NCM 109 Care of Mother and Child at Risk Midterm PDF
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This document provides an overview of high-risk infants, focusing on assessment and characteristics unique to infants small or large for gestational age. It includes descriptions, and assessments for infants considered to be high-risk. This document seems to be lecture notes, not a past paper.
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# NCM 109: Lecture 5 & 6 ## HIGH RISK CHILD ### Small for Gestational Age * An infant is SGA (microsomia) if the birth weight is below the 10th percentile on an intrauterine growth curve for that age. * SGA infants are small for their age because they have experienced intrauterine growth restric...
# NCM 109: Lecture 5 & 6 ## HIGH RISK CHILD ### Small for Gestational Age * An infant is SGA (microsomia) if the birth weight is below the 10th percentile on an intrauterine growth curve for that age. * SGA infants are small for their age because they have experienced intrauterine growth restriction (IUGR) or failed growth at the expected rate in utero. #### Etiology * A woman's nutrition during pregnancy plays a major role in fetal growth, so a lack of nutrition may be a major contributor to IUGR. * Adolescents are prone to having a high incidence of SGA infants because, if they eat only enough to meet their own nutritional and growth needs of the fetus can be compromised. * The most common cause of IUGR is placental anomaly either the placenta did not obtain sufficient nutrients from the uterine arteries or it was inefficient at transporting nutrients to the fetus. #### Assessment * The SGA infant may be detected in utero when fundal height during pregnancy becomes progressively less than expected. * The infant may have poor skin turgor and generally appears to have a large head because the rest of the body is so small. * Skull sutures may be widely separated. * Hair may be dull and lusterless. * The child may have a small liver, which can cause difficulty regulating glucose, protein, and bilirubin levels after birth. * The abdomen may be sunken. * The umbilical cord often appears dry and may be stained yellow. #### Laboratory Findings * Blood studies at birth usually shows a high hematocrit level (less than normal). * Amount of plasma in proportion to RBC are present because of lack of fluid) and an increase in the total number of RBC (Polycythemia). * Acrocyanosis (blueness of the hands and feet) may be prolonged and persistently more marked than usual. * SGA infants have decreased glycogen stores Hypoglycemia develop. ### Large for Gestational-Age Infant * An infant is LGA (also known as macrosomia) if the birth weight is above the 90th percentile on an intrauterine growth chart for the gestational age. #### Etiology * Such babies appear deceptively healthy at birth because of the weight but a gestational age examination often reveals immature development. * Infants who are LGA have been subjected to an overproduction of nutrients and growth hormones in the utero - obese and diabetic. * Multiparous women may also have large babies because with each succeeding pregnancy, babies tends to grow larger. #### Assessment * A fetus is suspected to descend CS may be necessary because shoulder dystocia (the wide fatal shoulders cannot pass through the outlet of the pelvis) would halt vaginal birth. #### Appearance * At birth LGA infants may show immature reflexes and low scores on gestational age examinations in relation to their size. * They may have extensive bruising on birth injury such as broken clavicle. * Because the head is large, it may have been exposed to more than usual. * Pressure during birth causing a prominent Caput Succedaneum, Cephalhematoma or molding. ### Caput Succedaneum * Bruising and edema of presenting part extending beyond the margin of the skull bone. * Prolonged delivery, ventouse delivery. * Pressure from uterus and vaginal wall during vaginal delivery. * Detected on ultrasound/vaginal examination. * Resolves in a few days. * Usually no complications ### Cephalhematoma * Bleeding between the baby's skull bones and the lining over the bones (the perineum). * Swelling appears 8-48 hours after birth, which has clear edges that end at the suture lines. * May be associated with fracture of the underlying skull bone. * Can cause anaemia and/or jaundice in newborn. * Gets spontaneously absorbed in some weeks. #### Cephalhematoma vs. Caput Succedaneum * **Cephalhematoma** * Periosteum peeled off bone * Does not cross the sagittal suture * **Caput Succedaneum** * Periosteum remains next to bone * Crosses the sagittal suture ### The Post term Infant * Is one born after the 41st week of pregnancy. * Infants who stay in utero past week 41 are at special risk because a placenta appears to function effectively for only 4 weeks. * After that week it seems to lose its ability to carry nutrients effectively to the fetus and th fetus begins to lose weight) post term syndrome. #### Features include * Wrinkled, patchy, peeling skin. * Long thin body suggesting wasting * Advanced maturity i.e., open-eyed, usually alert and appears old and worried. * The nails are typically long. * 10% of pregnancies born 41 and 43 weeks, 33% at 44 weeks. * Associated with oligohydramnios increases the likelihood of post maturity. * Post mature infant delivered at 43 weeks gestation. Thick, viscous meconium coated the desquamating skin. * Demonstrate many of the characteristics of the SGA infant. * Dry, cracked, almost leather-like skin from lack of fluid and absence of vernix. #### They may be SGA, and the amount of amniotic fluid surrounding them may be less at birth than usual and it may be meconium stained. * Fingernails will have grown well beyond the end of the fingertip #### Because they are older than term infants, they may demonstrate an alertness much more like a 2-week-old baby than a newborn. ### Respiratory Distress Syndrome * Formerly termed Hyaline Membrane Disease #### Often occur in * Preterm infants * Infants with diabetic mother * Or those who have decreased blood perfusion of the lungs. #### The pathologic feature is a hyaline (fibrous membrane formed from exudate of an infant's blood thst begins to line the terminal bronchioles, alveolar ducts and alveoli. * This membrane (hyaline) presents the exchange of oxygen and carbon dioxide at the alveolar-capillary membrane that interferes with effective oxygenation. ### Cephalhematoma * Collection of blood between cranial (usually parietal) bonne and periosteal membrane. * Does not cross suture lines. * Appears between first and second day. * Disappears after 2 to 3 weeks or may take months. ### Caput Succedaneum * Collection of fluid, edamatous swelling of the scalp. * Crosses suture lines. * Present at birth or shortly thereafter. * Reabsorbed within 12 hours or a few days after birth. ### The Post term Infant * Is one born after the 41" week of pregnancy. * Infants who stay in utero past week 41 are at special risk because a placenta appears to function effectively for only 4 weeks. * After that week it seems to lose its ability to carry nutrients effectively to the fetus and th fetus begins to lose weight) post term syndrome. #### Features include * Wrinkled, patchy, peeling skin. * Long thin body suggesting wasting * Advanced maturity i.e., open-eyed, usually alert and appears old and worried. * The nails are typically long. * 10% of pregnancies born 41 and 43 weeks, 33% at 44 weeks. * Associated with oligohydramnios increases the likelihood of post maturity. * Post mature infant delivered at 43 weeks gestation. Thick, viscous meconium coated the desquamating skin. * Demonstrate many of the characteristics of the SGA infant. * Dry, cracked, almost leather-like skin from lack of fluid and absence of vernix. #### They may be SGA, and the amount of amniotic fluid surrounding them may be less at birth than usual and it may be meconium stained. * Fingernails will have grown well beyond the end of the fingertip #### Because they are older than term infants, they may demonstrate an alertness much more like a 2-week-old baby than a newborn. ### Respiratory Distress Syndrome * Formerly termed Hyaline Membrane Disease #### Often occur in * Preterm infants * Infants with diabetic mother * Or those who have decreased blood perfusion of the lungs. #### The pathologic feature is a hyaline (fibrous membrane formed from exudate of an infant's blood thst begins to line the terminal bronchioles, alveolar ducts and alveoli. * This membrane (hyaline) presents the exchange of oxygen and carbon dioxide at the alveolar-capillary membrane that interferes with effective oxygenation. ### The Cause is low or absence of Surfactant, the phospholipid that normally lines the alveoli and reduces surface tension to keep the alveoli from collapsing on expiration. * Surfactant does not form until the 34 week of gestation. #### Most infants have difficulty initiating respirations at birth. * After resuscitation they appear to have free symptoms for hours and day because of initial release of surfactant. #### During this time subtle signs may appear such as: * Low body temperature * Nasal tachypnea. * Sternal and subcostal retractions. * Tachypnea (more than 60 breaths per min.) * Cyanotic mucous membrane. * Within several hours, expiratory grunting occurs caused by closure of glottis. ### As distress increases, an infant may exhibit: * Seesaw respirations (on inspiration the anterior chest wall retracts and the abdomen protrudes on expiration the sternum rises). * Heart failure evidenced by decreased urine output and edema of the extremities. * Pale gray skin. * Periods of apnea. * Bradycardia. * Pneumothorax. ### Therapeutic Management: * Surfactant replacement (Survanta) to restore naturally occurring lung surfactant to improve lung compliance. * Oxygen administration. * Kept warm - reduces the infant's metabolic oxygen demand. ### Prevention * Magnesium sulfate can help prevent preterm birth. * Betamethasone steroids appear to quicken the formation of lecithin (24 - 34 weeks). ### Meconium Aspiration Syndrome * Is present in the fetal bowel as early as 10 weeks gestation. * If hypoxia occurs, a vagus reflex is stimulated, resulting in a relaxation of the recta sphincter. * This relaxes the meconium into the amniotic flui Babies born breech may expel meconium into the amniotic fluid from pressure on the buttocks. #### Assessment * Difficulty in establishing respirations at birth. * The APGAR score is apt to be low. * Almost immediately, tachypnea, retractions and cyanosis begin. * Tachypnea * Retractions - the inflammation of bronch tends to trap air in the alveoli, limiting entrance of oxygen. * This trap air may cause enlargement of the anteroposterior diameter of the chest (barrel chest). ### Therapeutic Management: * Amino-infusion can be used to dilute the amount of meconium in the amniotic fluid and reduce the risk for aspirations. * Deeply stained amniotic fluid - cesarean birth is recommended. * After birth and tracheal suctioning. * Oxygen and assisted ventilation. * Antibiotic therapy to forestall the development of Pneumonia as a secondary problem. * If lung compliance is poor. Surfactant may be administered. * Observe infants for air trapping in the alveoli because the alveoli can expand only so far and then will rupture, sending air into the pleural space (Pneumothorax). * Warm environment. * Chest Physiotherapy with percussion and vibration to encourage removal of remnant of meconium from the lungs. ### Sudden Infant Death Syndrome * Sudden unexplained death in infancy. * It occurs higher than the usual rate in infants of adolescent mothers, infants of closely spaced pregnancies and underweight and preterm infants. * The peak age of incidence is 2 to 4 months of age. * Cause is unknown. In addition to prolonged but unexplained apnea. #### SIDS risk factors may include: * Teen pregnancy. * Alcohol use during pregnancy. * Premature birth. * Low birth weight. * Tobacco use during pregnancy. * Assigned male at birth (AMAB). ### Other Possible Contributing Factors includes: * Sleeping prone rather than supine. * Viral respiratory infection. * Exposure to secondary smoke. * Pulmonary edema. * Brain stem abnormalities. * Neurotransmitter deficiencies. * Heart rate abnormalities. * Distorted familiar breathing patterns. * Decreased arousal responses. * Possible lack of surfactant in the alveoli. * Sleeping in room without removing air currents (the infant rebreathes expired carbon dioxide. * Typically affected infants were well nourished. * Parents may report an infant who has a slight head cold - after being put to bed at night, the infant is found dead a few hours later. * An autopsy often reveals petechia in the lungs and mild inflammation an congestion in the respiratory tract. ### Hemolytic Disease of the Newborn: HYPERBILIRUBINEΜΙΑ * Hemolytic a latin for destruction (lysis) of RBC. * A certain degree of lysis of RBC in the newborn results from destruction of RBC. * Hemolytic Disease is present when there is excessive destruction of RBC, which leads to elevated bilirubin level (hyperbilirubinemia). * Cord blood has a total serum bilirubin level of 0 to 3 mg/ml. * An increasing bilirubin level becomes dangerous if the level rise to 20 mg/dl in a term infant and as low as 12mg/dl in preterm infant - brain damage (invasion of bilirubin into the brain cells). * Liver and spleen may be enlarged * Extreme edema * Anemia * Progressive jaundice occurs within 24 hours ### Therapeutic Management: * The initiation of early breastfeeding. * Bilirubin is removed from the body into feces. * Therefore, the sooner the bowel elimination begins the sooner bilirubin removal begins. * The light are placed 12 to 30 inches above the newborn's bassinets or incubator. #### Term newborns are scheduled for phototherapy when the total serum bilirubin level rises to 10 to 12 mg/d at 24 hours of age. * Preterm infants may have treatment begin at level lower than this. Continuous exposure may be harmful to the newborn. * Infant's eye must always be covered while under bilirubin lights. * Check the dressings frequently to be certain they have not slipped or are causing corned irritation. * Stools are usually bright green because of excessive bilirubin being excreted as a result to the therapy. * Stools are frequently loose and may be irritating to the skin. ### CONGENITAL HEART DISORDERS #### Classifications * **ACYANOTIC HEART DISEASE:** involves heart or circulatory anomalies that involve either a stricture to the flow of blood from the atrial to the venous system (oxygenated to unoxygenated blood from the left to right shunts). * Cause the heart to function as an ineffective pump and make the child prone to heart failure. * **CYANOTIC HEART DISEASE:** Occurs when blood is shunted from the venous to the arterial system as a result of abnormal communication between the two systems (deoxygenated blood or from right to left shunts). * **VENTRICULAR SEPTAL DEFECT:** An opening is present in the septum between the two ventricles, blood shunts from the left to right across a septum. * This impairs the effect heart because the blood that should go into the aorta and out of the body is shunted back into the pulmonary artery. #### Signs and symptoms: * easy fatigue * loud harsh pansystolic murmur becomes evident along the left sternal border at the 3'0 or 4' interspace. ### Therapeutic Management: * up to 85% of VSD are so small they close spontaneously. * moderate in size - interventional cardiac catheterization. * Larger ones (over 3mm) require open heart surgery. * **ATRIAL SEPTIC DEFECT:** Is an abnormal communication between the two atria, allowing blood to shift from the left to the right atrium (oxygenated to deoxygenated) because of the stronger contraction of the left side of the heart. * This causes an increase in the volume of the right side of the heart and generally results in ventricular hypertrophy and increased pulmonary artery blood flow. * **PATENT DUCTUS ARTERIOSUS:** The ductus arteriosus is an accessory fetal structure that connects the pulmonary artery to the aorta. * If it fails to close at birth (closure should begin with the first breath, bit complete closure may noy occur until months of age), blood will shunt from the aorta (oxygenated blood) to the pulmonary artery (deoxygenated blood) because of the increased pressure in the aorta. * The shunted blood returns to the left atrium of the heart passes to the left ventricle, out of the aorta, and shunts back to the pulmonary artery. * This causes an increase pressure in the pulmonary circulation from the extra shunted bloodfil this leads to right ventricle hypertrophy. #### Signs and Symptoms: * On physical examination, the child has wide pulse pressure. * Typically, continuous machinery like murmur can be heard at the upper left sternal border or under the left clavicle in older children. ### Therapeutic Management: * Ibuprofen is the drug of choice * Surgery 6 months - 1 year * **COARCTATION OF THE AORTA:** A narrowing of the lumen due to a constricting band, blood pressure increases proximal to the coarctation and decrease distal to it. * This results in increased blood pressure in the heart and upper portions in the subclavian artery increases. #### Signs and symptoms: * Headache and vertigo * Because the child is under 3 years of age, has difficulty describing these sensations, exceptional irritability may be the main clue. * Epistaxis (nosebleed) * Absence of palpable femoral pulse * As child grows older, they may experience leg pain on exertion, because of the diminished blood supply to the lower extremities. ### Therapeutic Management: * Interventional angiography (a balloon catheter) or surgery. ### TETRAGOLY OF FALLOT: It is called tetralogy because of the four anomalies are present ventricular septal defect, overriding aorta, pulmonary stenosis and right ventricular hypertrophy. #### 4 ANOMALIES: * **1. VENTRICULAR SEPTAL DEFECT (VSD):** Is a hole in the heart. It's a common heart problem present at birth (congenital heart defect). The hole occurs in the wall that separates the heart's lower chambers (ventricles). * **2. PULMONARY STENOSIS:** A narrowing or thickening of the valve that connects the right ventricle to the pulmonary artery. * **3. RIGHT VENTRICULAR HYPERTROPHY:** Thickening of the muscular wall of the right ventricle. The thickened wall can contribute to blocking the flow of blood through the pulmonary valve. * **4. OVERRIDING OF THE AORTA:** The artery that carries high oxygen blood to the body is out of place and arises above both ventricles instead of just the left ventricle as in the healthy heart. #### Signs and symptoms: * As newborn becomes more active, their skin acquires a bluish tint as cyanosis begins. * Polycythemia occurs as the body attempts to provide enough RBC supply oxygen to all body part. * Severe dyspnea, growth restriction and clubbing of the finger * Squatting or knee chest position when resting. #### Squatting gives physiologic relief to an overstressed heart by trapping blood in the lower extremities. * Syncope (fainting), hypoxic episodes (tet spells) - decreased blood to supply to the brain. * Surgery to correct heart defects done at 1 to 2 years of age. * Interventional cardiac catheterization - is used to correct an abnormality such as dilating a narrowed valve by the use of a balloon catheter. ### CLEFT LIP AND PALATE: The maxillary and median nasal processes normally fuse between weeks 5 and 8 of intrauterine life. * In infants with cleft lip, the fusion fails to occur in varying degrees, causing this disorder to range from a small notch in the upper lip to total separation of the lip and facial structure up into the floor of the nos with even the upper teeth and gingiva absent. #### The deviation may be unilateral or bilateral. * The nose is generally flattened because the incomplete fusion of the upper lip has allowed it to expand in a horizontal dimension. * Cleft lip is more prevalent among boys than girls. * Cleft lip occurs as a familial tendency or most likely occurs from the transmission of multiple genes. * Formation may be aided by teratogenic factors present during weeks 5 to 8 of intrauterine life, such * A viral infection or possibly a deficiency of folic acid. #### The palatal process closes at approximately weeks 9 to 12 of intrauterine life. * A cleft palate, an opening of the palate, is usually on the midline and may involve the anterior hard palate, the posterior soft palate, or both. * It may be a separate anomaly, but as a rule it occurs in conjunction with cleft lip. * It tends to occur more frequently in girls than boys. #### Assessment * Cleft lip may be detected by sonogram while the infant is in utero. * Cleft palate can be determined by pressing the newborn's tongue with a tongue blade. * This reveals the total palate and the extent of clef palate. * Be sure to have good lighting to visualize the palate clearly. * The repair of cleft palate is usually postponed until a child is 6 to 18 months old to allow the anatomic change in the palate contour that occurs during the first year of life to take place. * Repairs made before this change may be ineffective and may have to be repeated. #### Preoperative period * It may be possible for an infant with a cleft lip to breastfeed because the bulk of the mother's breast trends to form a seal against the incomplete upper lip. * The best feeding method for the child with cleft lip may be to support the baby in an upright position and feed the infant gently using a commercial cleft lip nipple. * A Breck feeder, am apparatus similar to a bulb syringe, or a Haberman feeder may be used. * If the surgical repair will be done immediately, the mother will be able to breastfeed as early as 7 to 10 days after surgery. * Be certain an infant with a cleft lip is bubbled well after feeding because of a tendency to swallow air caused by the inability to grasp a nipple or syringe edge securely with the mouth. * If a cleft extends to the nares, an infant will breathe through the mouth, causing the oral mucous membranes and lips to become dry. * Offering small sips of fluid between feedings can help keep the mucous membranes moist and prevent cracks and fissures that could lead to infection. * Infants with cleft palate cannot suck effectively either, because pressing their tongue or a nipple against the roof of their mouth could force milk up into their pharynx, leading to aspiration. * The most successful method for feeding this infant, like the child with cleft lip, is to use commercial cleft palate nipple that has an extra flange of rubber to close the roof of the mouth. * The nipple can be used with a plastic bottle that can be squeezed gently to increase the flow of the feeding to compensate for poor sucking. #### Postoperative period * After surgery for cleft lip or palate, an infant is kept NPO for approximately 4 hours. * The infant is then introduced to small amount of liquids (plan water) to prevent vomiting * No tension is placed on a lip suture line to keep the sutures from falling apart and leaving a large scar. * The infant is usually feed using a specialized feeder because this causes less suture line tension than bottle or breastfeeding. #### After palate surgery: * After palate surgery liquids are generally continued for the first 3 to 4 day and the soft diet is filled diet heating is complete. * When the child begins eating soft food he should not use a spoon because a child will invariably put it against the roof of the mouth and possibly disrupts sutures. * Be certain milk is not included in the first fluids offered because milk tend to adhere to the suture line. * After feeding offer the child clear water to rinse the suture line and keep it as clean as possible. ### TRACHEOESOPHAGEAL ATRESIA AND FISTULA: Between weeks 4 and 8 of intrauterine life, the laryngotracheal groove develops into larynx, trachea and beginning lung tissue. * A number of anomalies may occur if trachea and esophagus are affected by some teratogen that does not allow the two organs go separate but remain connected. ### ESOPHAGEAL ATRESIA: * Refers to obstruction of esophagus. Often a fistula (opening) occur between the closed esophagus and the trachea. * If a radiopaque catheter is used, it can be demonstrated coiled in the blind end of the esophagus on x-ray. #### Assessment: * Tracheoesophageal Atresia must be ruled out in any infant born to a woman with hydramnios (excessive amniotic fluid). * Diagnosing a tracheoesophageal fistula before an infant is first fed is important. * The infant will cough, become cyanotic and have obvious difficulty breathing as fluid is aspirated. * A newborn who has so much mucus in the mouth that he or she appears to be blowing bubbles. * The condition can be diagnosed with certainty if a catheter cannot be passed through the infant's esophagus to the stomach or the stomach contents cannot be aspirated. * Use of a firm catheter is necessary because a soft one will curl in a blind end esophagus and appear to have passed. ### Therapeutic Management * Emergency surgery for the infant with tracheoesophageal fistula is essential to prevent the development of pneumonia from leakage of stomach secretions into the lungs or dehydration or an electrolyte imbalance from lack of oral intake. * Antibiotics may be prescribed to help prevent infection. * Gastrostomy may be performed and the tube allowed to drain by gravity to keep the stomach empty of secretions and prevent reflux into the lungs. * Upper right lobe pneumonia from aspiration is one of the major complications of this disorder. * Surgery consists of closing the fistula and anastomosing the esophageal segments. * Observe infants closely at post operative days 7 to 10 when sutures dissolve because leaks occurring at anastomosis sites can occur at this time. * If this occurs, fluid and air leak out into the chest cavity and pneumothorax (collapse of the lung) may occur. ### OMPHALOCELE: * Is a protrusion of abdominal contents through the abdominal wall at the point of junction of the umbilical cord and abdomen. * The herniated organs are usually the intestines, but they may include stomach and liver. #### They are usually covered and contained by a thin transparent layer of peritoneum. * This condition occurs because at approximately weeks 6 to 8 of intrauterine life, the fetal abdominal contents, growing faster than the fetal abdomen, are extruded from the abdomen into the base of the umbilical cord. * At 7 to 10 weeks, when the abdomen has enlarged sufficiently, the intestine returns to the abdomen. * Omphalocele occurs when the abdominal contents fail to return in the usual way. ### Therapeutic Management * Most infants will have immediate surgery to replace the bowel before this peritoneal membrane surrounding it ruptures or becomes infected. * If the Omphalocele is large, infants may be prescribed a topical application of a solution such as Silver Sulfadiazine to prevent infection of the sac, followed by delayed surgical closure. ### **Before Surgery** * It is important that the lining of the peritoneum covering the Omphalocele not be ruptured or allowed to dry out and crack. * Exposure of intestine to air also causes a rapid loss of body heat. * Therefore, immediately place the baby in a warmed incubator. * Do not leave infants under a radiant heat source because this will quickly dry the exposed bowel. * It may be revealed by an elevated MSAFP examination during pregnancy. ### **Assessment** * If not, the presence of Omphalocele is obvious on inspection at birth. * When it is identified in utero, Cesarean birth may be performed to protec the exposed intestine. * Be sure to document the Omphalocele's general appearance and its size in centimeters at birth. * To keep the sac moist, cover it with either sterile saline-soaked gauze or a sterile plastic bowel bag until surgery. * Because of the large amount of exposed intestinal surface, the saline used must be at body temperature to prevent lowering body temperature. * A nasogastric tube is inserted at birth to prevent intestinal distention, which would enlarge the bowel lumen, making it even more difficult to replace. * Don't feed the infant orally or allow him or her to suck on a pacifier until the bowel repair is complete. * Observe infants carefully for signs of obstruction (abdominal distention, constipation, diarrhea or vomiting) when they begin oral feedings. ## **GASTROSCHISIS:** * Is a condition similar to Omphalocele, except that the abdominal wall disorder is a distance from the umbilicus and abdominal organs are not contained by peritoneal membrane but rather spill freely from the abdomen. * Also, a greater amount of intestinal contents tends to herniate, increasing the potential for Volvulus and obstruction. * The surgical procedure is the same as that for Omphalocele. #### Children with Gastroschisis often have decreased bowel mobility, and even after surgical correction they may have difficulty with absorption of nutrients and passage of stool. ### **SPINA BIFIDA:** * Used as a collective term for all spinal cord disorders. This occurs because of a lack of fusion of the posterior surface of the embryo in early intrauterine life. * Incidence ranges from 1 to 10 per 1,000 live births. * Incidence decreases include Folic Acid 600ug in prenatal Vitamins and the mandatory inclusion of; * Folic Acid in all cereal and grain products. * Thus, reduces the rate to 2 in 10,000 live births. #### **Types of Disorders:** * **a. ANENCEPHALY:** is the absence of cerebral hemispheres. It occurs when the upper end of the neural tube fails to close in early intrauterine life. * It is revealed by an elevated level of MAFP, amniocentesis or a prenatal sonogram. * Labor may be prolonged because the infant may present in breech presentation or the underdeveloped head may not engage the cervix well. On visual inspection the disorder is obvious. * Because the respiratory and cardiac sphincters are located in the intact medulla, infants may survive for several days after birth but cannot survive further because they have little or no cerebral function. * Need concerned support in the first few days of life as they realize the baby is ill and incomplete as predicted. * **MICROCEPHALY:** Is a disorder in which the fetal brain grows so slowly that it falls more than 3 standard deviations below normal on a growth chart at birth. * The cause might be a disorder in brain development associated with an intrauterine infection such as Rubella, Cytomegalovirus or Toxoplasmosis. * May result from severe malnutrition or anoxia following birth or in early infancy. * Generally, the infant is cognitively challenged because of lack of functioning brain tissue. * **SPINA BIFIDA OCCULTA:** Occurs when the posterior laminae of the vertebrae fail to fuse. This occurs most commonly at the fifth lumbar or first sacral level but may occur at any point along the spinal canal. * May be first noticed as dimpling at the point of poor fusion. * Abnormal tufts of hair or discolored skin may also be present. * Simple Spina Bifida Occulta is a benign disorder and it can occur a frequently as in one out of every four children. * Help clarify to parents that a surface of bone is missing, and the spinal cord is intact. * **MENINGOCELE:** * The spinal cord is protected by 3 layers of meninges or membranes: 1. Pia Mater 2. Arachnoid 3. Dura Mater If the membranes herniate through an unformed vertebra, they protrude as a circular mass, about the size of an orange at the center of the back and is termed Meningocele. The protrusion generally occurs in the lumbar region, although it might be present anywhere along the spinal cord. The protrusion is either covered by a layer of skin or more frequently only the clear dura mater. * **No sensory or motor deficits accompany the disorder unless the membrane sac should rupture, but the damage of the cord occur and infection could enter the unprotected Cerebrospinal fluid.** * **MENINGOMYELOCELE:** Most common birth defect affecting the CNS. In Meningomyelocele, not just the meninges protrude through the vertebrae but the spinal cord usually ends at the point of protrusion. * Motor and sensory function will be decreased or absent beyond this point. * The child will have partial or complete paralysis, partial or complete lack of sensation of the lower extremities, as well as loss of bowel and bladder control. * Hydrocephalus develops in as many as 90% of infants because of the lack of an adequate subarachnoid membrane for CSF absorption and obstruction of CSF circulation from the spinal deformity. * **ENCEPHALOCELE:** Is a cranial meningocele. It occurs most often in the occipital area of the skull but may occur as nasal or nasopharyngeal disorder. * Generally covered fully by skin, although they may be open or covered only by the dura mater. * Transillumination of the sac will reveal whether brain tissue is in the sac CT, MRI or ultrasound will reveal the size of the skull disorder and help predict the extent of surgery which will be needed. ### **Assessment:** * Neural tube disorders may be discovered during intrauterine life by prenatal ultrasound, fetoscopy, amniocentesis (discovery of AFP in amniotic fluid), or analysis of MAFP. * An infant may be born by Cesarean birth to avoid pressure and injury to the spinal cord. * Observe and record whether an infant born with neural tube disorder has spontaneous movement of the lower extremities to assess if the child has lower motor function. * Assess the nature and pattern of voiding and defecation; * The usual newborn appears to be "always wet" from voiding. * An infant without motor or sphincter control voids continually. ### Therapeutic Management: * Children with Spina Bifida Occulta need no surgical correction because ther is no tissue extruding from the vertebrae. * Parents should be made aware of the defect and watch for more serious symptoms as the child grows such as numbness, weakness, or pain which might indicate a need for reevaluation. * Some children may eventually need surgery to prevent vertebral deterioration because of unbalanced spinal column. * Treatment for a Meningocele or Encephalocele involves immediate surgery to replace the meninges and to close the gap in the skin to prevent infection. * This is done as soon as after birth (usually 24 to 48 hours) so an infection through the exposed meninges does not occur. * If large portion of meninges have to be removed by surgery, this can limit the rate of absorption of CSF, which can lead to build up of CSF and Hydrocephalus. * Children with meningomyelocele have the same surgery to return the meninges to the spinal cord and close the gap in the skin surface. * The child will continue to have partial or complete paralysis of the lower extremities and loose of bowel and bladder function because, although the lesion on the back can be repaired, the absent lower cord cannot be replaced. * AFP more than twice if there is neural tube disorder. * Decrease - chromosomal disorders such as Trisomy 21. ### **NURSING CARE OF A WOMAN AND FAMILY EXPERIENCING A POSTPARTAL COMPLICATION** ### **POSTPARTUM HEMORRHAGE** * is any blood loss from the uterus greater than 500ml in a 24-hour period. * Early hemorrhage occur within the first 24hrs. * Late hemorrhage anytime after firs 24hrs during the remaining days of the 6 weeks puerperium. #### **The 4 causes of postpartum hemorrhage are called the four Ts (tone, trauma, tissue and thrombin). The most common causes of PPH are:** * **1. UTERINE ATONY - Uterine atony **(or uterine tone) refers to a soft and weak uterus after delivery. This is when your uterine muscles don't contract enough to clamp the placental blood vessels shut. This leads to a steady loss of blood after delivery. **Conditions that leave the uterus unable to contract readily: * Maternal age greater than 30yrs * Previous and difficult labor. * Deep anesthesia or analgesia * Labor initiated with Oxytocin * High parity * Possible Chorioamnionitis, endometritis * Secondary maternal illness (anemia) * Prior history of postpartum hemorrhage * Prolonged use of Magnesium Sulfate * Vaginal bleeding is copious and the client exhibit symptoms of shock. * **Subinvolution** incomplete return of the uterus to its pre-pregnant size and shape. * At 4 to 6 weeks