PROBLEMS COLLABORATIVE of the NEWBORN
Dysmaturity Syndrome
Placental function deterioration in postterm pregnancies which causes interference w/oxygen & nutrient supply. This results in hypoxia & malnourishment in the fetus. Also known as postmaturity syndrome 6-12% of pregnancies go postterm postterm infants have a 2-3 x higher perinatal mortality rate than infants born at term major concern is how well placenta functions during the last wks of pregnancy
Postmature Infants Look like babies who are 1-3 weeks old Skin is typically dry and cracked May have long hair and nails. May have meconium stained finger nails d/t meconium release in utero. May weigh more than a term infant, but often appear physically wasted. They can look malnourished d/t uteroplacental insufficiency. Lack of SQ fat due to intrauterine deprivation (poorly functioning placenta). Placenta is old, becomes calcified. Prone to meconium aspiration syndrome: if baby gets hypoxic (from aged placenta), rectal sphincter relaxes causing meconium release. May give amnio infusion to reduce effects of meconium aspiration. Post term infants with oligohydramnios are prone to cord compression Prone to problems associated with their macrosomia (shoulder dystocia, prolonged birth) ----------------------------------------------------------------------------------------------
Preterm Infants
Account for the largest # of admissions to NICU Typically very small, minimal SQ fat (brown fat) Immaturity affects every body system More prone to ineffective thermoregulation: d/t minimal brown fat. Also have friable (easily broken or pulverized) capillaries. Poor muscle tone. More prone to respiratory distress: caused by insufficient production of surfactant, which is needed to keep alveoli open during exhalation. Periodic breathing with 5-10 seconds of respiratory pauses is normal. More prone to hyperbilirubinemia More prone to hypoglycemia ----------------------------------------------------------------------------------------------
Kangaroo Care
Method of providing skin-to-skin contact between preterm infants and their parents. Begin ASAP. Infant, wearing only a diaper and hat, is placed under the mothers clothes between her breasts. Increases attachment. Infants better able to maintain temperature. Also, more stable heart rates and oxygen saturation levels. Found safe for stable infants, even if intubated. May breastfeed if they wish & if infant is able 1
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Bilirubin
Although newborns liver is able to conjugate bilirubin, it may not be mature enough to prevent development of jaundice during the first week of life. Jaundice occurs in 60% of term & 80% of preterm Principle source of bilirubin is hemolysis of RBCs. This is a normal occurrence after birth, when fewer RBCs are needed than during fetal life. Only bilirubin remains as an unusable residue in the blood. It is toxic to the body and must be excreted. Hemoglobin is split into heme and globin: globin is used by the body, heme is converted into unconjugated bilirubin (indirect) Unconjugated/indirect bilirubin is not water-soluble but fat-soluble. The liver must change it to a water-soluble form by a process called conjugation before excretion can occur. When unconjugated bilirubin is released into the blood stream, it attaches to binding sites on albumin in the plasma and is carried to the liver. There, unconjugated bilirubin is converted to conjugated bilirubin. Conjugated bilirubin is excreted into the bile and then into the duodenum. In the intestines, the normal flora acts on bilirubin to reduce it to urobilinogen, which is excreted in stool. Because unconjugated bilirubin is fat-soluble, it may be absorbed by sub Q fat, causing a yellowish discoloration of skin. If enough unconjugated bilirubin accumulates in the blood, staining of the brain may occur (kernicterus) and may result in bilirubin encephalopathy which causes severe brain damage.
Hyperbilirubinemia
Refers to excessive accumulation of bilirubin in the blood Characterized by jaundice/icterus: yellow discoloration of skin & other organs. @ higher levels, sclera will be jaundiced. Typically benign, but may indicate a pathologic state. Almost all infants experience elevated bilirubin levels. Due to fact that neonate has large circulating volume of RBCs & immature liver RBCs have a shorter lifespan (40-90 days) than adult RBCs (120 days).
Physiologic vs. Pathologic Jaundice
Physiologic Jaundice: transient hyperbilirubinemia that usually begins around 2nd day after birth &that occurs for any number of reasons: excess production of bilirubin (bilirubin is produced in infants during 1 st 2 wks of life at a rate twice that in adults), fetal red blood cells break down more quickly than do adults, newborns immature liver may not produce adequate amounts of glycuronyl transferase (converts unconjugated to conjugated), intestines of newborns are sterile and bilirubin cant be reduced to urobilinogen, delayed feeding: feeding helps establish normal intestinal flora. Early frequent feedings keep bili level down because stimulates intestinal peristalsis to excrete meconium. Meco-nium causes bili levels to increase. Passage of meconium within 24 hrs is very important. trauma during birth may result in increased hemolysis of RBCs: use of forceps, vacuum extractor, or creation of cephalhematomas. fatty acids released during brown fat breakdown in response to cold stress have a greater affinity than bilirubin for binding sites on albumin & bind to albumin in place of bilirubin. Physiologic Jaundice becomes visible when serum bilirubin reaches 5-7 mg/dl. And any reading under 12 mg/dl is considered benign. Pathologic Jaundice: bilirubin levels over 12 mg/dl. Abnormal & must be differentiated from physiologic. One of the most important differences is the time at which jaundice appears. Pathologic jaundice occurs during the first 24 hours after birth or persists beyond 7 days, whereas physiologic never occurs that early. It is due to abnormalities causing excessive RBC 2
destruction. These abnormalities include: o Hemolytic disease of the newborn caused by incompatibilities between mothers blood and fetus. The best known cause is Rh incompatibility. Also, ABO incompatibilities. o Infection/sepsis o Cold stress o Metabolic disorders Nursing Care of Hyperbilirubinemia Observe for evidence of jaundice Look at overall color Apply direct pressure to skin to cause blanching Dark skinned infants: note color of sclera, conjunctiva, oral mucosa. Can still blanch on darkskinned infants. Use bilimeter Lab Work Total Direct Bilirubin level (dont have to know these numbers for the test) 12 mg/dl 24 48 hours old 15 mg/dl 49 72 hours old 17 mg/dl > 72 hours old TREAT!! Direct Coombs test on cord blood. Positive result indicates detection of maternal antibodies attached to fetal/neonatal RBCs. Follow up with serum bilirubin levels. Complications of Hyperbilirubinemia Bilirubin encephalopathy (Kernicterus): brain stained yellow. At term, total serum bilirubin over 25 mg/dl Syndrome of severe brain damage Results from deposition of unconjugated bilirubin in brain cells May result in irreversible brain damage May manifest as cerebral palsy, seizure disorder, mental retardation Implementation of Nursing Care Phototherapy (aka: ,,bili lights) commonly used. SE of phototherapy: loose green stools d/t ^^ bile flow & peristalsis. This is desired result: it leads to more rapid excretion of excess bilirubin. Phototherapy may cause temporary lactose intolerance. Some may need lactose-free formula During phototherapy, bilirubin in the skin absorbs the light and changes into water-soluble products that dont require conjugation by liver and can be excreted in bile & urine. Place infant under light source with frequent repositioning Eye mask on @ all times. Also, must keep diaper on them. Genitals and eyes will burn up. Monitor temperature carefully Observe skin for evidence of dehydration and drying Keep clean & educate parents Must feed at least Q 2-3 hrs to keep well hydrated. Also, must increase amount of feeding by additional 20 ccs. Also helps to push bile thru intestines. ----------------------------------------------------------------------------------------------
Hemolytic Disease of the Newborn
Erythroblastosis fetalis: excessive destruction of erythrocytes (mature RBCs capable of carrying oxygen) & the proliferation of erythroblasts (immature RBCs, incapable of carrying oxygen). Because of rapid hemolysis of erythrocytes, bilirubin increases markedly. The fetus becomes anemic, jaundiced, & edematous (hydrops fetalis). This is usually due to incompatibility of maternal and fetal blood types. In most cases, the fetus is Rh+ and the mother is Rh-. Occurs w/Rh or ABO incompatibility The more severe of the two is Rh incompatibility which is also known as isoimmunization. 3
Pathophysiology of Hemolytic Disease in Newborn Rh- mom forms antibodies to Rh+ positive fetus. Or, when mom has O type blood and baby has any combination of AB. Antibodies cross placenta to attack & destroy fetal RBCs. In utero, fetus accelerates erythropoiesis (RBC formation) Immature RBCs (erythroblasts) appear in fetal circulation. These RBCs cannot carry oxygen. Term erythroblastosis fetalis derived from presence of immature RBCs. Mom will get shot of RhoGam (immune globulin) to prevent her from forming antibodies against Rh+ fetal blood. This greatly decreases incidence of erythroblastosis fetalis. Given at 28 wks as preventative measure and again within 72 hours after birth if she is still unsensitized to prevent development of antibodies that might affect subsequent pregnancies. Most severe form of disease, hydrops fetalis
Hydrops Fetalis
Heart failure & generalized edema in the fetus secondary to severe anemia resulting from destruction of erythrocytes Progressive hemolysis causes Fetal hypoxia Cardiac failure, generalized edema Effusions into pericardial, pleural, & peritoneal spaces Fetus may be delivered stillborn or in severe respiratory distress. Placenta is often edematous which, along with edematous fetus, can cause overdistention rupture & of uterus. Post Delivery Signs & Symptoms Jaundice appears within 24 hours after birth Hepatosplenomegaly may be present Severe cases o Signs of anemia (marked pallor) o Hypovolemic shock o Symptoms present at birth Therapeutic Management Aimed at prevention Use of RhoGAM injections May have to give exchange transfusions in the case of hydrops fetalis. Exchange transfusions are necessary when phototherapy doesnt reduce dangerously high bili levels quickly enough. This treatment removes sensitized RBCs before they break down & release large amts of unconjugated bili. Also removes antibodies and unconjugated bili in blood & corrects severe anemia. Nursing Care May have to give exchange transfusion if severe. Monitor for reactions: Electrolyte imbalance Infxn Hyper or hypovolemia Cardiac arrhythmias Increase or decrease in BG Decreased perfusion to intestines Bleeding Thrombosis or embolism Do labs before and after exchange transfusions: CBC Bili level Ca level 4
Watch thermoregulation (procedure occurs under radiant warmer) If cold stressed, neonate increases O2 and glucose consumption, causing metabolic acidosis ----------------------------------------------------------------------------------------------
Respiratory Distress Syndrome (RDS)
Name applied to respiratory dysfunction in neonates Primarily related to developmental delay in lung maturation. Insufficient production of surfactant. When there is too little surfactant, alveoli collapse each time the infant exhales. And they resist reexpansion. Severe retractions will occur with each breath. Common in premature infants May be caused by sepsis, exposure to cold, hypoglycemia Pathophysiology of RDS At birth, infants must initiate breathing and keep their lungs inflated with air. Central factor responsible for this adaptation is surfactant. Surfactant Phospholipid secreted by alveolar epithelium Reduces surface tension in alveoli Results in uniform expansion and maintenance of lung expansion. Without surfactant, lungs dont remain inflated and infant must exert great deal of effort with each subsequent breath to reinflate the lungs. They use more oxygen & more energy. This leads to exhaustion. Deficient surfactant causes unequal inflation of alveoli on inspiration and collapse of alveoli on expiration. Severe retractions occur w/each breath, drawing weak muscles of chest wall inward. The resulting pressure on the lungs further interferes with expansion. May cause return to fetal circulation patterns. Eventually leads to widespread atelectasis, hypoxemia, hypercapnia, and lowered pH. This leads to acidosis. This is usually more of a problem in preterm infants. They will put an e-tube down and put surfactant down tube. Therapeutic Management of RDS Maintain adequate ventilation and oxygenation, maintain acid-base balance, neutral thermal environment (keep them warm), adequate hydration & electrolyte status. Surfactant replacement therapy (via ET tube) Signs/Symptoms of RDS Tachypnea (>70), dyspnea Pronounced retractions Fine inspiratory rales Audible expiratory grunt Flaring of the external nares Cyanosis &/or pallor, poor color
RDS Nursing Care Based on good assessment of respiratory status: watch heart monitor Observe/assess infants response to therapy: watch for bradycardia Watch thermoregulation of infant Suction prn, but not routinely. Too much may cause soft tissue damage leading to edema. Maintain patent airway! ----------------------------------------------------------------------------------------------
Transient Tachypnea of the Newborn (TTN)
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Condition of rapid respirations due to inadequate absorption of fetal lung fluid by pulmonary capillaries & lymph vessels. This causes decreased lung compliance and air trapping and brings about signs similar to respiratory distress syndrome. it is possible for them to progress to RDS. Noted soon after birth, lasts 24 to 72 hours More common in prematurity (mild immaturity of surfactant production); C/S; babies of diabetic mothers, mothers who smoke; SGA, maternal analgesia, asphyxia. Signs/Symptoms Rapid, labored breathing (tachypnea) of more than 60 breaths a minute Grunting or moaning sounds when the baby exhales Flaring nostrils or head bobbing Retractions (when the skin pulls in between the ribs or under the ribcage during rapid or labored breathing). Subclavicular retractions are REALLY serious. Cyanosis around the mouth and nose Diagnosing TTN Chest x-ray Pulse oximetry CBC Arterial blood gas Treating TTN Respiratory support IV Antibiotics Dont nipple feed if RR > 70 d/t risk for aspiration. Gavage feed via NG tube. If RR persists, start IV and give fluids, keep NPO. ----------------------------------------------------------------------------------------------
Meconium Aspiration Syndrome (MAS)
Occurs most often in postterm infants who have decreased amniotic fluid and are prone to cord compression. Also occurs in infants who have suffered intrauterine asphyxia which causes anal sphincter to relax. If aspirated, can lead to airway obstruction. This may be complete or partial. In partial, air can enter but not escape from alveoli. This results in air trapping. In addition, meconium is irritating to lung tissue and causes an inflammatory reaction and chemical pneumonitis. Creates environment for infection Treatment Amnio infusion prior to delivery to dilute meconium amniotic fluid. Surfactant lavages after birth Thorough suctioning after delivery of head but before delivery of rest of body. Get it out before infant takes first breath and draws it in deep. Oxygen support ---------------------------------------------------------------------------------------------6
Neonatal Sepsis
Systemic infection with bacteria in the bloodstream Neonates more susceptible d/t immature immune system. They have decreased ability to localize infxn allowing infxn to spread from one organ to another. The blood-brain barrier is less effective in keeping out organisms, so there is greater chance for CNS infxn. Bacterial infection can be acquired prenatally or during labor from infected amniotic fluid, across the placenta, or by direct contact with maternal tissue during birth. Most common causative agents: GBS & e. coli May be caused by complications of labor such as prolonged rupture of membranes, prolonged labor, or chorioamnionitis. May be caused by exposure to organisms during 1 st few days of life. Diagnosing Neonatal Sepsis Characterized by subtle, vague, nonspecific physical signs. Hard to dx. Confirmed by lab examination (blood cultures) Signs/Symptoms Infant "not doing well" Poor temperature control (up or down) Pallor, cyanosis, mottling Cool, clammy skin Abnormal heart rate, respiratory distress Lethargy, hypotonic Irritability, tremors, seizures Full/bulging fontanel Poor feeding leading to hypoglycemia Vomiting, diarrhea Jaundice, purpura, petechiae, ecchymoses
Medical Management Aimed at circulatory/respiratory support Antibiotic therapy Isolation of infant Nursing Care of Neonatal Sepsis Good assessment know maternal history (GBS status, fever d/t chorioamnionitis, PROM) and course in labor & delivery Observe infants carefully for changes in condition IV therapy, antibiotics Decrease stress to baby: good hydration & neutral thermal environment ----------------------------------------------------------------------------------------------
INFANTS OF DIABETIC MOTHERS
Pathophysiology 7
Tend to become hypoglycemic after birth Due to transient state of hyperinsulinism Infant still responding as though receiving high levels of maternal glucose Precipitous drops in blood glucose levels can cause serious neurologic damage or death.
Nursing Care Infant is LGA (large for gestational age) Observe for hypoglycemia Check blood glucose on admit and per protocol, check prn Provide early feeds d/t hypoglycemia Prevent cold stress: all available glucose may be depleted to increase metabolism and raise body temperature. Educate parents S&S of Hypoglycemia in the Neonate Hyperirritability, tremors, jitteriness Irregular respiratory effort Cyanosis Weak, high-pitched cry
Diaphoresis Feeding difficulty, hunger Lethargy, hypotonia ----------------------------------------------------------------------------------------------
Infants of Substance Abusing Mothers
Cocaine CNS stimulant: blocks presynaptic reuptake of neurotransmitters norepi & dopamine, producing excess of these @ nerve terminals. This produces a state of hyperarousal, euphoria. Side effects are hyperglycemia, anorexia, hyperthermia, & tachypnea. Cocaine is a cardio stimulant & vasoconstrictor that causes increased BP, heart rate, & demand for O2. Decreases uterine blood flow & stimulates uterine contractions. Increased incidence of spontaneous abortion, abruption (d/t cocaine-induced vasoconstriction of placental vessels), PROM, precipitous delivery Infants may look normal at birth OR may show neurologic problems. Neonatal S&S of Cocaine Exposure Will go into withdrawal in 2-3 days Neurotoxic symptoms can persist for 3-4 months Baby may have vomiting & diarrhea Baby may have lowered intellectual development Depression o Lethargy, hypotonia, difficult to arouse o Poor suck, weak cry Excitable behavior 8
o Hypertonicity, rigidity, irritability o High-pitched cry o Inability to be consoled inability to adapt to any kind of environmental change Nursing Care Providing adequate hydration, nutrition Comfort measures Optimal mother-baby attachment Assist mothers to begin drug rehab Alcohol (FAS) Leading cause of mental retardation (more cases than Downs or SB) Retards cell growth and division. Affects cell membranes and alters the organization of fetal tissue. Women with history of heavy drinking should be counseled Assist women to rehab, treatment Characteristics of FAS Specific facial features o flat midface o no philtrum o small head o thin upper lip o low-set ears Neurologic deficits: CNS impairment leading to mental retardation, high activity level, short attention span, and poor short term memory. Average IQ of 70. Growth retardation (growth restriction IUGR) Behavioral problems
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