HIGH RISK NEWBORNS

RESPIRATORY DISTRESS SYNDROME
Description
‡ A disease related to immaturity of lung tissue ‡ May also be called Hyaline Membrane Disease ‡ A complex disorder manifested by signs of respiratory distress ‡ Risk factors: prematurity, maternal DM, and stress during delivery that produces acidosis in the neonate ‡ Is seen almost exclusively in preterm neonates ‡ Is associated with a high risk of long-term respiratory and neurologic complications

‡Prenatal diagnosis can evaluate lung maturity while the fetus is in utero - Evaluation of lecithin/sphingomyelin ratio of the amniotic fluid is performed - Lecithin and sphingomyelin are two surfactant phospholipids - Evaluation of fetal lung maturity gives insight into how the fetus will face after birth and may precipitate treatment to delay labor or to mature the neonate·s lungs before delivery

keeping them open so gas exchange can occur In preterm neonates. the lungs may not be fully developed and therefore may not have sufficient surfactant available The result is the inability to maintain alveolar stability .Pathophysiology ‡ RDS is characterized by poor gas exchange and ventilatory failure due to lack of surfactant in the lungs Surfactant is a phospholipid secreted by the alveolar epithelium It coats the alveoli.

which decreases blood flow to the lungs ‡ Right-to-left shunting of blood perpetuates fetal circulation by keeping the foramen ovale and dactus arteriosus patent ‡ The alveoli can become necrotic and the capillaries are damaged ‡ Ischemia allows fluid to leak into the interstitial and alveolar spaces and a hyaline membrane forms ‡ The membrane greatly hinders respiratory function by decreasing the compliance of the lungs . labored breathing. and hypoxemia ‡ With worsening atelectasis. pulmonary vascular resistance increases.‡ The lack of surfactant leads to atelectasis. respiratory acidosis.

Assessment Findings ‡ RDS can produce respiratory distress acutely after birth or within a few hours of birth ‡ Initial assessment may reveal various findings Increase respiratory rate Retractions Satisfactory color Good air movement on auscultation .

‡ As respiratory distress becomes obvious. other findings may be noted Further increased respiratory rate Labored breathing More pronounced substernal retractions Fine crackles on auscultation Cyanosis Nasal flaring Expiratory grunting .

& acidosis are non-specific to RDS Specific laboratory tests must be carried out to evaluate the neonate for complications Tests include: blood.‡ S/Sx such as hypoxemia. serum calcium & arterial blood gas (ABG) levels ‡ Radiographic evaluation reveals various findings Alveolar atelectasis shown by a diffuse granular pattern that resembles ground glass over all lung fields Dilated bronchoiles shown by dark streaks within . urine & CSF cultures and blood glucose. hypercapnia.

parlyzant and diuretic Protection from infection Administration of parenteral feedings . sedative. if needed Prevention of hypotension Prevention of hypovolemia Correction of respiratory acidosis by ventilatory support Correction of metabolic acidosis by sodium bicarbonate administration Administration of surfactant and such other drugs like antibiotic.Treatment Thermoregulation Oxygen administration Mechanical ventilation.

effective after the 72nd hour.Glucocorticoid (Celestone) ± artificial surfactant given at birth before the first breath or after diagnosis of RDS. continuous positive airway pressure. including mechanical ventilation. hastens lung maturity. Nursing Interventions: Provide continuous monitoring and close observation Obtain necessary specimens for laboratory testing Continuously monitor pulse oximetry or transcutaneous oxygen levels administer oxygen as ordered anticipate the need for ventilatory support. or positive end-expiratory pressure .

and procedures as well as what to expect and provide emotional support during the acute stage . treatments. disturb the neonate with RDS as little as possible to decrease oxygen consumption Administer drugs as ordered Provide meticulous skin and mouth care Educate the parents about the disease.Suction the neonate as indicated Institute measures to maintain thermoregulation Provide parenteral nutrition and avoid gavage and oral feedings during the acute stage of the disease because these situations decrease respiratory rate and oxygen consumption Cluster nursing activities to provide the neonate with rest periods.

typically beginning after birth and generally lasting about 2 days ‡ Results from delayed absorption of fetal lung fluid after birth .Transient Tachypnea of the Neonate (TTN) Description ‡ Also known as type II respiratory distress syndrome or wet lung ‡ A mild respiratory problem in neonates.

TTN is commonly observed in neonates born by cesarean delivery ± did not receive thoracic compression that helps expel fluid during vaginal delivery. the neonate usually recovers completely & has no increased risk for further respiratory problems . 7 ± 42 ml of amniotic fluid are squeezed from the lungs during vaginal delivery Neonates who are small or preterm. or who were born rapidly by vaginal delivery (may not have received effective squeezing of the thorax to remove fetal lung fluid) ‡ Resolution of symptoms generally occurs within 48 hours Once TTN goes away.

Any fluid that remains is later coughed out or reabsorbed into the bloodstream . the fetal lungs are filled with fluid .After birth. the remaining fluid is pushed out of the lungs as the lungs fill the air . some of the neonate¶s lung fluid is squeezed out as he passes through the birth canal .All of the fetus¶s nutrients and oxygen come from the mother through the placenta .During the birth process.Pathophysiology ‡ Before birth.The fetus doesn¶t use his lungs to breathe .

usually 48 hours of life as respiratory activity becomes effective .‡ TTN results from aspiration of amniotic or tracheal fluid compounded either by delayed clearing of the airway or by excess fluid entering the lungs ‡ TTN spontaneously fades as lung fluid is absorbed.

reveals streaking (correlates with lymphatic engorgement of retained fetal lung fluid) .Assessment findings ‡ Increased RR ( greater than 60 bpm) ‡ Expiratory grunting ‡ Nasal flaring ‡ Slight cyanosis ‡ Retractions ‡ Tachypnea ‡ ABG levels may reveal hypoxemia and decreased carbon dioxide levels ‡ Increased CO2 levels may be a sign of fatigue and impending respiratory failure ‡ Chest x-ray the diagnostic standards for TTN.

coordination of neonatal mechanisms of sucking. swallowing. and breathing High risk of aspiration due to rapid RR ‡ Transcutaneous oxygen monitoring .Treatment ‡ Oxygen administration ‡ Ventilatory assistance (rarely needed) ‡ Maintenance of acid-base balance ‡ Thermoregulation ‡ Adequate nutrition via gavage feedings or IVF Difficulty with oral feedings because of increased RR and increased work of breathing.

and oxygenation status ‡ Provide respiratory support. including mechanical ventilation.Nursing Interventions ‡ Closely monitor the neonate·s HR. RR. if necessary ‡ Institute measures to maintain a neutral thermal environment ‡ Minimize stimulation by decreasing lights and noise levels ‡ Provide nutritional support via gavage feedings or parenteral nutrition ‡ Educate the parents about the condition and its usually quick resolution ‡ Provide emotional support to the parents and family .

and greenish black * MAS results when the neonate inhales the meconium mixed with amniotic fluid.Meconium is the neonate¶s first feces . sticky.it may be seen in the amniotic fluid after 34 weeks gestation and is thick. typically occurs with the first breath or while the neonate is in utero .MECONIUM ASPIRATION SYNDROME (MAS) ‡ Involves aspiration of meconium into the lungs .

Maternal diabetes .Intrauterine hypoxia .Poor intrauterine growth .Maternal hypertension .Fetal distress .Advanced gestational age (greater than 40 weeks) .‡ Risk factors for MAS .Difficult delivery .

Neonates with MAS increased respiratory efforts to create greater negative intrathoracic pressures and improve air flow to the lungs .Right-to-left shunting commonly follows .Hyperinflation. passage of meconium into the amniotic fluid. and reflex gasping of amniotic fluid into the lungs .Pathophysiology ‡ Asphyxia in utero leads to increased fetal peristalsis. and acidemia cause increased peripheral vascular resistance . relaxation of the anal sphincter. hypoxemia.

again preventing adequate gas exchange ‡ Cardiac efficiency can be compromised from pulmonary hypertension .‡ Meconium creates a ball-valve effect. trapping air in the alveolus and preventing adequate gas exchange ‡ Chemical pneumonitis results causing the alveolar walls and interstitial tissues to thicken.

such as neonate appearing limp. Apgar scores below 6.Assessment findings ‡ Fetal hypoxia as indicated by altered fetal activity and heart rate ‡ Dark greenish staining or streaking of the amniotic fluid noted on rupture of membranes ‡ Obvious presence of meconium in the amniotic fluid ‡ Greenish staining of neonate·s skin (if the meconium was passed long before delivery) ‡ Signs of distress at delivery. pallor. air trapping. or hyperinflation . cyanosis. and respiratory distress ‡ Coarse crackles when auscultating neonate·s lungs ‡ Chest x-ray may show patches or streaks of meconium in the lungs.

Treatment ‡ Respiratory assistance via mechanical ventilation ‡ Maintenance of a neutral thermal environment ‡ Administration of surfactant and an antibiotic ‡ Extracorporeal membrane oxygenation in sever cases .

as ordered . such as oxygen and respiratory support.Nursing Interventions ‡ During labor. continuously monitor the fetus for S/Sx of distress ‡ Immediately inspect any fluid passed with rupture of membranes ‡ Assist with immediate endotracheal suctioning during delivery as indicated ‡ Monitor lung status closely. including breath sounds and RR and character ‡ Frequently assess the neonate·s vital signs ‡ Administer treatment modalities.

treatments. and procedures a well as what to expect ‡ Provide the parents and family with emotional support and guidance .‡ Institute measures to maintain a neutral thermal environment ‡ Teach the parents about the condition.

during. Acrobacter. or after delivery ‡ Most common causative organisms are the gram (-) Escherichia coli.SEPSIS Description ‡ Occurs when pathogenic microorganisms or their toxins occur in the blood or tissues ‡ Can occur before. and Klebsiella and the gram (+) beta-hemolytic streptococci ‡ Prolonged rupture of membranes increases the neonate·s risk of sepsis .

such as lethargy and hypotonic ‡ Temperature instability ‡ Feeding pattern changes. including mottling. and cyanosis ‡ Positive blood cultures . such as poor sucking and decreased intake ‡ Apnea ‡ Hyperbilirubinemia ‡ Abdominal distention ‡ Skin color changes. pallor. nonspecific behavioral changes.Assessment findings ‡ Subtle.

‡ Lumbar puncture to rule out meningitis ‡ Urine. skin. blood. and nasopharyngeal cultures ‡ Gastric aspiration ‡ Antibiotic administration Nursing interventions ‡ Collect specimens to identity the causative organism ‡ Assess the neonate·s V/S at least once per hour or more frequently as indicated .

including maintenance of a neutral thermal environment ‡ Administer nutritional support ‡ Assist with respiratory support measures. administer IVF therapy as ordered ‡ Institute measures to provide cardiovascular support . including oxygen therapy as ordered ‡ Monitor F/E balance.‡ Expect to administer a broad spectrum antibiotic before culture results are received & to switch to specific antibiotic therapy after results are received ‡ Provide supportive care.

HYPERBILIRUBINEMIA ‡ Also called pathologic jaundice ‡ Characterized by a bilirubin level that exceeds 6 mg/dl within the first 24 hours after delivery and remains elevated beyond 7 days in a full-term neonate and beyond 10 days in a pre-term neonate .A level that¶s greater than 12 mg/dl in premature or term neonates .Conjugated (direct) bilirubin level that exceeds 1.A bilirubin level that rises by more than 5 mg/day .5 to 2 mg/dl ‡ The prognosis for hyperbilirubinemia varies depending on the cause .

and hypoalbuminemia) can disrupt conjugation and usurp albumin-binding sites . and sulfonamides) and conditions (such as hypothermia. anoxia.Biliary obstruction or hepatitis may block normal bile flow .Certain drugs (such as aspirin.Pathophysiology ‡ Hyperbilirubinemia can develop several ways . hypoglycemia.Increased erythrocyte production or breakdown can accompany a hemolytic disorder or Rh or ABO incompability . tranquilizers.Maternal enzymes present in breast milk can inhibit the neonate¶s glucuronosyltransferase-conjugating .Decreased hepatic function can result in reduced bilirubin conjugation .

resulting in hyperbilirubinemia ‡ Unconjugated bilirubin can infiltrate the nuclei of the cerebral cortex and thalamus. forming direct bilirubin ‡ Unconjugated bilirubin is fat-soluble and cant be excreted in the urine or bile. which binds with albumin for trasport to liver cells to conjugate with glucuronide. hemoglobin separates into globin (protein) and heme (iron) fragments ‡ Heme fragments form unconjugated (indirect) bilirubin. leading to kernicterus (an encehalopathy) . it may escape to extravascular tissue. especially fatty tissue and the brain.‡ As erythrocytes breakdown at the end of their neonatal life cycle.

. & high-pitched cry ‡ Possible causes include include hemolytic disease of the neonate. decreased reflexes. hypothermia. imparied hepatic functioning. polycythemia. opisthotonos. seizures. enclosed hemorrhage.. and asphyxia neonatorum ‡ Glucose-6-phosphate deficiency (G6PD) increases the incidence of jaundice. hypoglycemia. sepsis. kernicterus may occur with serum bilirubin levels at or above 20 mg/dl (full-term) and at lower levels (about 14 mg/dl) in preterm neonates .Although exact level is unknown.S/Sx of kernicterus: lethargy.

levels greater than 15 mg/100 ml in a preterm neonate. or levels that increase more than 5 mg/100 ml in 24 hours ‡ hepatoaplenimegaly .Assessment findings ‡ Jaundice appearing anytime after the first day of life and persisting beyond 7 days ‡ Elevated serum bilirubin levels ² levels greater than 12 mg/100 ml in a term neonate.

‡ Exchange transfusion to replace the neonate·s blood with fresh blood (less than 48 hours old).Usually discontinued after bilirubin levels fall below 10 mg/100 ml and continue to decrease for 24 hours .Considered the treatment of choice for hyperbilirubinemia due to hemolytic disease of the neonate (after the initial exchange transfusion) .uses fluorescent light to decompose bilirubin in the skin by oxidation . removing some of the unconjugated bilirubin in serum ‡ Phototherapy .

done 1 to 2 hours before exchange or as a substitute for a portion of the plasma in the transfused blood ‡ Treatment of anemia caused by hemolytic disease .‡ Albumin administration (1g/kg of 25% salt-poor albumin) to provide additional albumin for binding unconjugated bilirubin.

Don·t skip feedings because fasting stimulates the conversion of heme to bilirubin. Also. don·t supplement non-dehydrated breastfed infants with water or water and dextrose ‡ Assess and record the neonate·s jaundice in the first 24 hours after birth.‡ To prevent hyperbilirubinemia encourage the mother to breastfeed at least 8 to 12 times per day. G6PD. which may include blood type. CBC. immediately report the jaundice and serum or transcutaneous bilirubin levels ‡ Obtain lab values as ordered. U/A & total and direct bilirubin . Coomb·s test. and note the time it began. reticulocyte count.

or after spontaneous or elective abortion .Clean the neonate¶s eyes periodically to remove drainage .Offer extra water to promote bilirubin excretion . as ordered. to an Rh (-) mother after amniocentesis or to an Rh (-) mother during the third trimester (for the purpose of preventing hemolytic disease once the neonate is born).Explain that the neonate¶s stool contains some bile and may be breenish ‡ Assist with an exchange transfusion if indicated ‡ Administer Rho (D) immune globulin (human).‡ Institute phototherapy as ordered . after the birth of an Rh (+) neonate.

its causes. provide written information ‡ Assess all neonates for risk of hyperbilirubinemia before discharge ‡ Explain the importance of follow-up visit to assess for hyperbilirubinemia . and treatment. diagnostic tests.‡ Reassure parents that most neonates experience some degree of jaundice ‡ Explain hyperbilirubinemia.

The average range is 6 to 8 µw/cm2/nanometer  Explain the procedure to the parents  Record the newborn¶s initial bilirubin level and his axillary temp. place the phototherpay unit at least 3´ (7.Performing Phototherapy  Set up the phototherapy unit about 18 inches (45. and turn on the lights  Place a photometer probe in the middle of the bassinet to measure the energy emitted by the lights.6 cm) above the incubator. .7 cm) above the neonate¶s bassinet & verify placement of the lightbulb shield  If the neonate is in an incubator.

 Place the opaque eye mask over the neonate¶s closed eyes, & fasten securely  Undress the neonate, & place a diaper under him. Cover male genitalia with a surgical mask or small diaper to catch urine & prevent possible damage from the heat & light waves  Take the neonate¶s axillary temp every 2 hours & provide additional warmth by adjusting the warming unit¶s thermostat  Monitor elimination, & weigh the neonate twice daily. Watch for signs of DHN (dry skin, poor turgor, depressed fontanels), & check urine specific gravity with a urinometer to gauge hydration status

Take the neonate out of the bassinet, turn off the phototherapy lights, & unmask his eyes at least every 3 to 4 hours (with feedings). Assess his eyes for inflammation or injury Reposition the neonate every 2 hours to expose all body surfaces to the light and to prevent head molding and skin breakdown from pressure Check the bilirubin level at least once every 24 hours ± more often if levels rise significantly. Turn off the phototherapy unit before drawing venous blood for testing because the lights may degrade bilirubin in the blood. Notify the health care provider if the bilirubin level nears 20 mg/dl fullterm or 15 mg/dl if premature.

HEMOLYTIC DISEASE
Description ‡ Formerly called Erythroblastosis fetalis ‡ Involves a breakdown of RBCs ‡ The majority of neonates affected are female Pathophysiology ‡ During pregnancy, maternal antibodies are passed via the placenta to the fetus, causing RBC breakdown ‡ The disorder is usually caused by ABO incompatibility but may also be caused by Rh incompatibility

The most common incompatibility occurs when a type O mother carries a type A or type B fetus.ABO incompatibility can occur with the first pregnancy and is usually milder and of shorter duration than Rh incompatibility . causing jaundice & hepatosplenomegaly . type O blood contains anti-A and anti-B antibodies that travel transplacentally to the fetus.eABO incompatibility can occur when fetal blood type differs from maternal blood type .

Maternal antibodies are produced in response in a subsequent pregnancy with an Rh (+) fetus.Leakage of fetal Rh antigens commonly occurs during delivery. at the time of placental separation . causing erythroblastosis Assessment findings ‡ Hemolytic anemia ‡ Hyperbilirubinemia w/in 24 H after birth ‡ Jaundice ‡ Hepatosplenolegaly . maternal antibodies enter the fetal circulation transplacentally.dRh incompatibility occurs when the Rh (-) mother carries an Rh (+) fetus .

or bottle-feeding) ‡ Family support ‡ Phototherapy ‡ Exchange transfusion ‡ Monitoring of bilirubin levels .Treatment ‡ Drug therapy such as erythropoietin to stimulate RBC formation ‡ Initiation of early feeding (breast.

RhoGAM can be administered at 28 weeks¶ gestation to decrease the incidence of maternal isoimmunization . Du (-) patient who has had an abortion or whose neonate is Rh (+) or Du (+) .Nursing interventions ‡ During pregnancy. institute preventive measures .RhoGAM is ineffective when the patient is already sensitized .RhoGAM should be administered to an Rh (-).Prevention involves administration of Rh immune globulin (RhoGAM) within 72 H of delivery to prevent antibody formation .

if appropriate ‡ Prepare the neonate and parents for treatment procedures. such as phototherapy or exchange transfusion .‡ Keep in mind that Rh sensitization can occur during pregnancy if the cellular layer separating maternal & fetal circulation is disrupted ‡ Encourage the patient to feed the neonate.

TRACHEOESOPHAGEAL FISTULA Description ‡ Refers to a congenital anomaly resulting from exposure to some teratogen that doesn·t allow the esophagus and trachea to separate normally ‡ There·s an abnormal connection between the trachea and esophagus .

the esophagus ends in blind pouch with trachea communicating by a fistula with lower esophagus and stomach Assessment findings ‡ Signs of respiratory distress ‡ Excessive frothy oral mucus ² outstanding symptom ‡ Difficulty inserting a NGT ‡ Difficulty feeding (results in choking or aspiration) ‡ Triad ´Cµ: Choking.Pathophysiology ‡ Abnormal development of the trachea and esophagus occurs during the embryonic period ‡ Typically. Coughing and Cyanosis .

with fistula ± head is extended 30o .Treatment ‡ Maintenance of patent airway ‡ Withholding of food and fluids (NPO) until repaired ‡ Surgical correction ² esophageal anastomosis & division of fistula ‡ Positioning of neonate in high Fowler·s position to prevent aspiration of gastric contents .Without fistula ± Trendelenberg position to drain secretions ‡ Laryngoscope and endotracheal tube at bedside in case of extreme edema causing obstruction ‡ Frequent shallow suctioning ‡ Pacifier to meet sucking needs ‡ Possible gastrostomy tube feedings postoperatively .

Nursing intervention ‡ Keep the neonate on NPO status ‡ Administer IVF to maintain hydration & provide nutrition. offer a pacifier to meet the neonate·s sucking needs ‡ Assess airway for patency ‡ Frequently monitor V/S and respiratory status. watch for S/Sx of aspiration ‡ Position the neonate upright or on his right side to minimize the risk of gastric secretions entering the lungs ‡ Maintain a neutral thermal environment .

Change position frequently & stimulate baby to cry BUT avoid hyperextension of the neck to prevent tension on the suture line ‡ Offer emotional support to the parents and family . the risk for vomiting & aspiration increases without crying because air entering the stomach from the fistula leads to distention ‡ Prepare the parents and neonate for surgical correction ‡ Provide post-op care as appropriate .‡ Provide comfort measures & institute measures to reduce the risk of neonate·s crying.

DEVELOPMENTAL DYSPLASIA OF THE HIP Description ‡ Refers to the improper formation & function of the hip socket ‡ Commonly called congenital hip dysplasia ‡ Causes the femur head to ride out of or dislocate from the acetabulum Pathophysiology ‡ Exact cause is unknown ‡ The acetabulum is flattened or too shallow ‡ As a result the head of the femur dislocates upward & backward .

or Pavlik harness ‡ Hip-spica cast & braces if other means prove ineffective ‡ Possiblr surgical correction ‡ Parent education about use of device for maintaining position . a Frejka pillow splint.Assessment findings ‡ Positive Ortholani·s sign ‡ Positive Barlow·s sign ‡ Shortened femur on affected side ² Galeazzi·s sign ‡ Asymmetrical gluteal folds ‡ Waddling gait Treatment ‡ Positioning & maintaining the head of the femur in the acetabulum with triple diapers.

especially areas under the device ‡ Offer emotional support & guidance to parents ‡ Encourage parents to interact w/ the neonate & hold the neonate even with a device in place ‡ Inform parents about the possibility of the need for surgical correction later on when the neonate is older. ‡ Maintain skin integrity .Teach the parents how to apply triple diaper.Show parents how to properly care for the skin. abducted position ‡ Instruct the parents in measures to position & maintain the head of the femur .Nursing interventions ‡ Maintain the affected hip in a flexed. a splint or a harness .

CONGENITAL SYPHILIS Description ‡ Results fro infection by the spirochete of Treponema pallidum ‡ Occurs when the spirochete crosses the placenta froma pregnant infected patient to her fetus ‡ Diagnosed with serologic tests at 3 to 6 months ‡ The development of antibodies is necessary to make a diagnosis .

soles. and palm Treatment ‡ Penicillin therapy ‡ Infection-control precautions ‡ Covering of neonatal hands to minimize skin trauma from scratching .Assessment findings ‡ Vesicular lesions on the soles and palms ‡ Irritability ‡ Small for gestational age ‡ Failure to thrive ‡ Rhinitis ‡ Red rash around mouth and anus ‡ Copper rash on face.

Nursing interventions ‡ Make sure all pregnant patients are screened for syphilis at the first prenatal visit ‡ Assist with laboratory testing (VDRL or rapid plasma reagin) on neonatal cord blood ro check for intrauterine exposure ‡ Administer drugs as ordered .

OPHTHALMIA NEONATORUM Description ‡ A severe eye infection that occurs in neonates at birth or during the first few months ‡ Results from exposure to the causative organism during vaginal delivery ‡ Most commonly cause by Neiserria gonorrhea or Chlamydia trachomatis ‡ Prophylactic administration of antibiotic ointment at birth to all neonates is a primary preventive strategy .

if untreated ‡ Culture of exudate reveals causative organism Treatment ‡ I.V. antibiotic therapy ‡ Standard & contact infection ² control precautions ‡ Sterile saline solution eye irrigation ‡ Treatment of mother for infection .Assessment findings ‡ Fiery red conjunctivae ‡ Thick purulent discharge from the eye ‡ Eyelid edema ‡ Corneal ulceration and destruction.

wear goggles is splashing is likely ‡ Advised the mother to receive treatment for her infection. also suggest treatment for the mother·s sexual partners .Nursing Interventions ‡ Administer prophylactic antibiotic eye ointment to all neonates after delivery ‡ Monitor the appearance of the eyes for redness and drainage ‡ Institute standard and contact precautions ‡ Perform eye irrigation as ordered.

which causes potentially harmful pressure on the brain tissue ‡ Compression of brain tissue and cerebral blood vessels may lead to ischemia and. eventually.Non-communicating hydrocephalus occurs as a result of obstruction of CSF flow .HYDROCEPHALUS ‡ An excessive accumulation of CSF within the ventricular spaces of the brain ‡ This accumulation leads to dilation of ventricles. cell death ‡ May be communicating or non-communicating: .Communicating hydrocephalus results from faulty absorption of CSF .

‡ Causes of hydrocephalus aren·t well understood.Complications of preterm birth such as intraventricular hemorrhage .Tumors . such as spina bifida and enancephalocele .Prenatal maternal infection .Traumatic head injury .Subarachnoid hemorrhage .Neural tube defects. possible causes include: .Genetic inheritance .Meningitis .

CSF production is increased.Pathophysiology ‡ With hydrocephalus. ‡ As a result. or reabsorption is altered. flow is obstructed. intracranial pressure increases causing brain displacement or motor and mental damage Assessment findings ‡ Increased head circumference ‡ Bulging fontanels ‡ ´Sunset eyesµ ‡ Widened sutures .

shrill cry ‡ Projectile vomiting ‡ Feeding problems .‡ Forehead prominence ‡ Thin. shiny fragile-looking scalp skin ‡ Irritability ‡ Weakness ‡ Seizures ‡ Sluggish pupils with unequal response to light ‡ High-pitched.

‡ Monitor S/Sx of increasing ICP .Treatment ‡ Skin care to prevent breakdown and infection ‡ Careful head support during handling ‡ Measurement of head circumference ‡ Emotional support and education for the parents ‡ Assessment of neurologic status and progression of symptoms ‡ Shunt insertion to eliminate excess CSF ‡ Management of shunt and prevention of infection at the surgical site.

treatments and procedures . allowing extra time for feedings as necessary ‡ Provide meticulous skin care. frequent feedings. repositioning the neonate·s head often to reduce the risk of skin breakdown ‡ Teach the parents about the condition. reporting any changes ‡ Maintain adequate nutrition  Provide a flexible feeding schedule to accommodate schedule  Offer small.‡ Nursing Intervention ‡ Assess closely for S/Sx of increasing ICP ‡ Frequently measure HC.

‡ Provide the parents and family with emotional support ‡ Prepare the neonate for shunt insertion as indicated. monitoring the surgical site closely. including positioning the neonate on the unaffected side. complete all preoperative procedures and teaching ‡ Perform postoperative care. and obtaining head circumference .

fetus. Cytomegalovirus. or neonate Pathophysiology:  Infection results when the organisms cross the placenta or travel up through the birth canal  Once present. Rubella. Herpes virus type III) ‡ Can lead to serious complications in the embryo.TORCH SYNDROME ‡ Refers to a group of maternal infectious diseases (Toxoplasmosis. the organisms can cause severe problems with fetal growth and development .

severe congenital anomalies. neonatal deaths. seizures. deafness. retinochoroiditis. and coma  Maternal treatment involves anti-infective .TOXOPLASMOSIS ‡ Is transmitted to the fetus primarily via the mother¶s contact with contaminated cat box filler  A therapeutic abortion is recommended if the diagnosis is made before the 20th week of gestation  Effects include increased frequency of stillbirths.

intrauterine growth retardation. cataracts. and emotional support to for parents ‡ Women of childbearing age should be tested for immunity and vaccinated if necessary ‡ The neonate may persistently shed the virus for up to 1 year . and hearing impairment ‡ Management includes therapeutic abortion if the disease occurs during the first trimester.RUBELLA ‡ Is a chronic viral infection ‡ The greatest risk occurs within the first trimester ‡ Effects include congenital heart disease. mental retardation.

liver and blood ‡ Other effects include auditory difficulties and a birth weight that¶s small for gestational age .CYTOMEGALOVIRUS (CMV) ‡ CMV is a herpesvirus that can be transmitted from an asymptomatic mother transplacentally to the fetus or via the cervix to the neonate at delivery ‡ It¶s the most common cause of viral infections in fetuses ‡ CMV is a common cause of mental retardation ‡ Principal sites of damage are the brain.

‡ The neonate may also demonstrate a characteristic pattern of petechiae called BLUEBERRY MUFFIN SYNDROME ‡ antiviral drugs cant prevent CMV or treat the neonate .

increased temperament.V. seizures. and characteristic vesicular lesions ‡ a cesarean delivery can protect the fetus from infection ‡ Pharmacologic treatment may include acyclovir and vidarabine I. after exposure .HERPESVIRUS TYPE II ‡ The fetus can be exposed to the herpesvirus through indirect contact with infected genitals or via direct contact with those tissues during delivery ‡ Affected neonates may be asymptomatic for 2 to 12 days but then may develop jaundice.

fragile retinal blood vessels  Subsequent rupture of vessels occur with partial or complete retinal detachment .RETINOPATHY OF PRETERM BIRTH ‡ Refers to an alteration in vision leading to partial or total blindness ‡ Typically results from prolonged exposure to high concentrations of oxygen or fluctuations in oxygen administration levels Pathophysiology:  High concentrations lead to vasoconstriction of immature retinal blood vessels  Fluctuating oxygen administration levels lead to rapid vasodilation and vasoconstriction of immature.

E (reduces the incidence of retinopathy or prematurity by modifying tissues¶ response to effects of oxygen)  Cryosurgery or laser surgery . which are evident upon ophthalmologic examination Treatment  Monitoring of oxygen concentration  Monitoring ABG levels  Monitoring of transcutaneous oxygen levels and pulse oximetry  Ophthalmologic examinations at regular intervals during and after hospitalization  Administration of vit.Assessment Findings  Include retinal changes.

Nursing Interventions  Closely monitor oxygen concentration levels being administered; obtain transcutaneous oxygen and ABG levels and pulse oximetry readings as ordered  Administer oxygen carefully, ensuring that the lowest concentration necessary is being used  Explain the condition and its treatments to the parents  Instruct the parents in the need for follow-up eye examination  Provide preoperative and postoperative care as indicated

FETAL ALCOHOL SYNDROME (FAS)
‡ A cluster of birth defects (growth retardation, CNS abnormalities, and facial malformations) resulting from in utero exposure to alcohol. ‡ Commonly found in neonates of patients who ingested varying amounts of alcohol during pregnancy ‡ Birth defects associated with prenatal alcohol exposure can develop in the first 3 to 8 weeks of pregnancy before a woman even knows she¶s pregnant.

‡ The risk of teratogenic effects increases proportionally with increased daily alcohol intake ‡ No safe level of alcohol intake during pregnancy has been established ‡ FAS has been detected in neonates of moderate drinkers (7 to 2 oz or 30 to 59 ml of alcohol daily. PATHOPHYSIOLOGY  Alcohol is teratogenic substance that¶s particularly dangerous during critical periods of organogenesis  alcohol interferes with the passage of amino

 When a pregnant woman ingests alcohol, so does her unborn child  Alcohol crosses through the placenta and enters the blood supply of the fetus  Alcohol interferes with healthy development of the fetus  Variables that affect the extent of damage caused to the fetus by alcohol include the amount of alcohol consumed, timing of consumption, and pattern of alcohol use

ASSESSMENT FINDINGS  Prenatal and postnatal growth retardation  Characteristic findings within the first 24 hours of life  Difficulty establishing respirations  Irritability  Lethargy  Seizure activity  Tremulousness  Opisthotonos  Poor sucking reflex  Abdominal distention

receding jaw ‡ CNS dysfunction. such as microcephaly. uptumed. ptosis.short palpebral fissures. and Eyes . neurologic abnormalities such as decreased muscle tone. strabismus. and small brain . including decreased IQ. flat or absent groove above upper lip Mouth ± thin upper lip. maxillary hypoplasia. poor coordination. myopia Nose ± short.‡ Facial anomalies. developmental delays. learning disabilities. microophthalmia.

TREATMENT  Prevention through public education  Careful prenatal history and education  Identification of women at risk. with referral to alcohol treatment centers if necessary  Prompt identification of neonates with FAS to ensure early intervention and appropriate referrals .

NURSING INTERVENTIONS ‡ Institute measures for prevention  Increase public awareness about the dangers of alcohol consumption during pregnancy  Ensure increased access to prenatal care  Provide educational programs  Assist with screening women of reproductive age for alcohol problems  Use appropriate resources and strategies for decreasing alcohol use ‡ Closely assess any neonate born to a mother who has used alcohol .

including assessing breath sounds frequently. assist with developing measures to enhance neonate¶s intake ‡ Monitor weight and measure intake and output ‡ Promote parent-neonate attachment  Encourage frequent visiting and rooming in if possible  Encourage physical contact between the parents and the neonate  Educate parents about neonate¶s complications ‡ Provide emotional support .‡ Prevent and treat respiratory distress. being alert for signs of distress. and suctioning as needed ‡ Encourage successful feeding.

DRUG ADDICTION .

APNEA .

PRETERM BIRTH ‡ Born before the 38th week gestation or at 37 weeks or less .

sucking is weaker. nails are soft. and there is general weakness with sluggish movements.CHARACTERISTICS:  Weight is less than 2500 gm (2350 gm for Filipinos) and the length is less than 47 cm at birth  The cry is more feeble. physiologic weight loss is exaggerated . they often assume frog-like position  Scarf sign ± elbow passes the midline of the body  Square window wrist ± wrist at a 90o angle  There is abundance of lanugo.

minimal amount/ underdeveloped of subcutaneous tissue to act insulation. NEED: to place inside the incubator with temperature regulated to 33.3 ± 34. humidity of 55-56%.  The head appears relatively large. and frequent positioning on the right side to promote closure of the foramen ovale. Skin is thin and wrinkled.4oC. but the circumference is less than 33 cm with a characteristic wizened facie  Are poikilothermic (easily take on the temperature of the environment) .

SMALL FOR GESTATIONAL AGE ‡ Birth weight is less than expected for the specific gestational age. babies born on the 38th week of gestation who wiehgs 5 lbs . e.g.

‡ . baby born on the 36th week of gestation who weighs 8 lbs.. e.LARGE FOR GESTATIONAL AGE ‡ Birth weight is more than expected for the specific gestational age.g.

POSTMATURITY .

HUMAN IMMUNODEFICIENCY VIRUS INFECTION .

GENETIC DISORDERS .

‡ GENETICS ± is the study of heredity. including the tendency to develop certain diseases. .  Physical traits such as eye color are inherited as well as biochemical and physiological traits. the passing of traits from parents to their children.

or ova. .‡ INHERITANCE  Inherited traits are transmitted from parents of offspring through genes in germ cells.  DNA is a long molecule that is made up of thousands of segments called genes. Each of the traits a person inherits ± from blood type to toe shape and a myriad of others in between ± is coded in their genes.  Human gametes are eggs.  A person¶s genetic make-up is determined at fertilization.  Each chromosome contains a strand of genetic material called DNA.  In the nucleus of each germ cell are structures called chromosomes. and sperm. or gametes.

the corresponding chromosomes pair up.  When ovum and sperm unites. each 46 chromosome produces an exact duplicate of itself. .  The fertilized cell soon undergoes cell division (mitosis). The cell then divides and each new cell receives one set of 46 chromosomes.  The ova and sperm are formed by a different cell division process called meiosis.‡ HUMAN CHROMOSOMES  A human ovum and a sperm contains 23 chromosomes.  In mitosis.  Each cell in a person¶s body (except the ova and sperm) contains 46 identical chromosomes. The result is a fertilized cell with 46 chromosomes in the nucleus.

This allows each of the thousands of genes in an ovum to join the corresponding gene from a sperm when the chromosomes pair up at fertilization. ‡ The locus of each gene is specific and does not vary from person to person.‡ The location of a gene on a chromosome is called LOCUS. .

‡ When a gene mutates. ‡ Gene mutations in a gamete may be transmitted during reproduction. AND MULTIFACTORIAL GENETIC DISORDERS. .GENETIC MUTATION ‡ A mutation is a permanent change in genetic material. it may produce a trait that is different from its original trait. Some mutations cause serious or deadly disorders that occur in three different forms: SINGLEGENE DISORDERS. CHROMOSOMAL DISORDERS.

most heredity disorders are caused by autosomal defects. recessive genes do not produce abnormal traits unless both parents have the gene pass them to their offspring. Because there are 22 pairs of autosomes and only 1 pair of sex chromosomes. ‡ Dominant genes produce abnormal traits in offspring even if only one parent has the gene. .SINGLE-GENE DISORDERS ‡ are inherited in clearly identifiable patterns. sex-linked inheritance. ‡ In a third inheritance pattern. Two important inheritance patterns are called autosomal dominant and autosomal recessive. single-gene disorders are passed through the X chromosome.

‡ one of the parents is also usually affected. and if one parent is affected. and ‡ if both parents are affected.Autosomal Dominant Inheritance ‡ Male and female offspring are affected equally. Marfan syndrome .g. ‡ e. all of the children will be affected. the children have a 50% chance of being affected.

each of the offspring have a one in two chance of being affected and if certain autosomal recessive conditions are more common in specific ethnic groups. ‡ In many cases. cystic fibrosis in Whites & sickle cell anemia in Blacks.Autosomal Recessive Inheritance ‡ Male and female offspring are affected equally.. and ‡ If both parents are affected. ‡ If one parent is affected and the other is not a carrier.g. ‡ If both parents are unaffected but heterozygous for the trait (carriers). all of the offspring will be unaffected but will carry the altered gene. may be indicative that client has a ³negative family history´ . no evidence of the trait appears in past generation. ‡ If one parent is affected and the other is a carrier. e. all of their offspring will be affected. each of their offspring has a one in four chance of being affected.

‡ Because female receive two X chromosomes (one from each parent). the terms X-linked and sex-linked are interchangeable. or heterozygous. ‡ Because males have only one X-chromosome. a single X-linked recessive gene can cause disease in a male. they can be homozygous for a disease allele. In comparison.Sex-Linked Inheritance ‡ Because Y chromosome is not known to carry diseasecausing genes. a female needs two copies of diseased gene. . Therefore. males are more commonly affected by X-linked recessive diseases than female.

The family history may show miscarriages and the predominance of female offspring. . ‡ If a mother has a X-linked dominant disorder. there¶s a 50% chance that each of her children will be affected.X-linked Dominant Inheritance ‡ A person with the abnormal trait typically will have one affected parent. all of his daughters and none of his sons will be affected. and in X-linked dominant disorders are commonly lethal in males (prenatal or neonatal deaths). if the father has a X-linked dominant disorder. ‡ Evidence of the inherited trait most commonly appears in the family history.

‡ Unaffected sons cant transmit the disorder and the unaffected male children of a female carrier don¶t transmit the disorder.X-linked Recessive Inheritance ‡ In most cases. ‡ Sons of an affected male are unaffected.g. the father is affected and the mother is a carrier. ‡ In rare cases. affected people are males with unaffected parents.. ‡ e. ‡ All of the daughters of an affected male will be carriers. Hemophilia .

an endless variety of clinical manifestations may occur. . rearrangement. or exchange of genes. addition. ‡ If the remaining genetic material is sufficient to maintain life.CHROMOSOMAL DISORDERS ‡ May also be caused by chromosomal aberrations ± deviations in either the structure or the number of chromosomes. ‡ Deviations involve the loss.

. result in mosaicism. chromosomes normally separate in a process called disjunction. The effect on the offspring depends on the percentage of normal cells. Failure to do so ± is called disjunction ± causes an equal distribution of chromosomes between the two resulting cells. ‡ Gain or loss of the chromosomes is usually due to nondisjunction of autosomes or sex chromosomes during meiosis ‡ May occur during very early cell divisions after fertilization and may or may not involve all the resulting cells. some with a specific chromosome aberration and some with normal cells. A mixture of cells.Nondisjunction ‡ During cell division.

Fertilization of an ovum with a chromosome aberration by a sperm with a chromosome aberration usually does not occur. . ‡ A cell that contains one extra chromosome is called TRISOMY. Miscarriages cal also result from chromosomal aberrations.‡ The incidence of nondisjunction increases with parental age. ‡ A cell that contains one fewer than the normal number of chromosomes is called MONOSOMY. ‡ If the monosomy involves an autosome. the name of the affected cell contains the suffix ³somy´. However. the cell will be nonvisible. monosomy X can be viable and result in a female who has Turner¶s syndrome. ‡ When chromosomes are gained or lost.

. such as partial monosomie or partial trisomies. Parental age doesn¶t seem to be a factor. The children of parents with balanced translocations may have serious chromosomal aberrations. there are visible or measurable abnormalities. When the rearrangements preserve the normal amount of genetic material (balanced translocation). typically. ‡ When the rearrangements alter the amount of genetic material.Translocation ‡ Is the shifting or moving of a chromosome. It occurs when chromosomes break and rejoin in an abnormal arrangement. there are usually no visible abnormalities.

maternal infections during pregnancy or existing diseases in the mother. and poor-quality prenatal care. cleft palate.MULTIFACTORIAL DISORDERS ‡ Disorders caused by both genetic and environmental factors. and myelomeningocele. use of chemicals by father and mother. maternal or parental exposure to radiation. maternal nutrition or parental health. maternal smoking. maternal-fetal blood incompatibility. . high altitude. ‡ Examples are cleft lip. ‡ Environmental factors that contribute include: maternal age.

ACHONDROPLASIA ‡ Is a genetic condition that results in abnormally short stature with disproportionately short limb. ‡ The average height of an adult is 131 cm (52 inches. or 4¶4´) in males and 124 cm (49 inches or 4¶1´) in females. .

CLEFT LIP .

CLEFT PALATE .

CYSTIC FIBROSIS .

CYSTINURIA .

EHLERS-DANLOS SYNDROME .

HEMOPHILIA .

HUNTINGTON·S DISEASE .

JACOB·S SYNDROME .

KLINEFELTER·S SYNDROME .

LESCH-NYHAN SYNDROME .

MARFAN SYNDROME .

MUCOOPOLYSACCHARIDOSES .

MUSCULAR DYSTROPHY .

NEUROFIBROMATOSIS .

OSTEOGENESIS IMPERFECTA .

POLYCYSTIC KIDNEY DISEASE .

SICKLE CELL ANEMIA .

TAY SACH·S DISEASE .

TRISOMY 21 (DOWN·S SYNDROME) .

TRISOMY 13 (PATAU SYNDROME) .

TRISOMY 18 (EDWARD·S SYNDROME) .

TURNER SYNDROME .

XXX (TRIPLE X) SYNDROME .

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