children can not concentrate, and understanding to reduce slow response. Of infant apnea (breath. Bolding spells). School-age children in the classroom performance behavior abnormalities such as rampage, kept a little trick. These phenomena in relationship to the iron is not very, but the experimental proof of adrenaline in the urine of patients with iron deficiency anemia target = _blank> norepinephrine concentrations increased in recent years, to quickly returned to normal after iron, suggesting that the neuropsychiatric The changes may and norepinephrine catabolism. Urine norepinephrine increase by monoamine oxidase?? Neurochemical reaction from the management to the role. Now detect monoamine oxidase activity in platelets of patients with iron deficiency anemia decreased back to normal soon after taking the iron. Further confirmed the relationship of iron deficiency and neuropsychiatric symptoms in the future may wish to do more research in animal experiments.
Iron deficiency anemia in children are more prone to infection. Such patients E rosettes, active E rosette formation rate were decreased, of PHA skin test reaction was significantly lower than normal, indicating that T-leaching plant cell weakened. There are reports of peripheral blood T leaching correct cell subsets CD3CD4 lymphocytes to reduce OKT4/OKT8 ratio decreased. Were also reported in patients NBT test below normal. The iron content of myeloperoxidase due to a decrease, thus granulocytes kill attack reduced ability. After iron therapy, granulocyte bactericidal function of more than 4 to Heaven back to normal.
When the hemoglobin is reduced to 70g / L or less, there may be enlargement of the heart murmur, this unique signs of the general performance of the anemia rather than iron deficiency anemia. Due to the slow onset of iron deficiency anemia, the body's tolerance and strong, when the hemoglobin dropped to 40g / L, while from time to cardiac dysfunction in performance, but combined with respiratory infections, heart burden, can induce heart failure.Iron deficiency anemia in children - auxiliary examinationA biochemical test: before anemia appears, that is, a series of biochemical changes. When iron deficiency, the body first use stored iron in order to maintain the need of iron metabolism, ferritin and hemosiderin content decreased in liver and bone marrow; followed, serum ferritin decreased. 35ng/ml, serum ferritin, normal down to 10ng/ml the following can be biochemical or clinical aspects of iron deficiency. After serum ferritin fell below 50μg/dl, even as low as 30μg/dl below, while the serum iron binding capacity increased to 350μg/dl above, transferrin saturation dropped below 15%. Transferrin saturation less than 15%, synthesis decreased hemoglobin, free erythrocyte protoporphyrin accumulation can high to 60μg/dl, whole blood. Infants and young children during the increase in erythrocyte protoporphyrin and hemoglobin ratio (FEP / Hgb), to reduce the more meaningful for the diagnosis of iron deficiency anemia compared with transferrin saturation, and its ratio> 3μg / g is considered as abnormal if 5.5 ~~ 17.5μg / g, rule out lead poisoning can be diagnosed with iron deficiency anemia. Serum copper increased up to 146μg/dl. If iron deficiency continues to progress, namely the changes in the blood.
The bone marrow cytology. Blood: red blood cells and hemoglobin were lower, particularly lower hemoglobin. Accordingly reduce the hematocrit, mean corpuscular volume (MCV) is less than 80fl, can be as low as 51fl; mean corpuscular hemoglobin (MCH) of less than 26PG minimum 11.1pg; mean corpuscular hemoglobin concentration (MCHC) is lower than 0.30 can be as low as 0.20; mean corpuscular important measurement of the small number of cases, can be as low as 70pg. Smear of red blood cells become smaller, the majority of diameter less than 6μm, sometimes of varying sizes, mostly small. Price - Joan Secretary curve to the left, and basal widening. Red blood cell staining shallow, intermediate lucent zone to increase. Severe cases, red blood cells may be a ring. Network normal red blood cell percentage, but its absolute value is lower than normal, decreased erythrocyte fragility, are rarely seen in the peripheral blood nucleated red blood cells.
Morphologically normal white blood cell count normal, but severe cases of white blood cell count is likely to be reduced, and lymphocyte cells are relatively increased. Platelet majority within the normal range, in severe cases may be slightly lower, but rarely to the extent of causing bleeding.
Bone marrow: Bone marrow hyperplasia was phenomenon, bone marrow cell count increased slightly, the number of megakaryocytes is normal. According to the statistics of the Beijing Children's Hospital, the bone marrow cell counts between 150,000 and 400,000 / mm3, with an average of 300,000 / mm3, megakaryocytes 25 125 / mm3, with an average of about 70 / mm3.
Bone marrow classification of myeloid and the proportion of nucleated red blood cell nucleated red blood cells increased, indicating the strong red blood cell proliferation. Granulocytes of morphological changes in the count, neutrophils can be slightly higher. Erythrocyte count in the erythroblast and erythroblast-free increased, especially in young red blood cells to increase the more obvious. Promyelocytic, young and late erythroblast less cytoplasm, the hemoglobin content is extremely low, indicating the degree of maturity of full pulp behind in the nucleus, the cytoplasm of the edge is not very neat, with potassium ferrocyanide staining, showing sideroblasts reduce or even disappear, smear nibs do not see blue ferritin and containing haemosiderin.
(4) check: if there is chronic intestinal blood loss, positive fecal occult blood. Serious illness, longer duration, and skull X-ray shows like radiation-like stripes change of hemoglobin disease.Iron deficiency anemia in children - differential diagnosisThe diagnosis depends on the laboratory tests described above, to exclude the low color-small-cell anemia:
Thalassemia thalassemia: a family history, regional more obvious. Special face, significantly enlarged liver and spleen. The blood smear shows target-shaped cells and nucleated red blood cells, hemoglobin electrophoresis A2 and F increased, or hemoglobin H or Bart's. Increased serum iron, the increase of sideroblasts in the bone marrow.
2 pulmonary hemosiderosis disease: the performance of the onset of pale, weakness, cough, sputum with visible blood, sputum and gastric juice can be found in hemosiderin cells. The reticulocyte increased. X-ray lung fields visible outlets like Yin shadow.
Sideroblastic anemia: bone marrow smear extracellular iron significantly increased in the late erythroblast nuclear be seen around the iron particles in a ring arrangement, increased serum ferritin. Invalid with iron treatment. Some patients with vitamin B6 therapy can obtain better results.
Chronic infectious anemia: mostly small cell Stern, anemia, and even showed a low color rendering. Serum iron and iron binding capacity were decreased by the increase of sideroblasts in the bone marrow. Iron treatment nonresponders.
(5) Lead poisoning: red blood cells seen in basophilic stippling, lead levels in the serum, red blood cells and Protoporphyrin in urine increased significantly. FEP / of Hgb can be high to 17.5μg / g or more.

Iron deficiency anemia in children - PreventionThe therapeutic method of iron-deficiency anemia should first do the infant feeding guidance. The iron in breast milk is not enough, but its better absorption. If you can not use the breast-feeding should be used in fortified iron formula-fed. Or iron in food as soon as possible, appeal to the food sector, industrial production, manufacture infant foods fortified iron, ferrous sulfate in the milk, cereal, flour. 1000ml milk plus ferrous sulfate 0.06g equal to pure iron 12mg, will be able to meet the needs of the baby. Iron absorption by 10 percent calculations, the recommended supply of the children during the 10 to 15mg / day, adolescent girls 18mg / day.Was added to strengthen iron diet, full-term children from 4 to 6 months (no later than six months), premature infants and low birth weight children from 3 months. The easiest way to add milk, prescription or supplement of ferrous sulfate. Iron grains of breast-feeding children a day plus 1 or 2 times. Acceptable alternate use of ferrous sulfate drops, the amount of term infants pure iron does not exceed 1mg/kg / day (2.5% FeSO40.2ml/kg / day) in preterm infants does not exceed 2mg/kg · d. The maximum daily dose of 15mg in the family to use up ultrasound a month, in order to avoid the occurrence of iron poisoning.
Artificial feeding children in the 6 months after the feeding of milk iron, the total can not exceed 750ml, otherwise squeezed out into the amount of iron-containing diet.
For children and adults, the best plus iron 13 ~ 16mg per kilogram of flour. Rural grains, starchy diet, some places ancylostomiasis epidemic, we must pay attention also should be noted that to maximize the animal diet, due to iron in cereals, and its absorption is not such as animal food.
Do health checks, anemia census on a regular basis, so that early treatment of mild disease children. Hemoglobin 110g / L lower limit of normal infants should be given iron 3mg/kg · d, serving a total of 3 months. Experiments show that part of the baby after the application of iron hemoglobin slightly increased, these babies have a mild iron deficiency, necessary and correct.
Iron deficiency anemia in children - prognosisA good prognosis, with iron treatment, usually can be cured, if improvements in diet, removal of the cause, rarely relapse. For patients with very severe, and sometimes not timely rescue, may cause death. Severe infections and indigestion often fatal cause. Children for the treatment of late disease, anemia, although fully recovered, but the physical development, mental development will be affected.

Primary cardiomyopathy

Primary cardiomyopathy-What is a primary cardiomyopathy?

Primary cardiomyopathy is a group of slow onset, the cause is unknown, the characteristics of cardiac enlargement, and finally the development of heart failure heart disease. Initially may be no discomfort, shortness of breath, palpitations, chest tightness, difficulty breathing and other symptoms after tiredness or mild labor. Increase in heart weight, expansion of the various chambers of the heart, myocardial gray and loose; near-normal ventricular wall thickness, endocardial thickening, heart chamber enclosing the mural thrombus, often myocardial fibrosis, but also satisfying the wall into a piece of damaged cardiac pacing system can also be invaded.

Primary cardiomyopathy - Disease OverviewPrimary cardiomyopathy primary cardiomyopathy is a group of unknown cause heart disease cardiomyopathy. The disease is divided into three types: ① The dilated cardiomyopathy: the type characteristic for the left or right ventricle or both ventricles expand, and associated with cardiac hypertrophy, ventricular systolic dysfunction, with or without congestive heart failure, arrhythmia common condition was progressively increased, the death of the disease can occur at any stage, this type is most common, accounting for 70% to 80%. The ② hypertrophic cardiomyopathy: ventricular hypertrophy, typical in the left ventricular septal staggering, even showed concentric hypertrophy, normal or reduced left ventricular cavity volume, and occasionally lesions in the right ventricle, usually as an autosomal dominant inheritance. The type is more common, accounting for about 10% to 20%. ③ restrictive cardiomyopathy: invasive or non-invasive lesions of this type is characterized by primary cardiomyopathy, or myocardial endocardial fibrosis, diastolic dysfunction caused by obstruction of cardiac filling, very rare.Primary cardiomyopathy - disease etiologyPrimary cardiomyopathy dilated cardiomyopathy(1) virus infection, the immune response theory: that cardiomyopathy is caused by the autoimmune myocardial damage after viral infection, dilated cardiomyopathy, the incidence of doctrine.(2) intramyocardial small coronary artery lesions caused by spasm and the obstruction caused.(3) some cases there is a lack of certain enzymes in the process of myocardial metabolism may be one of the mechanisms.(4) in some cases and nutritional disorders, such as the lack of trace element selenium in food may cause myocardial changes.Hypertrophic cardiomyopathy that disease and genetic.Restrictive cardiomyopathy of unknown etiology.Primary cardiomyopathy - signs of illnessPrimary cardiomyopathy dilated cardiomyopathyApex beat to the left under the shift can be flattering beats the heart dullness to the left to expand, you can often hear the third and fourth heart sounds, rapid heart rate was gallop, mitral or tricuspid valve auscultation area can be heard systolic murmur hair samples, improved the heart function of the noise, reduce the blood pressure is normal, but patients with advanced blood pressure can drop small, pulse pressure, heart failure, diastolic blood pressure increased slightly, heart failure can occur when alternating pulse The pulse is often weakened, can smell the end of the lungs and moist rales, and visible enlargement of the liver, edema, or even chest, ascites, and a variety of arrhythmias may occur, led by the key performance, and a variety of arrhythmias in combination a complex arrhythmia can occur repeatedly. In addition, there are signs of embolism in the brain, kidneys, lungs, etc..(2) common signs of hypertrophic cardiomyopathy heart dullness to the left to expand the apex beat to the left shift, visible lifting of the impulse or apex pulsation; left sternal border apex can be heard inside the contraction of the mid-or late injection noise to the apical spread, may be associated with a systolic thrill, seen in patients with left ventricular outflow tract obstruction. Increase myocardial contractility or reduce the cardiac load measures (such as giving digitalis, isoproterenol, amyl nitrite, nitroglycerin, do the Valsalva maneuver, manual labor or premature beats) may make the noise enhancement; where decreased myocardial contractility or increase cardiac load measures (such as giving vasopressors, beta blockers, squat, clenched fist, etc.) can make the noise diminished to about half of patients could be heard and mitral regurgitation murmur; the second heart sound was unusual split, exhale significantly (due to left ventricular spurting blocked aortic valve delay the closure due to). Arrhythmia to atrial fibrillation. Non-obstructive hypertrophic cardiomyopathy only mild heart increases, the pulmonary valve sound split, anomalous reverse split, less and less noise.Lesions of restrictive cardiomyopathy with left ventricular-based can be the performance of left heart failure and pulmonary hypertension, such as could be heard the end of the lungs and rales, pulmonary second sound hyperthyroidism, etc.; lesions with right ventricular-based performance of the right ventricle returning blocked, such as neck vein distention, the inspiratory expansion of the (library's sign), hepatomegaly, leg edema, ascites, apex beat often weakened, mild increase of cardiac dullness, heart sound is low and blunt, heart rate fast, diastolic gallop and arrhythmias, pericardial effusion can exist, may have visceral embolism.

Primary cardiomyopathy - the clinical symptomsPrimary cardiomyopathy dilated cardiomyopathyMainly in congestive heart failure, which the shortness of breath and swelling are the most common. Initially in labor or exertion, shortness of breath, shortness of breath after mild activity or rest when, or paroxysmal nocturnal shortness of breath, and common dizziness, chest pain and other symptoms, a small number of patients with syncope, a variety of arrhythmias are visible , but also the occurrence of embolism and sudden death.(2) hypertrophic cardiomyopathyOnset of hypertrophic cardiomyopathy and more slowly. About 1/3 of patients have a family history, symptoms mostly start in before the age of 30, men and women suffering from the same. The main symptoms are: (1) difficulty in breathing, after more than tired; ② precordial pain, it resembles the tired, like angina, but may from typical; (3) fatigue, dizziness and fainting, and more in the activities; ④ palpitations; ⑤ The heart failure, more common in patients with advanced, often associated with atrial fibrillation.(3) restrictive cardiomyopathyRare and occurred in the south, was sporadic distribution, the onset is relatively slow. Early may have fever, and the gradual emergence of fatigue, dizziness, shortness of breath, shortness of breath than dilated cardiomyopathy lighter, lower extremity edema, ascites for the outstanding performance.Primary cardiomyopathy - disease diagnosisThe diagnosis of primary cardiomyopathy primary cardiomyopathy need except for other causes of heart disease. Such as clinical enlargement of the heart, arrhythmia, syncope, congestive heart failure, without a common rheumatic heart disease, coronary heart disease, congenital heart disease, high blood pressure, pulmonary heart disease or pericardial diseases should be considered when the disease. Further asked in detail about the history and physical examination, echocardiography, X-ray examination, electrocardiogram, myocardial enzymes and other tests to help diagnosis and classification of a definite diagnosis is sometimes dependent on myocardial biopsy, cardiac angiography.Primary cardiomyopathy - differential diagnosisPrimary cardiomyopathy, rheumatic heart diseaseCardiomyopathy can also be a systolic murmur of mitral or tricuspid valve, but generally not associated with diastolic murmur, and heart failure occurs when the noise than the ring, and heart failure after controlling noise weaken or disappear, and rheumatic heart disease, dilated cardiomyopathy is often suspicious of the cavity at the same time increases, unlike rheumatic heart disease, enlarged left atrium, left ventricle or right ventricular-based. Echocardiography contribute to the difference.(2) pericardial effusionCardiomyopathy apex beat to the left shift, in line with the left outer edge of the cardiac dullness; pericardial effusion the apex beat is often not obvious or in the left outer edge of the inside of the heart dullness. Ultrasound pericardial effusion see large amounts of liquid level in the pericardial segment or dark areas; cardiomyopathy, mainly for the expansion of the heart, although can also be a small amount of pericardial effusion, but not enough to cause cardiac tamponade, nor to affect the heart function and signs, in addition to cardiomyopathy were more audible heart murmur, electrocardiogram, see ventricular hypertrophy, abnormal Q spread a variety of complex arrhythmias, significant abnormality in cardiomyopathy, pericardial disease, normal systolic time interval (STI).Hypertensive heart disease, cardiomyopathy, may have a temporary blood pressure, but diastolic blood pressure does not exceed 14.67kPa (110mmHg), and acute heart failure, heart failure improves drop in blood pressure, eyes, urine, normal renal function tests.Coronary heart disease between the two is often difficult to identify, hypertension, high cholesterol or diabetes risk factors, wall activity was segmental abnormal coronary artery disease. A clear distinction between sometimes have to rely on coronary angiography.(5) the majority of congenital heart disease has obvious signs, it is easy to identify. Ebstein malformation of the noise of the tricuspid area, and can gallop, diminished heart sounds, right heart dilatation and failure, to identify with cardiomyopathy, but the former appears in the early years, left ventricular, cyanosis; ultrasound echocardiography can confirm the diagnosis.Secondary cardiomyopathy systemic diseases such as systemic lupus erythematosus, scleroderma, hemochromatosis, amyloidosis, glycogen storage disease, neuromuscular diseases, has its primary disease manifestations can be identified. In particular, the difference with myocarditis, acute myocarditis often occurs in viral infection at the time or shortly thereafter, chronic myocarditis and cardiomyopathy is more difficult to distinguish between the endomyocardial biopsy of some help. Followed by laboratory tests and antibodies, complement fixation or hemagglutination inhibition test was positive, coronary angiography negative helps to identify.Primary cardiomyopathy - pathophysiologyPrimary cardiomyopathy dilated cardiomyopathyIncrease in heart weight, expansion of the various chambers of the heart, myocardial gray and loose; near-normal ventricular wall thickness, endocardial thickening, heart chamber enclosing the mural thrombus, often myocardial fibrosis, but also satisfying the wall into a piece of damaged cardiac pacing system can also be invaded.Myocardial fiber hypertrophy, nuclear condensation, deformation or disappearance of intracytoplasmic vacuolization can be seen under the microscope. Increase in fibrous tissue, cardiac muscle fibers can be split by the cord-like fibrous tissue, collagen and elastic fibers in the endocardium also increased, showing varying degrees of degeneration, myocardial cells dissolve, especially in cases of long duration. Electron microscope, swelling of mitochondria of myocardial cells, cristae, or disappear, muscle serosal clearance to expand the fibrous material, and granular lipofuscin; the myofibrillar can disappear.(2) hypertrophic cardiomyopathy① hypertrophic obstructive cardiomyopathy: prominent septal high degree of hypertrophy to left ventricular cavity, contraction caused by left ventricular outflow obstruction.② hypertrophic non-obstructive cardiomyopathy: septal hypertrophy to a lesser extent, systolic left ventricular outflow tract without causing obvious obstruction.(3) restrictive cardiomyopathyIn invasive disease caused by restrictive cardiomyopathy, amyloidosis, sarcoidosis, hemochromatosis, glycogen storage disorders such species.

Primary cardiomyopathy - disease surveillancePrimary cardiomyopathy ECGA dilated cardiomyopathy, cardiac enlargement, mainly myocardial damage and cardiac arrhythmias. Left ventricular hypertrophy more common, often associated with myocardial strain, the late right ventricular hypertrophy, left or right atrial hypertrophy; often ST segment depression, T wave flat, two-way or upside down, 10% of patients with pathologic Q wave (more parts of the first interval of the V1, V2 lead), the common atrial and ventricular premature beats, atrial fibrillation, bundle branch block, atrioventricular block and arrhythmias.Hypertrophic cardiomyopathy more than 80% of patients with ST-T changes, a few seen huge inverted T wave; 60% of patients had left ventricular hypertrophy signs; visible abnormal Q wave in I, aVL, V5 and V6 leads Q-wave deep rather than wide, sometimes in II, III, aVF, V1 and V2 leads can also be Q-wave left atrial wave abnormalities; about 25% of patients: some patients with WPW syndrome.The low voltage of restrictive cardiomyopathy, atrial or ventricular hypertrophy, bundle branch block, the ST-T changes, atrial fibrillation, can also be abnormal Q wave in V1 and V2 leads.X-ray examinationA dilated cardiomyopathyGenerally increases the heart, was spherical, resembling a pericardial effusion; a small number of increases to the left ventricle, left atrium or right ventricle, similar to the appearance of mitral valve disease. Seen under fluoroscopy heart beat than normal for the weak, the aorta is generally not expansion. Longer course of pulmonary congestion and pulmonary interstitial edema often also common pleural effusion.(2) hypertrophic cardiomyopathyOrdinary chest X-ray to see increased left ventricle, but also in the normal range, late left atrial enlargement, pulmonary congestion. The aorta does not expand, the X-ray or radionuclide angiocardiography may show septal thickening, reduced left ventricular cavity. Radionuclide myocardial scan display cardiac hypertrophy of the location and extent.(3) restrictive cardiomyopathyVisible heart shadow to expand the shadow of the endomyocardial calcification, ventricular angiography shows the ventricular cavity narrow.Primary cardiomyopathy echocardiographyA dilated cardiomyopathyEarly you can see the chambers of the heart were enlarged, especially in left ventricular wall motion decreases, the late chambers of the heart to expand, the interventricular septum and left ventricular posterior wall movement weakened, the mitral valve the Ye Shuangfeng may disappear, but before and after the leaves are different to the activities , left ventricular-spurting index often reduced to less than 50%, myocardial shortening to reduce the number of a small amount of pericardial effusion.(2) hypertrophic cardiomyopathyVisible asymmetric septal hypertrophy, septal thickness and left ventricular posterior wall thickness ratio greater than 1.3:1; of mitral valve systolic forward; left ventricular cavity narrow outflow tract obstruction; left ventricular diastolic dysfunction. including compliance, reduced rapid filling time, Yung-time extension.(3) restrictive cardiomyopathyVisible endocardial thickening, apical ventricular cavity occlusion, myocardial endocardial structure density anomaly ultrasound echo wall motion decreased. Cardiomyopathy early myocardial enzymes check the activity increased, especially in the creatine kinase isoenzyme (CPK-MB), lactate dehydrogenase isoenzyme (of LDH1) increased valuable.Cardiac catheterizationA dilated cardiomyopathyEarly near-normal left and right ventricular end-diastolic pressure can be slightly increased, heart failure, cardiac index decreased, arteriovenous oxygen difference, pulmonary artery and left atrial pressure increased. Ventricular angiography showed a heart chamber to expand the weakened wall motion.(2) hypertrophic cardiomyopathyShow ventricular end-diastolic pressure, left ventricular outflow tract obstruction by systolic pressure difference between the ventricular chamber and outflow tract.(3) restrictive cardiomyopathyShow ventricular end-diastolic pressure gradually increased, resulting in subsidence after the platform wave, mainly in the left ventricle to pulmonary artery pressure increased, mainly in the right ventricular right atrial pressure, right atrial pressure curve in a significant wave of v replaced by a wave.

Primary cardiomyopathy - treatmentPrimary myocardial disease of unknown etiology of the disease, there is no effective therapy. Mainly for the treatment of myocardial damage, heart failure, arrhythmias and thromboembolism. Different pathological changes in the symptomatic treatment was also different.A dilated cardiomyopathyControl heart failure, prevention of cardiac arrhythmias, prevention of embolism.(1) General treatment: to avoid fatigue, adequate rest, heart failure should rest in bed, the infection should be actively control the infection and to prevent disease progression.(2) to correct ventricular dysfunction:① cardiac glycosides: Gexin to 0.125 ~ 0.25mg, orally, once daily. Attention to this disease due to extensive myocardial damage, digitalis drugs easy to poisoning, should be reduction application.② Non-digitalis cardiac drugs: dobutamine per minute 2.5μg ~ 10μg/kg speed static point 1 to 2 minutes after administration of onset. Ammonia pyrazole ketone intravenous loading dose of 1.5 to 3mg/kg per minute 10μ/kg intravenous infusion to maintain oral 100mg, 3 times a day.③ vasodilators: isosorbide dinitrate 5 ~ 10mg, 3 to 4 times daily, open Capoten 12.5mg ~ 25mg, 3 times a day, severe cases can be used sodium nitroprusside 25 to 50μg / static point.④ Diuretics: Hydrochlorothiazide 25 ~ 50mg, 1-3 times daily; triamterene 50 ~ 100mg, 1 to 3 times a day; edema or acute left ventricular failure furosemide can be used when oral or intravenous administration.(3) to correct the arrhythmia:① atrial premature beats, atrial fibrillation: dilated cardiomyopathy can be used to Gexin 0.125mg, oral, once daily, the ventricular rate is too fast, plus the service of small doses of beta blockers such as atenolol 6.25mg 2 or 3 times.The ② frequency or multiple derived PVCs or ventricular tachycardia, available mexiletine 100 ~ 200mg, 3 to 4 times daily; ethylamine iodine furosemide ketone 0.1 ~ 0.2g, 3 times a day. Intravenous drug use is optional, lidocaine, procainamide, propafenone, bromo benzylamine. Note that the anti-arrhythmic drugs on cardiac inhibition. Medical therapy, endangering the life or consciousness where forfeiture could be considered a shock cardioversion.③ slow arrhythmias may consider the installation of artificial cardiac pacemaker.Primary cardiomyopathy - prognosis processingCourse of primary cardiomyopathy dilated cardiomyopathy of varying lengths short by death within 1 year after the onset of the elderly can survive for more than 20 years. About 50% of the patients died due to heart failure and cardiac arrhythmias in 3 to 5 years. Where the heart is significantly expanded, heart failure, persistent or refractory arrhythmia poor prognosis. There are many patients with sudden death.Hypertrophic cardiomyopathy is relatively slow progression, prognosis is uncertain, can be stabilized unchanged for years, but once the symptoms gradually deteriorated. Sudden death and heart failure as the leading cause of death. A small number of patients with infective endocarditis complicated by thrombosis.The course of the development of restrictive cardiomyopathy is slow or fast, the prognosis is slightly better than the main left ventricular lesions than right ventricular disease. In recent years, surgical treatment of this type have a certain hope.