Deficiency of respiratory function:The respiratory impairments recorded a series of morpho-functional whose gravity is even more intense as the birth occurred earlier than normal time. At a gestational age ranging between 24 to 28 weeks, newborn lung to breathe air subject to change.The alveolar surface-substance is lacking lipoprotein surfactant molecules penetrate between the molecules of which the fluid covering the surface of alveoli, decrease their cohesion and thus lowers the surface tension, facilitating detachment of alveoli and pulmonary ventilation. Thus, surfactant deficiency will cause respiratory distress.Immaturity of the respiratory center leads to crises of apnea. These together with poor blood circulation causes hypoxia. It produces alterations in the vascular wall, alveolar epithelial injury occurs, with swelling and transudat with intraalveolar fibrin and ultimately the formation of hyaline membranes. Fibrinolytic system is deficient, there is deficiency of plasminogen and plasmin, thus explaining the absence of membranes resobtiei formats.
Chest narrow premature poorly mineralized ribs and muscle weakness are limited greatly favored trip lung circulation. The vesicular murmur is barely audible listening.
From these early impairments of fetal hemoglobin is protected with a high affinity for oxygen. Such is maintained oxygen saturation of 50-60% being covered about 15 volumes of oxygen in the 22 to 100 cm3 blood volume.
Hypoxia premature baby has severe consequences on the body, carbohydrates are consumed reserves used to liberate the energy needed and there is an accumulation of lactic acid and metabolic acidosis with hypercapnia. Acidosis will cause inhibition and cronotropismului inotropismului myocardium diminurea glomerular filtration and decreased tubular reabsorption. Also, metabolic acidosis disturb brain activity, inhibit glucose utilization and disrupts the function of sodium pump.Central nervous system (CNS) premature ventricular at risk of cerebral hemorrhage.
In the cardiovascular risk of producing a neonatal shock, especially septic shock. Botal hole permeability and is accompanied by the breaths arterialcare channel facilitates proper heart failure. Heart sounds are irregular and the pulse is 14-160/minut values. Low blood pressure 45-70 mmHg Tnsiunea mmHg/30-45 cause a slow and reduced irrigation in the extremities.
Hematology due hipofunctiei hemolysis and bone marrow may be premature in the first 2 months of life anemia normocitara normocroma called "anemia premature". After depletion of iron anemia is hypochromic, microcytic.
Nutritional deficiency function comprises several aspects. Due to the low amount of saliva dries the mouth and is easing stomatitis.Sucking reflex is missing in most premature and swallowing reflex is absent only in those with a birth weight less than 2000 g.In early gastric capacity is greatly reduced (30-90 ml), hypotonic intestinal muscles and promotes slow peristaltic movements flatulence and constipation.The liver has a structure of type embryo, the synthesis of serum proteins and clotting factors deficiency presenting large. Liver biochemical deficiency disorders will attract as hypoglycemia, hipoprotrombinemia, hypoproteinaemia, hipoglobulinemia.
Early gastrointestinal ulcerative-necrotic enterocolitis may present with a higher incidence of both gestational age is lower.
In the thermoregulatory function registers various changes. After nsatere, decreases body temperature by 2-3 degrees and return to normal of 37 degrees for 2-3 days or a week. The premature to fight cold is essential chemical thermogenesis. For this purpose we notice an increase in fatty acid oxidation in brown fat in the neck and mediastinum is releasing a large amount of heat to be distributed throughout the entire body through the bloodstream.The thermolysis is enhanced premature, he lost large amounts of heat due to greatly increased body surface compared with adipose panicle.Thermogenesis comes to balancing high energy losses by eating large amounts of oxygen and energy substances.Hypothermia to 32 degrees Celsius for 12 hours is fatal. Also, prolonged hypothermia cause serious tissue disorder called sclera (waxy induration of the skin and subcutaneous cellular tissue that does not allow formation of the skin fold, giving the feeling of plucking rubber skin).
Kidney deficiency can manifest itself in increased embryonic lobulatie kidney, heart ugly pronounced albuminuria increased glomerular permeability due to positive. Glomerular filtration is low and the dilution capacity and poor concentration. Premature dysfunction has a sodium pump, which you retain and make edema.
Specific humoral immunity of premature baby is much reduced.Immunoglobulin G from mother to fetus during passing last month of pregnancy, such as premature birth only to 0, 5-1 g / l IgG, compared with term newborn who arrives with 9-10 g / l .Cellular immune defense deficiency exposes the risk of nosocomial infections early. Lack blanket horny and absence of acidity on the sweat glands causes the skin to act as a barrier not being an open wound.
Ophthalmology can be found in newborns with low birth weight in prematurity retinopathy.
Risks of prematurity term frequently mental retardation and cerebral palsy register. The early distinction between gray and white matter is hardly possible. Development of brain cells is weak and almost nonexistent myelination process. Vasculature is low in cortex and subcortex.There is also a risk of damage to sensory (deafness, blindness to vision loss with retinopathy in prematurity) and bronchopulmonary dysplasia.
Thursday, June 23, 2011
Prematurity - premature baby care
Infant who is expected to be at risk at birth will be brought forth in aroom with a temperature of 26 degrees Celsius and is wrapped in swaddling clothes warm Speedlites has a high importance in order to combat shortages thermoregulation. When moving his salon,mercury thermometer inside the room has to climb to 26-28degrees Celsius. Premature infants whose gestational weight not exceeding 1800 g are placed in incubators. For a weight of 1000gtemperature must have a value of 34 degrees Celsius per 250 gbody weight plus or minus or minus 1 degree Celsius increase in temperatures. In early hypothermia, the temperature will be a degree lower than body temperature.
When body temperature oscillations do not exceed 1 degreeCelsius thermal homeostasis say is recorded.
The deficit will be countered by dezobstruarea respiratory airwaylateral decubitus layout avnd head higher than the body, aspirationof stomach contents into stasis to facilitate movement diaphragm,oxygen.
Acidosis will be controlled by oxygen and glucose 5% solution ofsodium bicarbonate addition, the mother in labor, then early in the first days of life according to values pHmetriei.
Fighting is bleeding tendencies in the administration of vitamin Kin the early days.
When body temperature oscillations do not exceed 1 degreeCelsius thermal homeostasis say is recorded.
The deficit will be countered by dezobstruarea respiratory airwaylateral decubitus layout avnd head higher than the body, aspirationof stomach contents into stasis to facilitate movement diaphragm,oxygen.
Acidosis will be controlled by oxygen and glucose 5% solution ofsodium bicarbonate addition, the mother in labor, then early in the first days of life according to values pHmetriei.
Fighting is bleeding tendencies in the administration of vitamin Kin the early days.
Prematurity
Is premature newborns with gestational age less than 37 weeks, weighing 2500 g and length of less than 47 cm. Premature weighs corresponding gestational age.
We know more degrees of prematurity. Depending on birth weight premature to classify these degrees: first degree corresponds children weighing between 2499-2000 g, grade II - 1999-1500 g, grade III - 1499-1000 g, grade IV - less than 1000 g.
Etiology of prematurity:
The causes that lead to preterm birth are numerous and diverse, often associating and being difficult to distinguish the contribution of each. It is difficult to separate causes from those that cause premature birth intrauterine growth delay.Known causes of premature births as generators can be divided into: causes obstetric, medical, social and Undiagnosed.
Obstetric causes include: uterine-womb infant, uterine malformations, chronic endometritis, uterine fibromatosis, dehiscence of the cervix, placenta, bleeding retroplancentare, detached early placenta, placenta praevia, pool starmt, twins, multipara, primary over 36 years and under 20 years.
Comprehensive medical causes vascular-renal syndrome.
Among the social causes are: trauma, excessive effort, vibrations, strong emotions, mental trauma, conflict, breach of hygiene rules.A 30% is the unknown causes.
Signs and symptoms of prematurity:
The clinical picture of premature baby provides a child with a large head circumference of which is third in size, anterior fontanelle is large and thinning hair. Newborn baby girl small, triangular, with a senile appearance. His mouth is big and sharp chin. Implanted ear pavilions are down, stuck to his head, with poor development of cartilage.On examination the devices and systems can notice a small chest, weak, comes in contrast with voluminous abdomen, flank widened due to weakness.The newborn attention inspctia red skin, thin, fragile, covered with lanugo abundant over the entire body, physiological descuamatia is extended lamellar or furfuracee.Elastic tissue is missing, and the fat is very poorly represented what enteritis wrinkled skin on the body. The muscle is hypotonic, hypotrophy, hipokinetic.
Different points of ossification are delayed, and help determine the approximate age prematurely: point of ossification appears calcanean 6 months of gestation, the astragalian 9 months, the distal epiphysis of the femur (Beclard) occurs close to birth.In making the necessary measurements to find a chest perimeter whose size varies between 25-31 cm, a thoracic perimeter of 23 cm has a poor prognosis, the infant in question was considered unsustainable.
Prematurity itself is a risk factor due to immaturity of organs and systems through short gestation and difficulties adapting to life outside the womb.
We know more degrees of prematurity. Depending on birth weight premature to classify these degrees: first degree corresponds children weighing between 2499-2000 g, grade II - 1999-1500 g, grade III - 1499-1000 g, grade IV - less than 1000 g.
Etiology of prematurity:
The causes that lead to preterm birth are numerous and diverse, often associating and being difficult to distinguish the contribution of each. It is difficult to separate causes from those that cause premature birth intrauterine growth delay.Known causes of premature births as generators can be divided into: causes obstetric, medical, social and Undiagnosed.
Obstetric causes include: uterine-womb infant, uterine malformations, chronic endometritis, uterine fibromatosis, dehiscence of the cervix, placenta, bleeding retroplancentare, detached early placenta, placenta praevia, pool starmt, twins, multipara, primary over 36 years and under 20 years.
Comprehensive medical causes vascular-renal syndrome.
Among the social causes are: trauma, excessive effort, vibrations, strong emotions, mental trauma, conflict, breach of hygiene rules.A 30% is the unknown causes.
Signs and symptoms of prematurity:
The clinical picture of premature baby provides a child with a large head circumference of which is third in size, anterior fontanelle is large and thinning hair. Newborn baby girl small, triangular, with a senile appearance. His mouth is big and sharp chin. Implanted ear pavilions are down, stuck to his head, with poor development of cartilage.On examination the devices and systems can notice a small chest, weak, comes in contrast with voluminous abdomen, flank widened due to weakness.The newborn attention inspctia red skin, thin, fragile, covered with lanugo abundant over the entire body, physiological descuamatia is extended lamellar or furfuracee.Elastic tissue is missing, and the fat is very poorly represented what enteritis wrinkled skin on the body. The muscle is hypotonic, hypotrophy, hipokinetic.
Different points of ossification are delayed, and help determine the approximate age prematurely: point of ossification appears calcanean 6 months of gestation, the astragalian 9 months, the distal epiphysis of the femur (Beclard) occurs close to birth.In making the necessary measurements to find a chest perimeter whose size varies between 25-31 cm, a thoracic perimeter of 23 cm has a poor prognosis, the infant in question was considered unsustainable.
Prematurity itself is a risk factor due to immaturity of organs and systems through short gestation and difficulties adapting to life outside the womb.
Postmaturity
Present syndrome postmaturitate any fetus from a pregnancy exceeding 42 weeks calculated from the first day of last period.As the pregnancy is prolonged, the greater the risk of intrauterine malnutrition.
Etiology:
Syndrome postmaturitate the causes can be divided into maternal and ovulare.Maternal factors are:- Hormonal and humoral factors that induce a decrease in excitability myometrium;- Mechanical factors: low responsiveness segmento-neck area, lack of cervical maturatiei;- Imbalances in the nervous control;- Primiparitatea after age 35 years;- Chronic poisoning;- Unfavorable socio-economic status, poor nutrition.Ovulari factors include:- Insufficient placental sulfatase;- Male because testosterone inhibit fetal oxytocin;- Anencephaly;- Absence of fetal pituitary.
Clinical signs:
Birth a child has dry skin, visible on inspection, "washerwoman hands," cellular tissue decreased on alert. There are also cases of children with skin imbued with meconium, meconium aspiration has a high incidence in children leading to increased mortality risk posmatur postpartum.
After crossing interval of 42 weeks gestation is recommended caesarean section if there are signs of fetal distress.Postnatal complications include: metabolic disorders (hyperglycemia, hypocalcemia), of meconium aspiration syndrome, polycythemia, persistent pulmonary hypertension.
Fetal prognosis is marked by increased perinatal morbidity and mortality compared with term sracinile. Degenerative changes affecting placental feto-maternal and fetal nutrition and oxygenation compromise causing hypoglycemia, hypocalcemia. The prognosis is influenced by the possibility of fetal malformations of existence, presentations pathological fractures collarbone, pelvis disparities fetus (macrosomia).
Etiology:
Syndrome postmaturitate the causes can be divided into maternal and ovulare.Maternal factors are:- Hormonal and humoral factors that induce a decrease in excitability myometrium;- Mechanical factors: low responsiveness segmento-neck area, lack of cervical maturatiei;- Imbalances in the nervous control;- Primiparitatea after age 35 years;- Chronic poisoning;- Unfavorable socio-economic status, poor nutrition.Ovulari factors include:- Insufficient placental sulfatase;- Male because testosterone inhibit fetal oxytocin;- Anencephaly;- Absence of fetal pituitary.
Clinical signs:
Birth a child has dry skin, visible on inspection, "washerwoman hands," cellular tissue decreased on alert. There are also cases of children with skin imbued with meconium, meconium aspiration has a high incidence in children leading to increased mortality risk posmatur postpartum.
After crossing interval of 42 weeks gestation is recommended caesarean section if there are signs of fetal distress.Postnatal complications include: metabolic disorders (hyperglycemia, hypocalcemia), of meconium aspiration syndrome, polycythemia, persistent pulmonary hypertension.
Fetal prognosis is marked by increased perinatal morbidity and mortality compared with term sracinile. Degenerative changes affecting placental feto-maternal and fetal nutrition and oxygenation compromise causing hypoglycemia, hypocalcemia. The prognosis is influenced by the possibility of fetal malformations of existence, presentations pathological fractures collarbone, pelvis disparities fetus (macrosomia).
Lobar pneumonia in children
Lobar pneumonia is a lung disease whose etiologic agent located is the pneumococcus.The main causes of this pathology are represented by: cold weather, allergy diseases recent respiratory mucosa irritation, physical debility.
The disease has a high incidence especially in large child, but can meet and at the age of the infant. Lobar pneumonia is lobar pneumonia franca by fibrin-leukocyte alveolitis, home pneumonia, the focus may be only segmental or round.
Signs and symptoms:
The clinical picture presents an atypical appearance compared to that of an adult can manifest itself in febrile syndrome (39-40 degrees C), chills, chest pain, cough, shortness of breath. The disease begins in children after previously had an infection of the upper airway aieriene with a feverish state. May appear misleading evocative aspects of acute appendicitis with symptoms: vomiting, abdominal pain (right iliac fossa at) the absence of muscular defense, fever, tachycardia. A clinical picture manifested by vomiting, fever, headache, neck stiffness to, but Valarie normal CSF may be suggestive of a diagnosis of acute meningitis false positive. A febrile syndrome without signs of localization can Simulta a typhoid fever, although more rare.There are several signs outlined in lobar pneumonia: facies vultuos, naso-labial herpes (most commonly of the pneumonic outbreak), which is initially dry cough polipneea.During the state specifies a set of functional and physical signs: fever with high (39-40 degrees) to keep the oscillations set up 0, 5 degrees, dry cough initially, then becomes productive (rarely rusty), tachycardia can reach values of 120-140 / minute.
On physical examination reveals lung Matita submatitate or limited, proper furnace condensation outbreak of rales crackles deeply perceived the end of inspiration, breath tubal exaggeration voice vibrations.
Positive diagnosis:
Positive diagnosis is based on clinical examination and performing laboratory investigations.Chest X-ray diagnosis is paramount for the issue. It shows a dense homogeneous opacity, pointing triangle to HIL (Weil-Mouriquand triangle), lobar or segmental. Right upper lobe is usually interested.Laboratory tests predict blood counts. This highlights hyperleukocytosis (20. 000/mmc) with polinucleoza (80-90%).Laboratory investigations also show a hiperfibrinemie (6-8 g 0 / 00), elevated ESR and CRP's site (C-reactive protein).
Differential diagnosis is made by clinical stage: acute appendicitis, meningitis, other pneumopathies, pleurisy. During radiological lobar pneumonia viral pneumonia will differentiate the disorders accompanied by segmentation ventilation (atelectasis).In case of an outbreak pneumonic round, it must be distinguished from a tumor or another process pneumonia with different etiology, such as the staphylococcal.
Treatment:
Treatment consists of antibiotics etiologic. In the past, penicillin was the antibiotic of choice, are given a dose of 1-2 million unitati/24h, divided in four doses at intervals of 6 hours or intra-venous infusion continues. Actualmentese antibiotics that is sensitive pneumococcus: Amoxicillin + clavulanic acid (Augumentin), ampicillin + sulbactam (Unasyn), cephalosporins (ceftriaxone Ceftriaxone 100 mg / kg / day), vancomycin, rifampicin, Imipenem dose of 50 mg / kg and . you only in special situations.Symptomatic states: controlling foot, treatment of heart failure, seizures, oxigeno therapy (oxygen wetting), cough suppressants.
The disease to establish the correct antibiotic within 24-48 hours apirexie produce, but physical and radiological signs persist for more. Healing is constant. Exceptionally lobar pneumonia complications can occur with: pleurisy, lung abscess.
Prophylaxis of pneumococcal vaccine is made with high-risk persons, such as splenectomizatii.
The disease has a high incidence especially in large child, but can meet and at the age of the infant. Lobar pneumonia is lobar pneumonia franca by fibrin-leukocyte alveolitis, home pneumonia, the focus may be only segmental or round.
Signs and symptoms:
The clinical picture presents an atypical appearance compared to that of an adult can manifest itself in febrile syndrome (39-40 degrees C), chills, chest pain, cough, shortness of breath. The disease begins in children after previously had an infection of the upper airway aieriene with a feverish state. May appear misleading evocative aspects of acute appendicitis with symptoms: vomiting, abdominal pain (right iliac fossa at) the absence of muscular defense, fever, tachycardia. A clinical picture manifested by vomiting, fever, headache, neck stiffness to, but Valarie normal CSF may be suggestive of a diagnosis of acute meningitis false positive. A febrile syndrome without signs of localization can Simulta a typhoid fever, although more rare.There are several signs outlined in lobar pneumonia: facies vultuos, naso-labial herpes (most commonly of the pneumonic outbreak), which is initially dry cough polipneea.During the state specifies a set of functional and physical signs: fever with high (39-40 degrees) to keep the oscillations set up 0, 5 degrees, dry cough initially, then becomes productive (rarely rusty), tachycardia can reach values of 120-140 / minute.
On physical examination reveals lung Matita submatitate or limited, proper furnace condensation outbreak of rales crackles deeply perceived the end of inspiration, breath tubal exaggeration voice vibrations.
Positive diagnosis:
Positive diagnosis is based on clinical examination and performing laboratory investigations.Chest X-ray diagnosis is paramount for the issue. It shows a dense homogeneous opacity, pointing triangle to HIL (Weil-Mouriquand triangle), lobar or segmental. Right upper lobe is usually interested.Laboratory tests predict blood counts. This highlights hyperleukocytosis (20. 000/mmc) with polinucleoza (80-90%).Laboratory investigations also show a hiperfibrinemie (6-8 g 0 / 00), elevated ESR and CRP's site (C-reactive protein).
Differential diagnosis is made by clinical stage: acute appendicitis, meningitis, other pneumopathies, pleurisy. During radiological lobar pneumonia viral pneumonia will differentiate the disorders accompanied by segmentation ventilation (atelectasis).In case of an outbreak pneumonic round, it must be distinguished from a tumor or another process pneumonia with different etiology, such as the staphylococcal.
Treatment:
Treatment consists of antibiotics etiologic. In the past, penicillin was the antibiotic of choice, are given a dose of 1-2 million unitati/24h, divided in four doses at intervals of 6 hours or intra-venous infusion continues. Actualmentese antibiotics that is sensitive pneumococcus: Amoxicillin + clavulanic acid (Augumentin), ampicillin + sulbactam (Unasyn), cephalosporins (ceftriaxone Ceftriaxone 100 mg / kg / day), vancomycin, rifampicin, Imipenem dose of 50 mg / kg and . you only in special situations.Symptomatic states: controlling foot, treatment of heart failure, seizures, oxigeno therapy (oxygen wetting), cough suppressants.
The disease to establish the correct antibiotic within 24-48 hours apirexie produce, but physical and radiological signs persist for more. Healing is constant. Exceptionally lobar pneumonia complications can occur with: pleurisy, lung abscess.
Prophylaxis of pneumococcal vaccine is made with high-risk persons, such as splenectomizatii.
Cleft palate, cleft lip and cheilo-palato-schizis - Medical Therapy
Neonatal care includes medical therapy and special diet techniques for children with craniofacial defects: cleft palate or cleft.
Neonatal care.A newborn with cleft face three major problems:-Risk of aspiration of liquids through oral communication between the mouth and nose-Airway obstruction and respiratory sequelae that occur if the defect is associated with migrognatia-Difficulty of Food and nasal regurgitation.These three major difficulties are compounded by the frequent association of other defects of craniofacial and neck area.
Feeding children with cleft.Most affected children are born with normal weight. Due to the difficult food and other problems encountered, therefore most frequently encountered in these children is weight loss. Most affected children are not breast fed. Those with cleft palate can not create a negative pressure necessary to suction the oral cavity.Mothers of children with cleft lip unilateral defect coverage can help your child through the breast.
There is no universally correct technique or method suitable for food. Most children finish eating in 18 to 30 minutes. If you need more than 45 minutes, the child struggles to suck and eat too much of their calories, Nelu weight. A child who is breast fed or bottle every 3-4 hours in weight tends to win more than one that is often fed to more than 2 hours for short periods.
Eating one cleft child.If one cleft lip, the child usually does not have eating disorders, besides learning how to keep nipple in the mouth. Children with cleft palate can suck the milk from the nipple through its compression between tongue and a portion of the palace.
It is helpful breast massage and hot compress for 20 minutes before feeding. Mom must press the areola with its finger to help angorjat nipple protrusion. The child should be kept in semi-raised position or football. Mother can maintain itself the breast, to ensure that the child's lower lip and the tongue is in its correct position is under the nipple.
If the child can not keep the nipple in the mouth for more tinp mother can collect the remaining milk with an electric or manual milking bottle meet. It is important to increase the amount of liquid consumed by the mother to increase the amount of milk.
Feeding with human milk from the bottle.For children who have cleft palate and lip bilateral, breast feeding is not possible. Mom can use a breast pump to gather and provide child milk bottle.
Feeding with formula milk bottle.Artificial milk formula that is required to be chosen by a child's pediatricians. Especially for these children are different types of teats and soothers. A soft nipple is more effective than the last one (which can be softened by boiling). You can use a nipple ribbed to prevent slipping. Any nipple can be channeled manually using a knife with teeth. It is important that the striate area to be in contact with the child's language.
String and the bottle must be relaxed, not gathered continuously.Nipple is oriented in the opposite corner of the mouth to the cleft.The child should be allowed a meal a few seconds to sneeze and cough when reflux occurred nose.
Complications of cleft besides eating difficult.
Upper airway obstruction.May be present in children with cleft palate, especially those with hypoplasia Pierre-Robin sequence manidibulara-. Obstruction result from posterior positioning of the tongue, which inspired prolapse into the pharynx. Nasal obstruction can result in tongue protrusion in the nasal cavity.Can be controlled by placing the child in position of pronation to prevent prolapse of the tongue. In severe cases where the obstruction is not resolved by conservative measures, may require a tracheotomy.
Otitis media.It is a common complication of cleft palate and is present in almost all children with cleft uncorrected. Although recurrent suppurative disease can be a problem, the primary complication of middle ear effusions is permanent hearing loss.
Therapeutic protocol used in the treatment of cleft centers include:-At the age of cleft lip repair 3 months, and placement of ventilation tubes-At the age of 6 months of orthodontics prechirurgicale interventions, if necessary, assessment of spoken language-At the age of 9 months to begin therapy, speech therapy spoken language-At the age of cleft palate repair 9-12 months, and placing a ventilation tube-At the age of 1-7 years-orthodontic treatment-At the age of 7-8 years, alveolar bone graftingAge-8 years-continuous orthodontic treatment.
Neonatal care.A newborn with cleft face three major problems:-Risk of aspiration of liquids through oral communication between the mouth and nose-Airway obstruction and respiratory sequelae that occur if the defect is associated with migrognatia-Difficulty of Food and nasal regurgitation.These three major difficulties are compounded by the frequent association of other defects of craniofacial and neck area.
Feeding children with cleft.Most affected children are born with normal weight. Due to the difficult food and other problems encountered, therefore most frequently encountered in these children is weight loss. Most affected children are not breast fed. Those with cleft palate can not create a negative pressure necessary to suction the oral cavity.Mothers of children with cleft lip unilateral defect coverage can help your child through the breast.
There is no universally correct technique or method suitable for food. Most children finish eating in 18 to 30 minutes. If you need more than 45 minutes, the child struggles to suck and eat too much of their calories, Nelu weight. A child who is breast fed or bottle every 3-4 hours in weight tends to win more than one that is often fed to more than 2 hours for short periods.
Eating one cleft child.If one cleft lip, the child usually does not have eating disorders, besides learning how to keep nipple in the mouth. Children with cleft palate can suck the milk from the nipple through its compression between tongue and a portion of the palace.
It is helpful breast massage and hot compress for 20 minutes before feeding. Mom must press the areola with its finger to help angorjat nipple protrusion. The child should be kept in semi-raised position or football. Mother can maintain itself the breast, to ensure that the child's lower lip and the tongue is in its correct position is under the nipple.
If the child can not keep the nipple in the mouth for more tinp mother can collect the remaining milk with an electric or manual milking bottle meet. It is important to increase the amount of liquid consumed by the mother to increase the amount of milk.
Feeding with human milk from the bottle.For children who have cleft palate and lip bilateral, breast feeding is not possible. Mom can use a breast pump to gather and provide child milk bottle.
Feeding with formula milk bottle.Artificial milk formula that is required to be chosen by a child's pediatricians. Especially for these children are different types of teats and soothers. A soft nipple is more effective than the last one (which can be softened by boiling). You can use a nipple ribbed to prevent slipping. Any nipple can be channeled manually using a knife with teeth. It is important that the striate area to be in contact with the child's language.
String and the bottle must be relaxed, not gathered continuously.Nipple is oriented in the opposite corner of the mouth to the cleft.The child should be allowed a meal a few seconds to sneeze and cough when reflux occurred nose.
Complications of cleft besides eating difficult.
Upper airway obstruction.May be present in children with cleft palate, especially those with hypoplasia Pierre-Robin sequence manidibulara-. Obstruction result from posterior positioning of the tongue, which inspired prolapse into the pharynx. Nasal obstruction can result in tongue protrusion in the nasal cavity.Can be controlled by placing the child in position of pronation to prevent prolapse of the tongue. In severe cases where the obstruction is not resolved by conservative measures, may require a tracheotomy.
Otitis media.It is a common complication of cleft palate and is present in almost all children with cleft uncorrected. Although recurrent suppurative disease can be a problem, the primary complication of middle ear effusions is permanent hearing loss.
Therapeutic protocol used in the treatment of cleft centers include:-At the age of cleft lip repair 3 months, and placement of ventilation tubes-At the age of 6 months of orthodontics prechirurgicale interventions, if necessary, assessment of spoken language-At the age of 9 months to begin therapy, speech therapy spoken language-At the age of cleft palate repair 9-12 months, and placing a ventilation tube-At the age of 1-7 years-orthodontic treatment-At the age of 7-8 years, alveolar bone graftingAge-8 years-continuous orthodontic treatment.
Cleft palate, cleft lip and cheilo-palato-schizis - Pathogenesis and causes
Physiology palate formation.Palate formation starts at the end of week 5 of pregnancy. At this stage the palace consists of two parts, called the palace above (primary) and the palace back (side). Median nasal protrusions form the intermaxillary segment, which includes primary and incisors palace. Extends back to the primary Palace incisive foramen.
Palace side, which consists of lateral palatal processes, starting from incisive foramen and includes a portion of a bone and muscle. Lateral palatine processes occurring in week 6 of pregnancy. Deep portion of the jaws comprise projections forming two structures horizontally, which will derive first brachial arch. They are found on either side of the tongue. As the tongue moves back in week 7, lateral processes grow medially. Hard palate before fusion begins and continue back in week 8 of gestation.
Physiology of upper lip formation.Embryonic development is characterized by fusion of the upper lip projections protruding jaws with lateral and medial nasal. This process begins in week 4 of pregnancy and is completely in week 7. Lack of complete mesenchymal migration to join one or both jaws with prominent median nasal prominence result in unilateral or bilateral cleft lip.
Genetic theory.Cleft palate is the genetic basis of heterogeneous and probably multifactorial. Pathways have been described autosomal recessive, autosomal dominant and X Linc. For all parents misfortune of having a child with velo-palatine defect is 1 in 700. In families in which no first-degree relative is affected, the rate of recurrence of cleft lip or cleft palate in infants is 2. 5%. Is affected when a relative degree, the recurrence rate is 10%. Similar recurrence rates occur in children of parents who were born with clefts. If the cleft is part of an autosomal dominant syndrome, the recurrence rate is 50%.
A cleft is associated with a syndrome in 30% of cases. The most common syndrome associated with cleft lip and palate is Van der Woude. It is an autosomal dominant disease characterized by cleft lip and / or palate, with blind sinuses or depressions of the lower lip.
The theory of externalities.Etiology of cleft palate is not well understood, though there is evidence of involvement of external factors. Quite a few of the factors known teratogenic cause cleft. Alcohol consumption during embryological history is present in many children with clefts. Other Teratogens associated with increased frequency of cleft palate include: phenytoin, retinoids and illegal rogurile-cocaine.
Palace side, which consists of lateral palatal processes, starting from incisive foramen and includes a portion of a bone and muscle. Lateral palatine processes occurring in week 6 of pregnancy. Deep portion of the jaws comprise projections forming two structures horizontally, which will derive first brachial arch. They are found on either side of the tongue. As the tongue moves back in week 7, lateral processes grow medially. Hard palate before fusion begins and continue back in week 8 of gestation.
Physiology of upper lip formation.Embryonic development is characterized by fusion of the upper lip projections protruding jaws with lateral and medial nasal. This process begins in week 4 of pregnancy and is completely in week 7. Lack of complete mesenchymal migration to join one or both jaws with prominent median nasal prominence result in unilateral or bilateral cleft lip.
Genetic theory.Cleft palate is the genetic basis of heterogeneous and probably multifactorial. Pathways have been described autosomal recessive, autosomal dominant and X Linc. For all parents misfortune of having a child with velo-palatine defect is 1 in 700. In families in which no first-degree relative is affected, the rate of recurrence of cleft lip or cleft palate in infants is 2. 5%. Is affected when a relative degree, the recurrence rate is 10%. Similar recurrence rates occur in children of parents who were born with clefts. If the cleft is part of an autosomal dominant syndrome, the recurrence rate is 50%.
A cleft is associated with a syndrome in 30% of cases. The most common syndrome associated with cleft lip and palate is Van der Woude. It is an autosomal dominant disease characterized by cleft lip and / or palate, with blind sinuses or depressions of the lower lip.
The theory of externalities.Etiology of cleft palate is not well understood, though there is evidence of involvement of external factors. Quite a few of the factors known teratogenic cause cleft. Alcohol consumption during embryological history is present in many children with clefts. Other Teratogens associated with increased frequency of cleft palate include: phenytoin, retinoids and illegal rogurile-cocaine.
Cleft palate, cleft lip and cheilo-palato-schizis - Surgical therapy
Unilateral cleft lip plasty.Unilateral cleft lip repair is usually performed in the first year of life.To the rule of 10: hemoglobin above 10 g, age over 10 weeks, weighing 10 kg. Patients who meet these criteria can better tolerate general anesthesia. All surgical procedures involve the application of local flaps for reconstruction and closure of defects.Prechirurgicale orthodontic interventions.
They use an applicator to reposition segments palace in normal alignment. The tape is placed over the cheeks and prolabiumul patient with bilateral deshizatura. They have the ability to convert a complete an incomplete cleft. In addition, realignment of the segments decreases preoperativa wound tension and the incidence of wound dehiscence.
Plasty cleft lip bilateral.This defect is unique because the control and postoperative results are affected by premaxilar segment status and degree of symmetry and completeness of the deformity. Target intervention includes correcting cleft nasal deformity and to establish a normal relationship between remaxilar and alveolar arches. Orthodontics prechirurgicala is useful to realign the maxillary arch and premaxila and to minimize voltage cleft closure.
Plasty cleft palate.The purpose of this procedure include palate defect closure and getting a normal spoken language, have a normal dental occlusion and facial growth and palate normal. Time of surgery remains controversial. Opinions are that although the most common early palate closure is associated with higher spoken language and better hearing would affect normal facial growth. In most centers, therapeutic intervention is practiced at the age of 12-18 months.
Complications of surgery include:-Obstruction is the most important respiratory complication during the immediate postoperative result and tongue prolapse in the neck by the patient is sedated as long as the anesthesia, intraoperative placement of a foreign language clips can be helpfulIntraoperative bleeding, is a common complication due to rich vascularization of the palace, can be dangerous in children because they have low blood reserved, epinephrine injection is performed in the palace and compresses oxymetazoline-hydrochloric-Palate fistulae or wound dehiscence can occur in the near postoperative or late, with an incidence of 34%, they occur at high tension in sutureMedium-facial abnormalities that occur in the interventions at an early age, when the girl was not fully developed, appearing through jaw growth restriction.
Therapeutic techniques include the use of the future of bone proteins to induce bone morfogenice.
They use an applicator to reposition segments palace in normal alignment. The tape is placed over the cheeks and prolabiumul patient with bilateral deshizatura. They have the ability to convert a complete an incomplete cleft. In addition, realignment of the segments decreases preoperativa wound tension and the incidence of wound dehiscence.
Plasty cleft lip bilateral.This defect is unique because the control and postoperative results are affected by premaxilar segment status and degree of symmetry and completeness of the deformity. Target intervention includes correcting cleft nasal deformity and to establish a normal relationship between remaxilar and alveolar arches. Orthodontics prechirurgicala is useful to realign the maxillary arch and premaxila and to minimize voltage cleft closure.
Plasty cleft palate.The purpose of this procedure include palate defect closure and getting a normal spoken language, have a normal dental occlusion and facial growth and palate normal. Time of surgery remains controversial. Opinions are that although the most common early palate closure is associated with higher spoken language and better hearing would affect normal facial growth. In most centers, therapeutic intervention is practiced at the age of 12-18 months.
Complications of surgery include:-Obstruction is the most important respiratory complication during the immediate postoperative result and tongue prolapse in the neck by the patient is sedated as long as the anesthesia, intraoperative placement of a foreign language clips can be helpfulIntraoperative bleeding, is a common complication due to rich vascularization of the palace, can be dangerous in children because they have low blood reserved, epinephrine injection is performed in the palace and compresses oxymetazoline-hydrochloric-Palate fistulae or wound dehiscence can occur in the near postoperative or late, with an incidence of 34%, they occur at high tension in sutureMedium-facial abnormalities that occur in the interventions at an early age, when the girl was not fully developed, appearing through jaw growth restriction.
Therapeutic techniques include the use of the future of bone proteins to induce bone morfogenice.
Cleft palate, cleft lip and cheilo-palato-schizis - Signs and symptoms
Most cleft palate are discovered at birth and occurs frequently in breast feeding difficulties of. Act may be compromised by the loss of sucking oral tightness of the nipple. If cleft palate is associated with hypoplasia can cause shortness of breath manidibulara because language prolapseaza by opening the posterior nasal cavity and oropharynx.
Mend partial or submucosa of the soft palate may be undiagnosed because they are asymptomatic. Initial manifestations consist of nasal reflux of liquids and solids. Later as they develop spoken language is manifested by nasal voice or nasal reflux of food.
In addition to the physical characteristics common to the cleft, children may have frequent upper respiratory infections: colds, sinusitis, ear infections, adenoid. Dental development is also affected. Teeth may be missing, supernumerary or bad can be replaced. These abnormalities may affect the act of chewing and facial appearance of the child.Patients with cleft associated otitis media and middle ear effusions air leakage.
Mend lip may occur as microforms, incomplete or complete. Mend microforms are characterized by a vertical groove and a notch with varying degrees of shortening purple lips. Incomplete unilateral lip is manifested by varying degrees of notching the lip associated with nasal septum intact or Simonart band (band of fibrous tissue at the end of the nasal floor until the red lip). Complete mend cestarea is characterized by lip, nasal septum and dental alveoli.
Mend bilateral cleft lips are always associated with the palace.Mend unilateral cleft lip palate are associated with in 68% of cases. Nasal regurgitation during suckling may indicate a cleft lip associated with one of the palace. All children with cleft lip should be examined fully and carefully for defects in the craniofacial and neck. The presence of a uvula bifida, a central translucent areas in the soft palate and posterior border of the notch detectable cleft hard palate submucosa indicate the palace.
Classification of cleft lip and palate of
Davis and Ritchie Classification:Group I previously cleft alveoli (cleft lip unilateral or bilateral median)Group II postalveolare clefts (cleft of the hard palate, cleft of the soft palate, cleft of hard and soft palate, submucous cleft).
Veau Classification:Group I (A), only the soft palate defectsGroup II (B), defects of the soft palate and hardGroup III (C)-defects of the soft palate and the alveoli, which involves lipGroup IV (D) complete bilateral cleft-.
Classification Kernahan and Stark points to the importance of anatomical and embryonic formation incisive foramen during week 4-7 of pregnancy. Palace forms the ceiling of the oral cavity side of incisive foramen until the uvula In the weeks 7-12 of pregnancy.
Diagnosis
Imaging studies.Ultrasound can detect some craniofacial defects if they change the appearance of fetal face. Some defects can be seen even from week 14-16 of pregnancy.
Mend partial or submucosa of the soft palate may be undiagnosed because they are asymptomatic. Initial manifestations consist of nasal reflux of liquids and solids. Later as they develop spoken language is manifested by nasal voice or nasal reflux of food.
In addition to the physical characteristics common to the cleft, children may have frequent upper respiratory infections: colds, sinusitis, ear infections, adenoid. Dental development is also affected. Teeth may be missing, supernumerary or bad can be replaced. These abnormalities may affect the act of chewing and facial appearance of the child.Patients with cleft associated otitis media and middle ear effusions air leakage.
Mend lip may occur as microforms, incomplete or complete. Mend microforms are characterized by a vertical groove and a notch with varying degrees of shortening purple lips. Incomplete unilateral lip is manifested by varying degrees of notching the lip associated with nasal septum intact or Simonart band (band of fibrous tissue at the end of the nasal floor until the red lip). Complete mend cestarea is characterized by lip, nasal septum and dental alveoli.
Mend bilateral cleft lips are always associated with the palace.Mend unilateral cleft lip palate are associated with in 68% of cases. Nasal regurgitation during suckling may indicate a cleft lip associated with one of the palace. All children with cleft lip should be examined fully and carefully for defects in the craniofacial and neck. The presence of a uvula bifida, a central translucent areas in the soft palate and posterior border of the notch detectable cleft hard palate submucosa indicate the palace.
Classification of cleft lip and palate of
Davis and Ritchie Classification:Group I previously cleft alveoli (cleft lip unilateral or bilateral median)Group II postalveolare clefts (cleft of the hard palate, cleft of the soft palate, cleft of hard and soft palate, submucous cleft).
Veau Classification:Group I (A), only the soft palate defectsGroup II (B), defects of the soft palate and hardGroup III (C)-defects of the soft palate and the alveoli, which involves lipGroup IV (D) complete bilateral cleft-.
Classification Kernahan and Stark points to the importance of anatomical and embryonic formation incisive foramen during week 4-7 of pregnancy. Palace forms the ceiling of the oral cavity side of incisive foramen until the uvula In the weeks 7-12 of pregnancy.
Diagnosis
Imaging studies.Ultrasound can detect some craniofacial defects if they change the appearance of fetal face. Some defects can be seen even from week 14-16 of pregnancy.
Subscribe to:
Posts (Atom)