High-Risk Newborns Are those whose incidence of illness (morbidity) & death (mortality) is increased because of prematurity, dysmaturity , postmaturity , congenital anomalies, acquired physical problems or birth complications .
Basic Nursing Actions in High-Risk Newborns Detect early Kept newborn warm. Provide immediate supportive care. Report/refer promptly.
Danger Signs of Newborn Distress Difficult respiration or tachypnea/increased rate (over 60/m in). The earliest sign of various problems, often respiratory in origin: asphyxia, respiratory distress, & sepsis Lethargy, failure to s uck: May be due to hypoglycemia, hypothermia, brain damage, sepsis & prematurity. Cyanosis (generalized or central) Central cyanosis that increases with crying, sucking or activity is likely because of a congenital heart defect. Central cyanosis that decreases with crying is most likely because of respiratory problem, often upper airway (nasal) obstruction. Excessive mucus/Drooling : A danger sign of congenital defect esophageal atresia or tracheoesophageal atresia. Assess for maternal polyhydramnios. Safety Alert : In suspected maternal polyhydramnios never place the NB in Trendelenburg position; instead elevate his head slightly. The most common type of esophageal atresia is the fistula type. Placing him with his down can drain gastric contents to the lungs via the fistula & can cause respiratory distress & aspiration pneumonia. Maintain a slight head-up position, frequent suctioning & NPO & refer promptly.
Danger Signs of Newborn Distress Sac or dimpling at the lower back over the lumbar region : spina bifida Safety Alert : Position the NB on his abdomen (prone position) or on his side (lateral) never supine; cover sac with sterile saline soak to keep it moist. Absent or sluggish moro reflex : Brain damage. Moro reflex is the best index of CNS integrity in the NB; its absence can signifiy brain damage or injury Twitching, seizures or tremors : hypoglycemia, brain damage Safety alert : For any suspicion of head/brain injury, never position the baby with the head down, as this will increase ICP & cause further brain damage. Prevent episodes of convulsion by gentle handling, & by decreasing environmental stimuli.
Danger Signs of Newborn Distress Bile-stained (greenish) vomitus : intestinal obstruction, intussusception, Hirschsprung’s disease . Safety alert : If there is any suspicion of GI obstruction do not feed infant ! And for any infant with vomiting or whatever type, prevent aspiration ! Yellowish discoloration of the sclera, skin in the first 24 hours : hemolytic disease or erythroblastosis fetalis Safety alert : The first thing to do when the NB is yellowish is to identify how old the NB is: jaundice in the first 24 hours is pathologic , whereas jaundice b/w 2 to 7 days is physiologic , due to fetal polycythemia & liver immaturity. Meconium staining of skin & nails : Chronic hypoxia (often from placental insufficiency in postmaturity ) if the amniotic fluid in cephalic presentation is meconium-stained; if only the amniotic fluid is meconium-stained & the infant’s skin & nails are not greenish, it means recent hypoxia/fetal distress. No passage of meconium in 1 to 2 days or meconium from an inappropriate opening (fistula): imperforate anus, the most common congenital anomaly that is compatible with life.
HIGH-RISKS CONDITIONS BIRTH INJURIES Head Injuries . The head is the most commonly injured part, as this is the biggest part of the baby’s body to pass through the narrow birth canal. It is also the most commonly presenting part. Caput succedaneum: presence of edematous fluid in the presenting part. Cause: pushing when the cervix is not yell fully – pressing fetal head against the soft cervix. Characteristics: bilateral, crosses suture line (not limited by cranial bones), self-resolving in a few days (3 to 5 days) with little symptoms. b. Cephalhematoma : presence of blood b/w the periosteum & the flat bones of the skull Cause: pressure from bony pelvis or blades of forceps Characteristics: unilateral, does not cross suture line (limited by cranial bones), disappears in a few weeks; may have jaundice as it resolves.
HIGH-RISKS CONDITIONS A. BIRTH INJURIES Head Injuries c. Intracranial hemorrhage Precipitating factors: forceps delivery, precipitate labor, premature birth (soft cranial bones) Signs: signs of increased ICP Tense, bulging fontanels High-pitched, shrill cry Projective vomiting Lethargy; failure to suck Twitchings /tremors Absent Moro reflex/startle reflex; the absence of this reflex indicates brain damage as this is best index of CNS integrity. Vital signs: decreased pulse & RR Nursing Implementation: Decreased environmental stimuli, gentle minimal handling & avoid Trendelenburg position, instead slight head elevation to 30 to 45 degrees.
HIGH-RISKS CONDITIONS A. BIRTH INJURIES 2. Nerve Injuries Facial Nerve Injury (Bell’s Palsy): 7 th cranial nerve injury Cause: Unknown; may be viral, autoimmune (congenital/acquired); may be acquired during labor from a difficult forceps delivery Signs: Complete paralysis of one side of the face – inability to move muscles on affected side – asymmetry in facial movements: Loss of expression on affected side Displacement of mouth toward unaffected side Inability to close eyelids (both or affected side only); only one eye is closed during sleep Forceps marked on the face; Complete recovery in 3 to 5 weeks in majority of cases
HIGH-RISKS CONDITIONS A. BIRTH INJURIES 2. Nerve Injuries Facial Nerve Injury (Bell’s Palsy): 7 th cranial nerve injury Nursing implementation Detect early: check for symmetry in the facial movements of infants delivered by forceps. Administer ordered drugs: corticosteroid to decrease edema & analgesic for pain Provide care to the affected eye: Artificial tears to prevent corneal drying Ointment & eye patch during sleep to keep eyelid closed Reassure parents that most cases are temporary.
HIGH-RISKS CONDITIONS A. BIRTH INJURIES 2. Nerve Injuries b. Brachial Nerve paralysis or upper arm paralysis/ ERB Duchenne Paralysis ( Erb’s Palsy); most common neurologic injury in NB’s Cause: Difficulty in rotating & delivering the shoulders (often because of the presence of large-sized babies – injury to the brachial nerve plexus or a subsequent injury to the fifth & sixth cervical nerves) Signs: In supine position. One or both arms extended with hand extension, unmoving (normally, flexed & moving) Decreased muscle tone, grasp reflex & negative arm recoil on the affected side – waiter’s sign Asymmetry in arm movements; incomplete tonic neck reflex (fencing); asymmetrical Moro reflex Prognosis: Majority of cases are resolved in 2 weeks of life Nursing Implementation Position at rest: Place arm gently in flexed position Arm support when holding Arm strengthening exercise that possibly flex & extend the arm Teach parents about position & simple exercises
HIGH-RISKS CONDITIONS A. BIRTH INJURIES 3. Bone Injury: clavicle fracture; clavicle – the bone most commonly injured in delivery & childhood Signs: Incomplete fracture – no pain or disability noticed at birth but a large callus will be discovered at fracture site by 2 to 3 weeks Complete fracture – signs evident at birth Refusal to move affected arm Tenderness at the site Crying with pain upon movement of the arm Hypermobility of the bone Hematoma & visible angulation Incomplete Moro reflex b. Diagnosis: X-ray
HIGH-RISKS CONDITIONS A. BIRTH INJURIES 3. Bone Injury c. Treatment: Figure – of – eight bandage &/or a triangular sling for about 2 weeks Remodeling of the bone, which corrects a residual deformity Completed in 6 months in the younger child Completed within 1 year in the older child (over 10 years) d. Nursing implementation: Apply appropriate sling or bandage Cotton or gauze placed in each axilla to protect the infant’s skin from rubbing against the bandage Tighten bandage daily to fit snugly around the shoulders Avoid lifting the affected arm Triangular sling to support the elbow to hold the arm up to prevent sagging of the shoulder Parental teaching: parents are asked to demonstrate positioning & handling of the infant in the sling during bathing, dressing & feeding; tightening & reapplication of it comes off
THE PREMATURE INFANT Born after 20 weeks & before 37 weeks’ gestation. A preterm is low in birth weight. A low in birth weight baby is one whose weight is 2.5 kg or less Risk Factors Maternal infection – viral/rubella Multiple/multifetal pregnancy Malnutrition Bleeding complications of pregnancy: placenta previa , abruption placenta PIH, DM, cardiac d/o PROM Severe isoimmunization Trauma Incompetent cervix
THE PREMATURE INFANT Assessment Findings Physical Appearance Old man’s facies Head: disproportionately large Hair: lanugo, fine, fuzzy Ears: flat Thorax: small Breast buds: 5 mm or below Abdomen: relatively large, protruding Testes: commonly undescended (cryptorchidism) Scrotum: pink, fine rugae ; labia: underveloped Skin: increased lanugo, thin & red & wrinkled, visible capillaries, decreased subcutaneous fats Muscle tone: poor Nails: soft
THE PREMATURE INFANT 2. Altered Physiology Respiratory system Poorly developed lungs/respiratory muscles Decreased surfactant – prone to atelectasis & respiratory distress syndrome (RDS) Difficulty breathing with apnea & cyanosis Poor/unstable chest walls – retractions Poor gag/cough reflex – aspiration b. Poor thermal control Poikilothermia : infant easily takes on the temperature of the environment; can stabilize temperature at a lower level 35 C - 36 C Decreased subcutaneous fats, muscle, fat & glycogen deposit Decreased activity; decreased sweat glands
THE PREMATURE INFANT 2. Altered Physiology c. Digestive system Poor sucking & swallowing (before 32 to 34 weeks) Small stomach – decreased gastric capacity Poor cardiac sphincter tone – vomiting/regurgitation Decreased enzymes – decreased tolerance Decreased bile salts – decreased digestion & absorption of fats & fat-soluble vitamins A,D,E & K Decreased ability to release insulin in response to glucose Poor glucose to glycogen conversion & vice-versa d. Liver function Decreased vitamin K – bleeding Decreased hemoglobin & blood production – anemia Poor bilirubin conjugation – hyperbilirubinemia Poor sugar storage & release – hypoglycemia
THE PREMATURE INFANT 2. Altered Physiology e. Renal system Decreased ability to conserve & excrete urine Decreased ability to concentrate urine – dehydration Decreased ability to acidify urine Increased sodium & decreased potassium excretion Imbalanced glomerular tubular function: (+) sugar, (+) protein, (+) amino acid and (+) sodium in the urine f. Nervous system Centers for vital function are poorly developed Poor reflexes Low responses to stimuli Poor muscle tone
THE PREMATURE INFANT g. Immune system No IgM & IgG at birth Decreased phagocytosis, chemotaxis (reaction to chemical stimuli) Decreased anti-inflammatory response due to decreased adrenal gland functioning h. Integumentary system Sensitive because of permeability & collagen instability Thin skin – increased risk of toxicity from topical applications Delayed skin pH recovery to acidity after washing 3. Associated problems Hyaline membrane disease (HMD) or respiratory distress syndrome (RDS) Hypothermia – decreased temperature below 36.5 C Hypoglycemia Sepsis Hyperbilirubinemia Bleeding & anemia Nutritional problems
THE PREMATURE INFANT D. Nursing Implementation Maintain respirations at less than 60/min Monitor pattern of respiration; check every 1 to 2 hours Suction gently as necessary Administer oxygen as ordered; frequently check concentration to prevent toxicity & blindness ( retrolental fibroplasia). Observe oxygen precautions. Auscultate lungs to assess expansion; turn every 1-2 hours for better lung expansion & to prevent exhaustion. Monitor for apnea; encourage breathing with gentle rubbing of back & feet Evaluate ABG results & electrolytes 2. Maintain thermoneural body temperature; prevent cold stress Maintain in incubator or radiant warmer if temperature is not stable as ordered; maintain appropriate humidity. Turn gently to increase body heat. Monitor temperature per axilla; maintain axillary temperature b/w 97 F and 99.5 F Keep dry; change wet diapers & blankets immediately Use heat source when bathing the infant. Wash small parts of the body one at a time, then dry first before proceeding to the next part.
THE PREMATURE INFANT D. Nursing Implementation 3. Meet nutritional, fluid & electrolytes needs: feed according to abilities Use “preemie” nipple if the baby is started bottle-feeding & has good sucking. Use small, rubber-tipped syringe or dropper if sucking is poor or if sucking causes too much fatigue & tachypnea Use gavage feeding as ordered for poor sucking & swallowing. Feed slowly & carefully as regurgitation & vomiting are more common in these infants. Monitor I&O, weight, passage of stools, signs of dehydration, hypoglycemia & hyperbilirubinemia Provide supplementary vitamins (particularly Vitamin C to prevent infection) & minerals, especially iron to prevent anemia, as ordered. Implement breastfeeding or use of mother’s pumped breast milk whenever appropriate. 4. Prevent bleeding Administer vitamin K injection as ordered Handle gently & carefully Monitor potential bleeding sites (umbilicus, injection sites, skin & urine)
THE PREMATURE INFANT D. Nursing Implementation 5. Prevent infection Implement meticulous handwashing before & after handling the infant. Handwashing is still the best way to prevent spread of nosocomial infection. Provide skin care giving special attention to the: Scalp (prevents “cradle cap”/seborrheic dermatitis) Periumbilical area (prevents omphalitis or inflammation of the cord) Creases at the perianal region (prevents “diaper rash”/ ammoniacal dermatitis) Monitor temperature Administer prophylactic antibiotic as ordered. Maintain high vitamin C, iron & protein formula as ordered to increase resistance to infection & promote growth & development. Provide meticulous but careful skin care & reposition to prevent breakdown.
THE PREMATURE INFANT D. Nursing Implementation 6. Provide support to the parents. Encourage verbalization of concerns, fears & anxiety. Provide complete explanations about treatments, procedures & plans as appropriate. Encourage involvement in the care of the infant. Encourage frequent visits. Promote confidence with infant care before discharge. Refer to self-help groups.
The Postmature Newborn Delivered after the completion of 42 weeks of pregnancy or one that exceeds 294 days, from the first day of the last menstrual period. Problems of the postmature newborns result from progressive inefficiency of an aging placenta. ASSESSMENT FINDINGS: Behavior: wide awake & mentally alert Skin features are secondary to prolonged malnutrition & dehydration Dry, cracked, desquamating, parchment-like appearance of the skin Yellowish-greenish from meconium staining Absent lanugo & vernix Depleted stored fats/subcutaneous tissues Old man’s look Long nails & scalp hair May have signs of distress due to aspiration of meconium (meconium aspiration syndrome) NURSING IMPLEMENTATION : Generally like the care given to premature infants
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease Difficult respiration due to deficient surfactant, leading to collapse lungs (atelectasis), which prevent adequate gas exchange. Etiology : immature lungs with decreased surfactant Incidence: Common in preterm NB’s, especially those weighing b/w 1000-1500 grams Incidence of this condition is also high in babies of diabetic mothers, babies delivered by CS, & those babies whose mothers had antepartum bleeding Complications/Associated Problems Hypoxia Retrolental fibroplasisa – from oxygen of high concentration, greater than 40% Atelectasis Bronchopulmonary dysplasia
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease ASSESSMENT FINDINGS: Use the Silverman-Anderson Scale for scoring difficult respiration. Score of 0-normal respiration ; score of 10-most difficult respiration, RDS Major signs Expiratory grunting – a major sign: late occurring Flaring of the nares – an early sign Retractions – sternal & intercostal due to the use of accessory muscles to aid respiration See-saw breathing: flattening of the chest during inspiration with bulging of the abdomen Tachypnea: rate of respirations is greater than 70/minute; an early sign
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease ASSESSMENT FINDINGS: 3. Minor signs Cyanosis Tachycardia Falling body temperature; color – pale gray Dyspnea Decreased activity level Respiratory acidosis On auscultation, fine rales & diminished breath sounds Decreased urine; edema of extremities Decreased muscle tone; absent bowel sounds Periods of apnea
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease DIAGNOSIS History Assessment findings (Silverman) Blood gas studies NURSING IMPLEMENTATION Keep airway patent/promote respiration Suction endotracheal tube 1 to 2 hours as needed. Suctioning time in the preterm is less than 5 seconds per suctioning Use a sterile catheter 2. Maintain & monitor oxygen concentration; maintain humidity. Maintain in a supine position with head slightly extended to improve respiratory function; do not hyperextend the neck.
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease NURSING IMPLEMENTATION 3. Administer prescribed oxygen under CPAP – continuous positive(oxygen) airway pressure. A mask or intubation can be used Administration by a mask fitted over the infant’s face: The bag should be compressed to supply oxygen by positive pressure at a rate of about 50 bursts a minute. A control valve should be used to ensure that pressure that does not exceed 44 cm H 2 O or the pressure may rupture the lung alveoli. Auscultate lungs simultaneously to be certain that oxygen reaches the lungs b. Administration by intubation (ET) – this method is used if administration by bag does not initiate spontaneous respirations after a minute’s trial Size – varies depending on the size of the infant (usually 10F to 20F) Extra gentleness when passing the ET to prevent hemorrhage due to the rupture of capillaries Before oxygen is given by ET, further aspiration should be done to ensure that swallowed maternal blood or mucus plug was not the reason for the infectivity of the mask.
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease NURSING IMPLEMENTATION Evaluate effectiveness of your measure: note rising of the chest (chest should raise & fall if the lungs are being filled). Oxygen is then given by infant respirator to control pressure. Pressures over 44 cm H 2 O should be used with extreme caution. Safety Alert: Mouth-to-Mouth Resuscitation is the wisest step when you are only one in the delivery room to establish respiration in an emergency situation & you are untrained in the use of ET Clear the airway. Use a bulb syringe. Place a clean piece of gauze over the infant’s mouth & nose. Begin mouth breathing at a rate of 40 per minute, utilizing only air in your mouth, delivering it with short, sharp puffs (prevents rupture of pulmonary alveoli or stomach). Allow the infant to exhale b/w each of your inhalations. 4. Frequent evaluation/monitoring: v/s, color, breath sounds, & blood gases
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease NURSING IMPLEMENTATION 5 . Maintain hydration & nutrition NPO for tachypnea Monitor I&O. daily weight Provide for IV therapy, gavage feeding or hyperalimentation . Gavage feeding : when infant is unable to suck or tires easily Measure the distance from the bridge of the nose to the ear to the xiphoid process against a No. 10 gavage tube & mark with a Kelly clamp to ensure the tube enters the stomach. Rationale : A tube passed too far will curl & end up in the esophagus & a tube not passed far enough will also end in the esophagus – aspiration of feedings into the lungs. Restrain or swaddle the infant loosely.
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease NURSING IMPLEMENTATION 5 . Maintain hydration & nutrition Lubricate the tip of the tube using sterile water (& NEVER an oil lubricant). Rationale: In accidental passing of the tube into the trachea, oil can be left in the trachea & can lead to lipoid pneumonia. The NB infant is a nose breather; therefore, pass tube through the mouth to lessen distress. Pass the catheter with gentle with gentle pressure to the point of the Kelly clamp. Check for position before any feeding is given. Rationale: To check for patency & to prevent aspiration: Remove the clamp & dip the proximal end of the tube into a glass of sterile water. If bubbles appear in the water with each expiration, the tube is in the trachea; therefore, remove & replace. Aspiration of the stomach contents; check pH; the best before any feeding is given. Instill with 1 -3 ml of air with a syringe into the tube, then listen with a stethoscope for air rushing into the stomach.
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease NURSING IMPLEMENTATION 5 . Maintain hydration & nutrition In gavage-feeding, the tube should not be elevated more than 12 inches above the infant’s abdomen to prevent a gravity flow that is too fast for the infant; never use a plunger of a syringe or bulb attachment to hurry feeding, as this can cause stomach overflow & aspiration. Provide a pacifier to suck during the gavage-feeding. After feeding, the tube is reclamped securely; & if this is a single feeding, gently but rapidly withdraw the tube. Rationale : Clamping before withdrawal prevents any milk remaining in the tube from flowing out as the tube is removed thus prevents aspiration. Hyperalimentation : meets the infant’s nutritional needs as this contains glucose, protein, vitamins, & electrolytes. Plasma transfusion may also be given to supply the infant with essential fatty acids & trace minerals.
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease NURSING IMPLEMENTATION 6. Prevent infection by: Handwashing Wearing proper attire: gown, bonnet, mask, gloves, googles as appropriate Taking antibiotics as ordered Avoiding exposure to infected personnel Isolating infected NB 7. Keep warm Maintain in isolette with high humidity Monitor temperature per axilla Prevent heat loss
Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease NURSING IMPLEMENTATION 8. Give supportive care to parents Allow verbalization of feelings & concerns Explain special procedures Inform of results & progress Encourage participation in care; provide support; provide positive feedback as appropriate 9. A special nursing concern is the prevention of respiratory distress syndrome by preventing prematurity. Prematurity is the leading cause of deaths in the neonatal period & hyaline membrane disease or RDS is the leading cause of deaths in premature NB. Other causes of premature deaths include infection, intracranial hemorrhage & congenital defects.
Hypoglycemia Decreased serum glucose. Normal value: 45 – 50 mg/100 mL. a blood glucose concentration of less than 35 mg/ dL , or a plasma glucose of less than 40 mg/ dL should be considered hypoglycemic, although this has not been correlated with severity of symptoms. Onset: First 12 hours of life (may be as early as 2 to 3 hours, or as later as 48 hours after birth). Earlier in the infant of a diabetic mother: 1 hour after birth. Risk Factors: Intrauterine growth retardation NB of diabetic mother Hemolytic disease Birth trauma Hypothermia Sepsis Hypoxia & asphyxia Developmental defects Lack of oral intake/prolonged NPO
Hypoglycemia ASSESSMENT FINDINGS Tremors & jitteriness Lethargy Poor feeding Hypotonia High-pitched cry Tachypnea, tachycardia Temperature instability Pallor, cyanosis Hyper irritability Apnea & convulsion are serious & late signs due to neuroglycopenia
Hypoglycemia NURSING IMPLEMENTATION Early detection: Dextrosix screening using capillary blood Anticipate heel-prick. With frequent monitoring, there is a need to record the amount of blood withdrawn. Done at birth & 30 minutes after for 6 times, then q2h for 6 times 2. On identification: Oral glucose stat 3. Administer 10% or 25% IV glucose as ordered. Take care not to run too fast to prevent hyperglycemia (blood glucose above 125 mg/100 mL). 4. Keep NB warm. 5. Prevent & observe for seizures: reduce environmental stimuli; minima, gentle handling. 6. Maintain blood sugar at greater than 45 mg/100 mL. s
Neonatal Sepsis Generalized infection in the NB; a clinical syndrome of systemic illness accompanied by bacteremia. RISK FACTORS: Prematurity & prolonged period b/w rupture of membranes & delivery, fever, chorioamnionitis & other conditions that increase the risk for complications r/t sepsis Dystocia Maternal infection Prematurity, SGA Resuscitation Aspiration of mucus, meconium & vaginal secretions Iatrogenic-infected personnel/equipment
Neonatal Sepsis ASSESSMENT FINDINGS: s/s are generalized & are not specific because neonate cannot yet localize infection due to immature immune system Lethargy Poor respiratory effort, apnea, cyanosis, persistent hypoglycemia or frank signs of respiratory distress Jaundice or pallor Decreased or increased temperature; (fever is the least important sign) Diarrhea, vomiting, dehydration, abdominal distention Weight loss, malnutrition Increased WBCs DIAGNOSIS Culture of body secretions, or blood if there is no focus of infection
Neonatal Sepsis NURSING IMPLEMENTATION Isolate NB – first nursing action; observe strict asepsis in handling the NB Handwashing 2 to 3 minutes scrubbing at the start of the tour of duty 15-second scrub b/w & before infants Gown-mask technique Decrease contact with unit equipment/areas Exclude infected persons from the nursery 2. Provide oxygen & respiratory support as indicated. 3. Administered ordered antibiotics stat 4. Keep the NB warm.
Neonatal Sepsis NURSING IMPLEMENTATION 5. Maintain nutrition & hydration. Administer IV fluids/oral food & fluids Monitor I&O, daily weight Assess for signs of dehydration Sunken fontanels – first Soft depressed eyeballs Non-elastic skin/poor skin turgor on thighs & abdomen Oliguria Fever Lethargy/weakness
Neonatal Sepsis NURSING IMPLEMENTATION 6. Meet the NB’s emotional needs: Provide touch, promote comfort, stimulate the senses. The crib mobile is an excellent play material, as the NB can fixate a bright light/an object. 7. Provide psychological support to parents Encourage verbalizations of concerns & anxieties Explain treatments & diagnostic examinations; inform results Inform of the NB’s progress
Hypocalcemia Decreased serum calcium below 7 to 7.5 mg/100 mL RISK FACTORS: Hypoglycemia Asphyxia Low Apgar score Lack of intake Prematurity NB’s of diabetics Birth trauma Treatment of acidosis with bicarbonate
Hypocalcemia TREATMENT Oral calcium if the infant can suck & swallow IV calcium can be given as 10% solution of calcium gluconate if it’s not possible for oral liquids to be taken safely. Administer sodium phenobarbital, in addition to calcium gluconate, to halt the seizures Safety Alert: Calcium gluconate should not be given IM, or subcutaneously, as this might cause necrosis at injection site. NURSING IMPLEMENTATION Administer ordered oral & IV calcium. Monitor rate of flow to prevent hypercalcemia. Maintain serum calcium at above 8 mg/100 mL. Prevention & management of seizures. Have ready emergency equipment for intubation to relieve laryngospasm. Maintain on oral calcium as ordered. Administer ordered vitamin D to facilitate absorption of calcium & phosphorus from the GIT.
Neonatal drug Addiction Addiction in the NB because of maternal substance abuse ONSET: Heroin: several hours after birth up to 3 to 4 days Paregoric ( Comphorated tincture of opium) p.o. TREATMENT: Phenobarbital p.o. Thorazine (Chlorpromazine) p.o. Diazepam Narcotic antagonist for respiratory depression in morphine addiction Methadone: 7 to 10 days – weeks PROGNOSIS Long-term effects are unknown; may have hyperactivity, temper tantrums, brief attention span, abnormal psychomotor development
Neonatal drug Addiction NURSING IMPLEMENTATION Early recognition & reporting Prevention & management of convulsion Minimized handling with well-organized care Decreased stimuli Medications with meals During convulsion: ensure a patent airway as (top priority) & protect from injury 3. Provide nutrition & hydration small, frequent feedings IV, I&O, weight Provision of activities: sucking pacifier 4. Promote respiration: semi-Fowler’s position; respiration monitor.
Neonatal drug Addiction NURSING IMPLEMENTATION 5. Prevent skin injuries a. Swaddle the infant – check temperature frequently to prevent hyperthermia b. Frequent skin care c. Positional changes d. Use of sheep skin 6. Provide psychological support Promote bonding Feed by demand Have mother feed infant 7. Provide follow-up care because infants are at risk for: Failure to thrive Child abuse SID – sudden infant death syndrome
Hyperbilirubinemia Bilirubin – is a waste product that is excreted from the body only in the form of conjugated bilirubin. Most bilirubin is released in the breakdown of RBC. The RBC gives off hemoglobin – heme & globin . The globin portion is a protein that probably returns to the intracellular amino acid pool. The heme portion is broken down – free bilirubin & iron . The iron is either stored in the form of ferritin (in liver) or used to produced new hemoglobin. Bilirubin bound to albumin & travels to the liver . It is called unconjugated, fat-soluble, or indirect bilirubin because it cannot be excreted in bile or through the kidneys . In the liver, it is converted on the smooth endoplasmic reticulum to a water-soluble from when it combines with glucuronic acid through the intervention of the enzyme glucuronyl transferase . Water-soluble or conjugated bilirubin , it can be excreted into bile & excreted by the intestine & kidneys. Most of the bilirubin is converted by to stercobilinogen , which is oxidized to stercobilin before being excreted in the feces. Stercobilin & other bile pigments impart the brown color to the feces.
Hyperbilirubinemia Excessive levels of serum bilirubin greater than 12-13 mg/100 mL. N ormal value: 2-6 mg/100 mL. RISK FACTORS: Prematurity – immature liver Sepsis/infection Exposure to drugs in uteru : excessive vitamin K Isoimmunization Polycythemia Hypothermia Birth trauma with bleeding: cephalhematoma Breastfeeding: because of pregnanediol rendering glucoronyl transferase ineffective in conjugating bilirubin Poor meconium/stool passage. Meconium is very rich in bilirubin so frequent stooling results to increased excretion of bilirubin.
Hyperbilirubinemia ASSESSMENT FINDINGS Pathologic jaundice Occurs in the first 24 hours Duration: lasts more than a week Dangerous levels at which kernicterus may set it: Full term: 20 mg/100 mL or above Preterm: 15 mg/100 mL or above d. Signs of kernicterus Sluggish-to-absent Moro reflex Opisthotonus (best: side-lying position) Severe lethargy Projectile vomiting Tense, bulging fontanel High-pitched cry Apnea Convulsion – a late sign 2. Pallor – from hemolytic anemia 3. Irritability, lethargy 4. Polycythemia – tachycardia, red hands/feet, distress 5. high-pitched cry 6. Increasing serum bilirubin
Hyperbilirubinemia Treatment Phototherapy & exchange transfusion Phototherapy Transports bilirubin from the skin to the blood, then to the bile where it is excreted & passed out through the stool. Infant is continuously exposed to 3 to 6 fluorescent light tubes with a total strength of 200-500 foot candles. Photo-decomposition is the normal alternate route of bilirubin conversion. The exposure to lights increases the rate of conversion. Have light tubes 16 inches (42-45 cm) away from the baby Prepare for phototherapy Undress NB Cover eyes & genitalia Rationale: covering the eyes prevents possible retinal damage & blindness ; covering the genitalia prevents possible painful penile erection (priapism) & sterility Safety alert: Make sure the eyes are closed before applying eye dressing or cotton balls & before finally securing with an additional dressing to prevent corneal damage.
Hyperbilirubinemia d. Provide continued care during the treatment. Feed regularly (every 2 to 3 hours) to prevent metabolic acidosis; remove the infant from under the light; remove eye shield, then cuddle him during feeding. Rationale: By regularly removing the eye shield & cuddling the infant during feeding, the nurse gives the infant ample sensory stimulation. Turn every 2 hours for maximum exposure of skin surfaces Increase fluid intake; give fluids in between feedings. Monitor temperature every 2 hours. Rationale : During phototherapy, the NB gains added heat through radiation, which can lead to hyperthermia. The body temperature must be monitored frequently. Safety Alert: The heat in the isolette must be turned down during temperature taking & the portholes left open to prevent overheating & inaccurate temperature reading.
Hyperbilirubinemia e. Assess for side-effects & manage as necessary Bronze skin (explain to the parents: temporary ) Dark, concentrated urine (increase fluids, give sterile water b/w regular milk feedings). Bright, green loose stools from excess bilirubin excretion (explain & reassure parents that this is not diarrhea) Priapism (turn to prone) Retinal damage (prevent by shielding the eyes) Dehydration (increase fluids; give sterile water b/w regular milk feedings) Elevated temperature/fever (monitor temperature; provide adequate hydration) f. Turn off lights if blood is to be extracted for serum bilirubin determination & obtain a darkened container for the blood specimen. Rationale: This is to get accurate results because bilirubin is destroyed by light.
Hyperbilirubinemia 3. Exchange transfusion Method of choice; effective in clearing indirect bilirubin levels; site of exchange – umbilical vein. Removal of blood & replacement is conducted by removing approximately 5mg/kg at once & replacing this with donor blood – continued until a total volume of 170 mL/kg of infant blood has been replaced, representing twice the infant’s total circulating volume of 85 mL/kg. Prepare blood: Amount is twice the infant’s blood volume (Assumption: NB circulation contains 85 mL of blood per kilogram of body weight) Blood that contains acid-citrate-dextrose to keep it from coagulating may cause hypocalcemia. Infant generally receives calcium gluconate infusion at the time of exchange. Fresh type O, Rh (-) & compatible with both NB & maternal serum. The use of fresh blood to prevents hypocalcemia, tetany & convulsion. At room temperature, in order to prevent cardiac arrest.
Hyperbilirubinemia b. Provide care: Observe NPO; aspirate stomach to prevent vomiting & aspiration. Prepare oxygen & suction in readiness for any emergency. Check v/s before & q15 minutes during the procedure. Keep NB warm during the procedure; procedure than under a radiant heat source (radiant warmer). Monitor exchanges: 10 to 20 mL of the infant’s blood is withdrawn & 10 to 20 mL of the donor’s blood is instilled until the exchange is complete. Administer calcium gluconate as ordered. Provide care after exchange transfusion: Observe for signs of hemorrhage from the exchange site (particularly when heparinized blood was use for transfusion) Observe for signs of hypocalcemia: jitteriness, ankle clonus, & hypothermia
Hyperbilirubinemia Inject protamine sulfate at the conclusion of the exchange of the exchange if heparinized blood was used to prevent bleeding by aiding blood coagulation. Provide rest. Keep umbilical stump covered & moist with wet sterile gauze (saline soak), for possible future use. c. Effects of e xchange transfusion: Lowers serum bilirubin – corrects hyperbilirubinemia Elevates hemoglobin – corrects anemia Reduces/prevents CHF, a leading cause of mortality in the most severe form of erythroblastosis fetalis : hydrops fetalis
Hemolytic Disease of the NB/ Erythroblastosis fetalis Severe hemolytic reaction characterized by: Severe anemia Severe hyperbilirubinemia Severe hypoxia Cardiac decompensation Edema Hydrothorax Ascites Death, if there is no adequate treatment Characteristic Features: Hemolytic anemia Hyperbilirubinemia
Hemolytic Disease of the NB/ Erythroblastosis fetalis Types: Rh incompatibility ABO incompatibility Pathophysiology: Blood incompatibility (Rh (-) mother with Rh (+) fetus) – Rh (+) antigens of the fetus (RBC) enter maternal circulation – sensitization occurs: maternal antibodies against fetal antigens begin to form – formed antibodies remain in maternal circulation – at the time of next pregnancy with Rh (+) fetus, antibodies cross placenta – antibodies enter fetal circulation & attack fetal RBC (hemolysis) resulting to hyperbilirubinemia & anemia with hypoxia, or the most severe form hydrops fetalis . In hydrops fetalis , the fetus & placenta have severe edema; fetus may develop pleural & cardiac effusions, cardiomegaly, & hepatosplenomegaly Once antibodies are formed, subsequent pregnancies are at risk for hemolytic disease of the fetus & NB.
Hemolytic Disease of the NB/ Erythroblastosis fetalis Diagnosis Prenatal detection: Early detection of Rh sensitization is vital because this is the most common & significant cause of maternal immunization & hemolysis in the fetus or NB. Determination of maternal blood type & Rh factor Incompatibility exists with: Rh-negative mother carrying an Rh positive fetus or Type O mother carrying a fetus who is with A, or B, AB blood. The first child is nor usually affected in Rh-incompatibility, for under normal circumstances, there is no mixture of fetal & maternal blood. Fetal cells enter maternal blood stream only ate the time of placental separation. This may also happen after an abortion, ectopic pregnancy, blood transfusion with incompatible blood, abruption placenta & normal delivery.
Hemolytic Disease of the NB/ Erythroblastosis fetalis Diagnosis b. I ndirect Coomb’s Test Determines presence of Rh sensitization using maternal blood. Titer determines number of maternal antibodies. Negative result: The mother has not been sensitized yet. Positive result: The mother already has been sensitized & now has circulating antibodies against Rh positive antigen. c. Amniocentesis by about 26 weeks’ gestation to determine severity of hemolytic activity by identifying bilirubin by-products. d. Percutaneous umbilical blood sampling (PUBS) is a direct sampling of fetal blood from the umbilical cord guided by UTZ. Also known as cordocentesis ; takes 10 minutes to get sample invasive:; provides direct access to fetal circulation; needs informed consent Involves direct aspiration of fetal blood Most common site: umbilical cord, within 2 cm of placental insertion site. Alternative sites: fetal cardiac ventricle & intrahepatic vein
Hemolytic Disease of the NB/ Erythroblastosis fetalis 2. Intranatal detection Observes character of amniotic fluid on membrane rupture: straw-colored fluid indicates mild disease while golden-colored fluid means severe disease. 3. Postnatal diagnosis Direct coombs test to detect the presence of antibodies on the RBCs of the NB; done on the blood taken from the cord at birth Negative result: The NB has not received any antibodies from the mother; NB is safe. Positive result: The NB has received antibodies from the mother; the NB is also likely to manifest early signs of hyperbilirubinemia & anemia & to receive the treatment after identification of serum bilirubin.
Hemolytic Disease of the NB/ Erythroblastosis fetalis Treatment Prevention: RhoGAM (Rh D gamma globulin) Give within 72 hours after termination of normal pregnancy, ectopic pregnancy or abortion route: IM Given to an Rh-negative mother who carried or delivered an Rh-positive baby (or abortion, ectopic pregnancy) with negative Coombs test b. Action of RhoGAM : to prevent or suppress sensitization in susceptible Rh-negative women carrying Rh-positive fetus; it can’t reverse isoimmunization (it also cannot destroy antibodies already formed) c. Women experiencing a first trimester pregnancy loss or those undergoing invasive procedures should receive RhoGAM . 2. Measures to prevent or control: Cardiac failure & related edema Hyperbilirubinemia & related kernicterus Anemia
Hemolytic Disease of the NB/ Erythroblastosis fetalis Nursing Implementation The same with hyperbilirubinemia Care of infants receiving phototherapy treatment & exchange transfusion Care of infants with convulsion due to jaundice of the brain known as kernicterus; observe two major principles of management: Keep airway patent; gently suction oropharyngeal secretions Prevent injury Pad railings of crib Do not apply tongue depressor Do not restrain extremities 3. Care of an infant with severe anemia 4. Providing support to the family