Sarah Maria C.

dela Cruz, RN, RM

y High Risk Neonates a newborn regardless of
gestational age or birth weight, who has a greater-thanaverage chance of morbidity or mortality because of conditions or circumstances superimposed on the normal course of events associated with birth and the adjustment to extrauterine existence.

y Encompasses human growth and development
from the time of viability ± 28 days following birth and includes threat to life and health that occur during the prenatal, perinatal, and postnatal periods.

y Viability ± gestational age at which survival

outside the uterus is believed to be possible, or as early as 23 weeks of gestation.

y Birth Weight y Gestational Age ± preterm/post term y Predominant Physiologic Factors ± associated with
state of maturity; chemical disturbances (hypoglycemia, hypocalcemia); consequences of immature organ systems (hypothermia, Respiratory Distress Syndrome,

y Very Low Birth Weight ± birth weight is less than 1500g. . y Extremely Low Birth Weight ± birth weight less than 1000g.CLASSIFICATION ACCORDING TO SIZE y ow Birth Weight ± less than 2500g regardless of gestational age y Moderately Low Birth Weight ± birth weight is between 1501g to 2500g.

CLASSIFICATION ACCORDING TO SIZE y Appropriate for Gestational Age (AGA) ± birth weight falls between the 10th and 90th percentile y Small for Gestational Age (SGA) ± birth weight falls below the 10th percentile y Large for Gestational Age (LGA) ± birth weight falls above the 90th percentile .

CLASSIFICATION ACCORDING TO GESTATIONAL AGE y Premature Infant ± born before the completion of 37 weeks of gestation. regardless of birth weight . regardless of birth weight y Full-Term Infant ± born between the beginning of the 38 weeks and the completion of the 42 weeks of gestation y Postmature Infant ± born after 42 weeks of gestational age.


born before body and organ system have completely matured. PREMATURE: to describe a baby .PRETERM INFANTS y An infant born before term (</=36 weeks). y PRETERM: refers to pregnancy (PT labor).2.5kg) y Born before complete maturity. premature or preterm y A low birth weight infant: </=1300-2000g (Philippine Standards) (.

PRETERM INFANTS INCIDENCE: y Highest among low socio economic class y Largest # of admission to NICU y 12% of all pregnancies y Multiple pregnancies y PIH y Placental problems .

vaginal infection) Drug Use (coccaine. alcohol) Abnormal structure of the uterus Previous PT Births . tobacco.PRETERM INFANTS CAUSES: y UNKNOWN y MATERNAL FACTOR y y y y y y y Malnutrition Preeclampsia (toxemia of pregnancy) Chronic Medial illness (Cardiac/kidney disease/DM) Infection (UTI.

multiple gestations .OM. poly/oligohydramnios y FETUS y Chromosomal abnormalities y Intrauterine Infection y Anatomic Abnormalities y IUGR.PRETERM INFANTS CAUSES: y PREGNANCY y Hypertension y Incompetent Cervix y Placental Previa/ Abruptio Placenta y PP.

PRETERM INFANTS DIAGNOSTIC EVALUATION: y Appraisal is made as soon as possible after admission to the nursery. eyes closed. y HEAD ± head circumference is large in comparison with chest (reflects cephalocaudal direction of growth) y The fontanels are small and bones are soft y Soft cranium subject to characteristic nonintentional deformation. and ears are poorly supported by cartilage (soft and pliable) y Bones of skull and ribs ± soft y Very small and appear scrawny ± less subcutaneous fat (skin is wrinkled) . ³preemie head´ y Absent eyebrows.

undescended testes y y . Small breast bud size with underdeveloped nipples Male Infants ± few scrotal rugae. fine & y y fuzzy on head Soles and palms ± minimal creases Harlequin color ± Skin color changes when preterm infant is moved.PRETERM INFANTS DIAGNOSTIC EVALUATION: y SKIN ± bright pink (often transluscent) with small blood vessels y Smooth and shiny (may be edematous) with small blood vessels clearly visible underneath thin epidermis y Fine lanugo hair abundant over body. upper half or one side of the body is pale or one side of the body is red. sparse.

complete relaxation with marked flexion and abduction of the thighs. swallow. cough reflexes ± ABSENT y Temperature instability ± Heat regulation poorly developed in the preterm infant because of poor development of CNS y Increased susceptibility to infection . gag. random movements are common with slightest stimulus y Activity ± Inactive and listless y Extremities maintain an attitude of extension and remain in any position in which they are placed. y Reflexes ± partially developed y Sucking absent.PRETERM INFANTS DIAGNOSTIC EVALUATION: y Labia and clitoris are prominent in females y Posture . weak or ineffectual.

chronic lung disease.PRETERM INFANTS DIAGNOSTIC EVALUATION: y Respirations are not efficient because of muscular weakness of lungs and rib cage and limited surfactant production. and a short shrill cry y Cerebral palsy. BPD. y Retraction at xiphoid is evidence of air hunger y Infants should be stimulated if apnea occurs y HMD/RDS. convulsions. altered intellectual functions . cyanosis. visual-motor deficits. abnormal respirations. apnea of prematurity y Greater tendency toward capillary fragility in the preterm infant y Red and white blood cell counts are low with resulting anemia during first few months of life. y Neuro ± Higher incidence of intracranial hemorrhage in the preterm infant y Muscle twitching.

the greater the degree of potential disability. y Higher ECF ± vulnerable to fluid and electrolyte imbalance y Cardio: (+) murmur y More susceptible to biochemical alterations ± hyperbilirubinemia. and slow emptying time of the stomach y Renal: Reduced glomerular filtration rate results in decreased ability to concentrate urine and conserve fluid. hypoglycemia y The greater degree of immaturity. small capacity of stomach. .PRETERM INFANTS DIAGNOSTIC EVALUATION: y GIT: Nutrition is difficult to maintain ± because of weak sucking and swallowing reflexes.

respiratory therapist y Incubator. Oxygen therapy y PREVENTION: y PRENATAL CARE: key factor y Good nutrition and education y ID mothers at risk y Educate on symptoms of PT labor y Avoid heavy/repetitive work or standing long periods of time . advance practice nurse. IV lines.PRETERM INFANTS THERAPEUTIC MANAGEMENT: y Team approach: neonatologist. nurse staff.

meds. bld extraction X-ray Special feedings of breastmilk/formula Medications Kangaroo care ± shorter stay in NICU . IVF Umbilical catheterization ± IVF.PRETERM INFANTS THERAPEUTIC MANAGEMENT: y TREATMENT: y y y y y y Oxygen.

follow up visits .PRETERM INFANTS THERAPEUTIC MANAGEMENT: y DISCHARGE: y Usually stay in hospital until reach pregnancy due date depending on their condition y GOALS: y Serious illness resolved y Stable temperature y Taking all feedings by breast/bottle y No recent apnea/bradycardia y Parents are able to provide care (meds and feedings) y Prior to discharge: eye examination.

y Maintain airway; check respirator function if employed; position
to promote ventilation; suction when necessary; maintain temperature of environment; administer oxygen only if necessary y Observe for changes in respirations, color, and vital signs y Check efficacy of Isolette: maintain heat, humidity, and oxygen concentration; monitor oxygen carefully to prevent retrolental fibroplasias y Maintain aseptic technique to prevent infection

y Adhere to the techniques of gavages feeding for safety of the

y Observe weight-gain patterns y Determine blood gases frequently to prevent acidosis y Institute phototherapy by letting them verbalize and ask

questions to relieve anxiety y Provide flexible and liberal visiting hours for parents as soon as possible y Allow parents to do as much as possible for the infant after appropriate teaching y Arrange follow-up before and after discharge by a visiting nurse or a Barangay Health Worker

y After 42 weeks AOG/ 294 days past 1st day of
mother¶s LMP; regardless of birth weight

y Post term, post maturity, prolonged pregnancy,
post datism

y 7% (3.5-15%) OF ALL PREGNANCIES

y CAUSES: unknown
y History of >/= 1 previous post term pregnancies &
miscalculated due date (not sure of LMP)

fetus may stop gaining weight/ weight loss y Decreased amniotic fluid may lead to cord compression during labor y Increased risk of MAS and hypoglycemia y Increasing size (mainly length) & hardening of skull may contribute to CPD y GREATEST RISK: during stresses of labor & delivery especially in infants of primigravidas. .may not function efficiently y Amniotic fluid volume decreases.POST MATURE INFANTS FETAL RISK: y Progressive placental dysfunction ± placenta (supplies nutrient & oxygen) ages toward the end of pregnancy -.

parchmentlike & desquamating) Wasted physical appearance (reflects intrauterine deprivation) Minimal fat deposit (depleted subcutaneous fat) ± thin.POST MATURE INFANTS CHARACTERISTICS OF INFANTS (1-3wks of AGE): y Absent lanugo. overgrown nails Dry. little if any vernix caseosa. peeling skin (cracked. abundant y y y y y scalp hair. elongated appearance Meconium staining ± seen in skin folds w/ vernix caseosa Visible creases palms/ soles .

E y UTZ.recommended . estimate amniotic fluid volume MANAGEMENT: y Check respiratory problems related to meconium y Blood test for hypoglycemia y PREVENTION: y Accurate due date and UTZ y Cesarean section/ induction of labor . non-stress testing.POST MATURE INFANTS DIAGNOSIS: P.


nails y Relatively benign but it can also be pathologic .HYPERBILIRUBINEMIA y Refers to excessive level of accumulated Bilirubin in the blood y JAUNDICE or ICTERUS ± yellowish discoloration of skin. sclera.

HYPERBILIRUBINEMIA PATHOPHYSIOLOGY: RBC DESTRUCTION Globin Protein (used by the body) Heme Unconjugated Bilirubin liver Bilirubin detched from albumin through enzyme glucoronyl transferase + glucoronic acid Conjugated Bilirubin Excreted into Bile (feces and urine) .

PATHOPHYSIOLOGY: y Result from increased unconjugated/ conjugated bilirubin y Bilirubin ± one of the breakdown products of hgb from RBC
destruction y Unconjugated Bilirubin ± insoluble, bound to albumin y Intestines ± (+) bacterial action ± reduces conjugated bilirubin y Urobilinogen ± pigment that gives stool its characteristic odor.

Decreased milk intake related to fewer calories consumed by infant before mother¶s milk is well established; enterohepatic shunting



CAUSE: Immature hepatic function + increased bilirubin load from RBC hemolysis

Possible factors is breast milk that prevent bilirubin conjugation Less frequent stooling

Blood antigen incompatibility causes hemolysis of large # of RBCs. Liver unable to conjugate & excrete excess bilirubin from hemolysis

2nd ± 4th day



ONSET: After 24 hours (preterm infants, prolonged) PEAK: 75 ± 90 hours DURATION: Declines on 5th-7th day

5th ± 7th day

During 1st 24 hrs (levels increase faster than 5mg/ml/day) Variable

3rd ± 5th day

10th ± 15th day


May remain jaundiced x 3-12 3weeks or more

Dependent on severity & treatment

Frequent (10(1012x/day) breastfeeding, avoid glucose water, water supplements or formula. Evaluate stooling pattern; stimulate as needed.



THERAPY: Increase frequency of feedings & avoid supplements. Evaluate stooling pattern. Monitor Transcutaneous Bilirubin (TcB)/ Total Serum Bilirubin (TSB)

Increase frequency of breast feeding; use no supplementations (glucose water); cessation of breastfeeding not recommended. Perform risk assessment.

Monitor TcB/TSB level. Perform risk assessment POST NATAL ± phototherapy; administer IVIG per protocol; if severe, perform exchange transfusion.

PRENATAL ± transfusion (fetus) Prevent sensitization (Rh Incompatibility) of Rh-negative Rhmother with Rhig (Rhogam) . direct and indirect serum bilirubin. Use phototherapy if bilirubin level increases significantly (>5mg/dl/day) or significant hemolysis is present. family history & others as necessary.HYPERBILIRUBINEMIA COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA PHYSIOLOGIC JAUNDICE BREASTBREASTFEEDINGFEEDINGASSOCIATED JAUNDICE (EARLY ONSET) Use phototherapy if bilirubin level increases significantly (17(1722mg/dl) or significant hemolysis is present. BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE THERAPY: Perform risk assessment. Consider performing additional evaluations: G6PD.

Assist mother with maintaining milk supply. evaluate benefits & harm of temporarily discontinuing breastfeeding.HYPERBILIRUBINEMIA COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA BREAST-FEEDINGBREAST-FEEDINGASSOCIATED JAUNDICE (EARLY ONSET) THERAPY: If phototherapy is instituted. BREAST MILK JAUNDICE (LATE ONSET) HEMOLYTIC DISEASE May include home phototherapy with a temporary (10-12hr) (10discontinuation of a breastfeeding. After discharge. may bottle-feed expressed milk bottleas appropriate to therapy. follow up according to hour of discharge. additional assessments may be required. Assist mother with maintenance of milk supply & reassurance regarding her milk supply and therapy. a subsequent TSB may be drawn to evaluate a drop in serum levels. Use formula supplements only at practitioner¶s discretion. assist with maintenance & storage of milk. . Minimize maternal-infant maternalseparation & encourage contact as appropriate. PRENATAL ± If mother is breastfeeding. feed expressed milk as appropriate.

method of feeding. no pathologic process (PREMATURITY): y Physiologic Jaundice / Icterus Neonatorum ± most common 2 PHASES: term infants y 1ST phase ± Bilirubin: 6mg/dl on 3rd DOL decreased to 23mg/dl by 5th day y 2nd phase ± Steady plateau without increase/decrease level 12th-14th day: levels decresed to normal (1mg/dl) y Pattern varies according to racial group.HYPERBILIRUBINEMIA POSSIBLE CAUSES: y PHYSIOLOGIC (DEVELOPMENTAL) FACTORS cause. . gestational age PRETERM: Bilirubin ± 10-12mg/dl at 4-5days slowly decrease by 2-4 weeks.

.HYPERBILIRUBINEMIA POSSIBLE CAUSES: y PHYSIOLOGIC (DEVELOPMENTAL) FACTORS (PREMATURITY): y Mechanisms Involved: y NB produce 2x as much bilirubin as do adults due to higher concentrations of circulating RBC & shorter life span of RBC (7090days) y Liver¶s ability to conjugate bilirubin reduced ± due to limited production of glucoronyl transferase y Lower plasma binding capacity for bilirubin because of lower albumin concentrations than other children.

HYPERBILIRUBINEMIA POSSIBLE CAUSES: y PHYSIOLOGIC (DEVELOPMENTAL) FACTORS (PREMATURITY): y Primary Mechanism : enterohepatic circulation/shunting y Normally: Conjugated bilirubin urobilinogen (excreted) y Sterile & less motile NB bowel is less effective in excreting urobilinogen y Conjugated bilirubin thru B-glucoronidase converted back to unconjugated bilirubin reabsorbed by intestinal mucosa liver .

12-13% of Breastfeeding infants y Related to process of breastfeeding.HYPERBILIRUBINEMIA POSSIBLE CAUSES: y An association with breast feeding or breast milk y BREASTFEEDING JAUNDICE ± early onset y Begins at 2-4days of age. facilitates meconium evacuation . results from decreased caloric & fluid intake by Breastfeeding infants before milk supply is wellestablished (fasting is associated with decrease hepatic clearance of bilirubin) y Feeding (+) peristalsis more rapid passage of meconium decreased amount of reabsorption of unconjugated bilirubin y Feeding introduces bacteria to aid in reduction of bilirubin to urobilinogen y Colostrums. natural cathartic.

12-13% of Breastfeeding infants Rising levels peak at 2nd week gradually diminish May remain jaundiced x 3-12 weeks or more infants are well May be caused by factors in BM (pregnanediol. fatty acids. Bglucorinidase) that either inhibit conjugation or decrease excretion of bilirubin y Less frequent stooling by Breastfeeding infants may allow for extended time for reabsorption of bilirubin from stools y y y y .HYPERBILIRUBINEMIA POSSIBLE CAUSES: y An association with breast feeding or breast milk y BREAST MILK JAUNDICE ± late onset Onset: 4th-7th day of age.

exchange transfusion ± severe y Prenatal ± transfusion (fetus) . liver unable to conjugate & excrete excess bilirubin from hemolysis y Onset: 1st 24 hours (levels increase faster than 5mg/dl/day) y Treatment: Postnatal ± phototherapy . bruises y Hemolytic disease ± blood antigen incompatibility ± hemolysis of RBC .HYPERBILIRUBINEMIA POSSIBLE CAUSES: y Excess production of bilirubin ± Hemolytic disease. biochemical defects. Rhogam .

Asians . bile duct obstruction y Combined overproduction & undersecretion ± sepsis y Some disease states ± hypothyroidism. galactosemia.HYPERBILIRUBINEMIA POSSIBLE CAUSES: y Disturbed capacity of liver to secrete conjugated bilirubin ± enzyme deficiency. infant of a diabetic mother y Genetic predisposition to increase production ± Native Americans.

infections) y Appears on 2nd or 3rd day. maternally-derived diseases (DM. nails. peaks on 3rd ± 4th day. skin y If it appears within 1st 24 hours: hemolytic disease of Newborn.HYPERBILIRUBINEMIA CLINICAL MANIFESTATIONS y Jaundice ± most obvious sign y Yellowish discoloration: sclera. declines on 5th ± 7th day: physiologic jaundice (varies according to ethnicity) y Intensity of jaundice is not always related to the degree of hyperbilirubinemia . sepsis.

2-1.HYPERBILIRUBINEMIA DIAGNOSTIC EVALUATION y Serum Bilirubin (B1: 0.4mg/dl) y Jaundice appears at >5mg/dl y Evaluation based on: y y y y y y y y Timing of appearance of clinical jaundice Gestational age at birth Age in days since birth Family history including maternal Rh factor Evidence of hemolysis Feeding method Infant¶s physiologic status Progression of serum bilirubin levels .

HYPERBILIRUBINEMIA DIAGNOSTIC EVALUATION y Indicators of physiologic jaundice ± warrants further investigation as to the cause of jaundice y Clinical jaundice within 24 hrs.5-2mg/dl y Total serum Bilirubin ± over 95th percentile for age (in hours) on hour-specific risk nomogram . of birth y Persistent jaundice over 2 weeks in full-term. upper limit for breastfeeding infant ± 15mg/dl y Increase serum bilirubin >5mg/dl/day y Direct bilirubin (B2) 1.9mg/dl (term infant) or over 15mg/dl (preterm). formula fed infant y Total serum bilirubin levels 12.

allow for repetetive estimations of bilirubin y Hour-specific Serum Bilirubin Levels ± predict newborn at risk for rapidly rising levels y Recommended by AAP for monitoring healthy Newborn >35wks AOG before discharge from hospital y Carbon monoxide indices in exhaled breath ± CO is produced when RBC is broken down .HYPERBILIRUBINEMIA DIAGNOSTIC EVALUATION y Transcutaneous Bilirubinometry ± noninvasive monitoring of bilirubin via cutaneous reflectance mechanisms.

HYPERBILIRUBINEMIA COMPLICATIONS y BILIRUBIN ENCEPHALOPATHY/ KERNICTERUS ± unconjugated bilirubin highly toxic to the neurons y Syndrome of severe brain damage due to deposition of unconjugated bilirubin in brain cells (extremely high B1 level increase crosses the blood-brain barrier) y KERNICTERUS ± yellow staining of brain cells that may result in bilirubin encephalopathy .

hypoxia. hypoglycemia . hypothermia.HYPERBILIRUBINEMIA COMPLICATIONS y FACTORS THAT CONTRIBUTE TO BILIRUBIN NEUROTOXICITY: y Serum bilirubin alone do not predict the risk of brain injury y Metabolic acidosis y Low serum albumin level y Intracranial infections (meningitis) y Abrupt increase in BP y Conditions that increase metabolic demands for oxygen and glucose ± fetal distress.

athetosis). deafness y Those who survived: NEUROLOGIC DAMAGE y Mental retardation. behavior disorders. sensorineural hearing loss . seizures y Athetoid CP.HYPERBILIRUBINEMIA COMPLICATIONS y SIGNS OF CNS DEPRESSION/ EXCITATION: y Prodrome: decreased activity. irritability. ADHD. hypotonia. perceptual problems. mental retardation. delayed/ abnormal motor movements (ataxia. lethargy.

HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT y Phototherapy ± main form y Exchange transfusion ± reduce high bilirubin levels that occur with hemolytic disease y Phenobarbital ± hemolytic disease. effective when given to mother several days before delivery y Promotes hepatic glucoronyl transferase synthesis increases bilirubin conjugation & hepatic clearance of pigment in bile y Promotes protein synthesis ± increase albumin for more bilirubin binding sites y Heme-oxygenase inhibitors ± decrease bilirubin production .

formula or water supplementation . decreases enterohepatic shunting.HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT y Early initiation of feedings & frequent breastfeeding ± promotes increased intestinal motility. establish normal bacterial flora in the bowel excrete B2 y Frequent breastfeeding every 2 hrs y Avoid glucose water.

HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT y Phototherapy ± application of fluorescent light (bili light) to infant¶s exposed skin y Light promotes bilirubin excretion by photoisomerization (alters structure of bilirubin to a soluble form ± lumirubin) for easier excretion y Blue Light ± more effective in reducing bilirubin but alters the color of the infant y Fluorescent bulbs with spectrum 420-460nm preferred y Infant skin is fully exposed .

blood is transported in covered tube to avoid false reading as a result of bilirubin destruction in test tube. better temperature control y Eliminates the need for eye patches y SPECIAL CAUTION: plastic pad must completely be covered to prevent exposing fragile skin of extremely immature/compromised infant to fiberoptic blanket (dermal injury) y When blood is drawn.HYPERBILIRUBINEMIA THERAPEUTIC MANAGEMENT y Phototherapy ± application of fluorescent light (bili light) to infant¶s exposed skin y Rapidly rising bilirubin/ critical level ± double intensive phototherapy y Conventional overhead lamps while infant is lying on fiber optic blanket y BEST RESULT: occur within 1st 24-48hrs of treatment y Fiberoptic blanket/panel ± light generating illuminator y blanket delivers therapeutic light consistently & continuously to infant & achieve same photoisomerization as conventional phototherapy y For home phototherapy. phototherapy lights are turned off. . permits more infant-parent interaction.

HYPERBILIRUBINEMIA MANAGEMENT OF HYPERBILIRUBINEMIA IN HEALTHY TERM NEWBORN TSB LEVEL (mg/dl/mmol/L) AGE (HOURS) CONSIDER PHOTOTHERAPY PHOTOTHERAPY EXCHANGE TRANSFUSION IF INTENSIVE PHOTOTHERAPY FAILS -->/= 20 (340) >/= 25 (430) >/= 25 (430) EXCHANGE TRANSFUSION AND INTENSIVE PHOTOTHERAPY -->/= 25 (430) >/= 30 (510) >/= 30 (510) 24 2525-48 4848-72 >72 -->/= 12 (170) >/= 15 (260) >/= 17 (290) -->/= 15 (260) >/= 18 (310) >/= 20 (340) .

delayed motor skills.HYPERBILIRUBINEMIA PROGNOSIS: y Early recognition prevents brain damage y Bilirubin encephalopathy: athetosis. paralytic gaze palsy. dental enamel hypoplasia . gaze abnormalities. sensorineural hearing loss.

conjunctiva. oral mucosa y Observe natural daylight y Evidence of jaundice that appears before infant is 24 hrs of age ± indication for assessing bilirubin levels . color of sclera & mucous membranes y Apply direct pressure to skin especially bony prominences (tip of nose or sternum) blanching allow yellow stain to be more pronounced y Dark-skinned ± color of sclera.HYPERBILIRUBINEMIA NURSING CONSIDERATIONS y ASSESSMENT y Observe for evidence of jaundice at regular intervals y Observe color from head-toe.

HYPERBILIRUBINEMIA NURSING CONSIDERATIONS y Phototherapy ± nude under light source. repositioned frequently to expose all body surface areas to light y Frequent bilirubin determination ± every 6-12hrs (visual assessment is no longer considered valid) .

correctly positioned without occluding the nares y Infant¶s eyelids are closed before mask is applied. corneal irritation y Removed during feedings y Infants in open crib must have a protective plexiglass shield between them & fluorescent lights to minimize amount of undesirable UV lights reaching skin & protect them from accidental bulb breakage y Temperature monitored y Maintain in flexed position w/ rolled blankets alongside body . excessive pressure on lids. corneas may become excoriated y Eyes checked every shift for discharge.HYPERBILIRUBINEMIA NURSING CONSIDERATIONS y PHOTOTHERAPY: y PRECAUTIONS: y Eye Shield ± opaque mask to prevent exposure to light y Properly sized.

Increase BMR. priapism . electrolyte imbalance (hypocalcemia). DHN. hypothermia.HYPERBILIRUBINEMIA NURSING CONSIDERATIONS y PHOTOTHERAPY: y ACCURATE CHARTING: Times that phototherapy is started and stopped Proper shielding of the eyes Type of fluorescent lamp Number of lamps Distance between surface of lamps & infant (not <18 in) Use of phototherapy in combination with an incubator or open bassinet y Photometer measurement of light intensity y Occurrence of side effects y y y y y y y Side effects: loose greenish stools transient skin rashes.

skin turn grayish brown hours after infant is placed under light y Due to retention of bilirubin breakdown product of phototherapy (copper prophyrin) y Infants with elevated B2 level & some degree of cholestasis y Resolves after discontinuation of phototherapy .HYPERBILIRUBINEMIA NURSING CONSIDERATIONS y PHOTOTHERAPY: y Informed consent prior to treatment y Oily lubricants/lotions not used ± ³frying effect´ y Full-term newborn ± additional fluid volume to compensate for fluid loss y Meticulous skin care y Rebound effect ± after phototherapy is permanently discontinued subsequent increase in serum bilirubin level. transient y ³Bronze Baby Syndrome´ ± serum. urine.


preeclampsia) y Rare in drug-exposed infants or those who have been exposed to y RDS of nonpulmonary origin in Newborn: sepsis. acute blood loss. Caesarean Section delivery. exposure to cold. low birth weight. history of previous RDS chronic intrauterine stress (HPN. precipitous delivery. infants of diabetic mothers. airway obstruction. cold stress.RESPIRATORY DISTRESS SYNDROME (RDS) y Condition of surfactant deficiency & physiologic immaturity of thorax y Seen almost exclusively in preterm infants. metabolic acidosis. drugs. cardiac defects. delivery before 37 weeks AOG. . seen in infants <32 wks AOG y A disease related to developmental delay in lung maturation y Also associated with multifetal pregnancies. asphyxia. IVH. hypoglycemia.

RESPIRATORY DISTRESS SYNDROME (RDS) y PATHOPHYSIOLOGY Deficient Surfactant Collapse of Alveoli Great deal of effort to reexpand the alveoli with each breath Exhaustion Fewer and fewer alveoli opens Atelectasis Hypoperfusion to the lung tissue Hypoxemia and hypercapnia .

RESPIRATORY DISTRESS SYNDROME (RDS) y PATHOPHYSIOLOGY y Preterm ± born before lungs are fully prepared for gas exchange (critical factor in RDS) y Combination of structural and functional immaturity of lungs y (+) fetal respiratory activity before birth: lungs have feeble respiratory movements. fluid excreted thru alveoli .

RESPIRATORY DISTRESS SYNDROME (RDS) y PATHOPHYSIOLOGY y Final unfolding of alveolar septa (increase surface area of the lungs) occurs on last trimester of pregnancy Preterms are born with underdeveloped and uninflatable alveoli Limited pulmonary blood flow Collapsed lungs Increased pulmonary vascular resistance Fetal blood shunted from lungs by ductus arteriosus and foramen ovale .

type 2 cells do not fully mature until about 36 wks AOG y Reduces surface tension of fluids that line the alveoli & respiratory passages expansion uniform expansion and maintains lung .RESPIRATORY DISTRESS SYNDROME (RDS) y PATHOPHYSIOLOGY y Rib Cage: weak and compliant y Fetal chest highly compliant because of predominance of cartilage. diaphragm is prone to fatigue y Fetal Lungs deficient in surfactant due to immaturity of surfactant producing type 2 alveolar cells y Surfactant ± 1st produced at 24 wks AOG.

collapse of alveoli of end expiration y Without surfactant ± infants unable to keep lungs inflated. exerts great effort to reexpand the alveoli exhaustion atelectasis .RESPIRATORY DISTRESS SYNDROME (RDS) y PATHOPHYSIOLOGY y Deficient surfactant ± unequal inflation of alveoli on inspiration.

RESPIRATORY DISTRESS SYNDROME (RDS) y PATHOPHYSIOLOGY Inadequate pulmonary perfusion and ventilation Hypoxemia and hypercapnia Markedly reactive pulmonary arterioles and thick Muscular layer decreased oxygen concentration Decreased oxygen tension + decreased blood pH Vasospasm in pulmonary arterioles Increased PVR Intrapulmonary shunting Anaerobic glycolysis Metabolic acidosis. cyanosis .

increased difficulty in breathing Hypoxemia. impaired gas exchange . and hypercapnia with respiratory acidosis Hypoperfusion of pulmonary circulation Tissue hypoxia & metabolic acidosis Hyaline membrane formation. atelectasis.RESPIRATORY DISTRESS SYNDROME (RDS) y PATHOPHYSIOLOGY y (+) pulmonary edema ± impaired gas exchange y (+) pulmonary interstitial emphysema ± overdistention of distal airways CAUSE Increased surface tension of alveoli (surfactant deficiency) Impaired gas exchange Increased pulmonary vascular resistance Hypoperfusion (with hypoxemia) Increased transudation of fluid into lungs MAJOR FACTORS IN RDS EFFECT Alveolar collapse.

audible expiratory grunt Flaring of external nares Cyanosis / pallor y As disease progresses y Apnea . absent spontaneous movement y Unresponsive . mottling y Severe disease: shock-like state y Decreased cardiac output and bradycardia y Low systemic BP . diminished breath sounds . flaccidity .RESPIRATORY DISTRESS SYNDROME (RDS) y CLINICAL MANIFESTATIONS: y Respiratory Signs and Symptoms: y y y y y Tachypnea (80-120/min) initially : dyspnea Pronounced intercostals and/or substernal retractions Fine inspiratory crackles .

pulse oximetry and carbon dioxide monitoring. diffuse.RESPIRATORY DISTRESS SYNDROME (RDS) y EVALUATION: y Blood glucose test y Chest x-ray with fine. recticogranular or ³ground glass appearance and air bronchogram y Arterial blood gas (ABGs) . pulmonary function tests .

y Prenatal diagnosis:
y Problems like maternal diabetes ± delay fetal lung maturation
y Antenatal administration of glucocorticoids ± enhance fetal lung

y Lecithin / sphingomyelin ratio (L:S ratio) : relationship

between these 2 lipids during gestation y L:S = 2:1 y ³Shake/ bubble test´ ± stable foam bubbles form when amniotic fluid is shaken in presence of ethanol y Tap Test ± abundant bubbles appear in test tube of amniotic fluid with 6N ± HCL and diethyl ether y TDx fetal lung maturity assay

y Immediate establishment of adequate oxygen and ventilation and
supportive measures required for a preterm, prevent further complications y SUPPORTIVE MEASURES: y Maintain adequate ventilation and oxygen y Maintain acid-base balance y Maintain neutral thermal environment y Maintain adequate tissue perfusion and oxygen y Prevent hypotension y Maintain adequate hydration and electrolyte status y NUTRITION: parenteral therapy during 1st phase of disease y Nipple and gavage feedings are contraindicated ± causes increase
RR, prone to aspiration y Enteral substrate to infant with transient hypoxia ± increase risk Necrotizing Enterocolitis

y y y y y y y y
Decrease oxygen requirements and mean airway pressure (MAP) Improves blood gas values & ventilator settings Decrease incidence of pulmonary air leaks Decrease deaths from RDS Decrease mortality rate COMPLICATIONS: pulmonary hemorrhage, mucous plugging Given at birth via endotracheal (ET) tube directly into infants trachea NURSING RESPONSIBILITIES: y Assist in delivery of the product, collection, and monitoring of ABG¶s,
scrupulous monitoring of oxygen with pulse oximetry y Assess infant¶s tolerance of procedure y Delay suctioning for an hour or so to allow maximum effects to occur

y Aggressive respiratory support: Oxygen, continuous positive y
airway pressure (CPAP), intubation, mechanical ventilation Goals of Oxygen therapy: provide adequate oxygen to tissues y Prevent lactic acidosis resulting from hypoxia y Avoid negative effects of oxygen barotrauma / toxicity Gas should be warmed before entering respiratory tract Oxygen can be supplied via plastic hood If oxygen saturation of blood cannot be maintained at satisfactory level and PaO2 rises ventilatory assistance

y y y

RESPIRATORY DISTRESS SYNDROME (RDS) y TREATMENT / MANAGEMENT: METHOD CONVENTIONAL METHODS Continuous Positive Airway Pressure (CPAP) Provides contrast distending pressure to airway in spontaneously breathing infant. maintains residual airway pressure Nasal prongs. endotracheal tube. nasal cannula Endotracheal intubation. face mask. Provides increase endendexpiratory pressure during expiration and between Mandatory breaths which prevents alveolar collapse. and either volume-limited or volumepressurepressure-limited ventilator DESCRIPTION HOW PROVIDED Positive End-Expiratory EndPressure (PEEP) .

airway pressure. assist/control mode facilities full inspiratory synchrony. or flow changes HOW PROVIDED Endotracheal intubation and ventilator Synchronized Intermittent Mandatory Ventilation (SIMV) PatientPatient-triggered infant ventilator with signal detector and assist/control mode. endotracheal tube . thoracic impedance. involves signal detection of onset of spontaneous respiration from abdominal movement.RESPIRATORY DISTRESS SYNDROME (RDS) y TREATMENT / MANAGEMENT: METHOD Intermittent Mandatory Ventilation (IMV) DESCRIPTION Allows infant to breath spontaneously at own rate but provides mechanical cycled respirations and pressure at regular preset intervals Mechanically delivered breaths are synchronized to the onset of spontaneous patient breaths.

endotracheal tube ALTERNATIVE METHODS High frequency Oscillation (HFO) Application of high-frequency. sine wave flow oscillations to airway at rates between 480 and 1200 breaths/min VariableVariable-speed piston pump (or loudspeaker.RESPIRATORY DISTRESS SYNDROME (RDS) y TREATMENT / MANAGEMENT: METHOD Volume Guarantee Ventilation DESCRIPTION Delivers predetermined volume of gas using an inspiratory pressure that varies according to infant¶s lung compliance (often used in conjunction with SIMV) HOW PROVIDED Volume guarantee ventilator with flow sensor. highlowlow-volume. endotracheal tube . fluidic oscillator) .

parallel. endotracheal tube . low compliant circuit and injector port to deliver small pulses or jets of fresh gas deep into airway at rates between 250 and 900 breaths/min HOW PROVIDED May be used alone or with lowlow-rate IMV.RESPIRATORY DISTRESS SYNDROME (RDS) y TREATMENT / MANAGEMENT: METHOD HighHigh-Frequency Jet Ventilation (HFJV) DESCRIPTION Uses separate.

inflammation y Palatal grooves. subglottic stenosis y Tube obstruction and infection .RESPIRATORY DISTRESS SYNDROME (RDS) y TREATMENT / MANAGEMENT: y COMPLICATIONS OF POSITIVE PRESSURE VENTILATION: y Increased incidence of air leaks that produce complications: y Pulmonary Interstitial Emphysema y Pneumothorax y Pneumomediastinum y Associated with Intubation: y Nasal/tracheal/pharyngeal perforation y Stenosis.

RESPIRATORY DISTRESS SYNDROME (RDS) y TREATMENT / MANAGEMENT: y INHALED NITRIC OXIDE (NO): for newborn with conditions that cause persistent pulmonary HPN. subsequent acidosis. highly diffusible gas: cause smooth muscle relaxation and y y y y y y reduce pulmonary vasoconstriction and subsequent pulmonary HPN when inhaled into lungs Administered through ventilator circuit and blended with oxygen Attaches readily to hemoglobin and deactivated so that systemic vasculature is not affected Toxic in large quantities Mucus may collect I respiratory tract as a result of infant¶s pulmonary condition interferes with gas flow and obstruct passages Catheter inserted gently but quickly. pulmonary vasoconstriction. intermittent suctioning (limited to <5secs) FiO2 increased by 10% before suctioning . and severe hypoxia y Colorless.

RESPIRATORY DISTRESS SYNDROME (RDS) y TREATMENT / MANAGEMENT: y Most advantageous position for facilitating an infant¶s open airway are on the side with head supported in alignment by small folded blanket y Back position ± keep neck slightly extended y Head in ³sniffing´ position y Inspection of skin ± position changes and use of water pillows (prevents skin breakdown) y Mouth care .

decrease lung compliance y Management: Oxygen therapy y Signs and symptoms similar to RDS 1 (hyaline membrane disease) but resolves 48-72 hrs. .RESPIRATORY DISTRESS SYNDROME (RDS) y TRANSIENT TACHYPNEA OF THE NEWBORN (RDS TYPE 2) y Delayed resorption of fetal lung fluid.


SEPSIS / SEPTICEMIA y Generalized bacterial infection in the bloodstream y Newborns are highly susceptible to infection as a result of diminished nonspecific (inflammatory) & specific (humoral) immunity: impaired phagocytosis. males > females . decreased complement levels y High-Risk Infant 4x greater chance. delayed chemotactic response. minimal/absent IgA & IgM.

ET tubes Administration of TPNs Nosocomial exposures ± NICU Infant born after a difficult or traumatic labor & delivery . mucous y y y y membranes Invasive procedures ± IV lines.SEPSIS / SEPTICEMIA y RISK FACTORS: y Prematurity y Congenital Anomalies y Acquired injuries that disrupt the skin.

parasitic infections y Early birth interrupts transplacental transmission of passive immunity (IgG) y Preterms ± low IgG. IgA & IgM not transferred to fetus .SEPSIS / SEPTICEMIA y PATHOPHYSIOLOGY: y Premature withdrawal of placental barrier ± leaves infants vulnerable to viral. bacterial. fungal.

syphilis can occur .SEPSIS / SEPTICEMIA y SOURCES OF INFECTION: y Acquired prenatally across placenta from maternal blood stream or during labor from ingestion or aspiration of infected amniotic fluid y Prolonged rupture of membranes ± maternal-fetal transfer of pathogenic organisms y Transplacental transfer of CMV. toxoplasmosis.

Coli y H. Candida albicans. Listeria organism.SEPSIS / SEPTICEMIA y SOURCES OF INFECTION: y Early Sepsis (< 3days) ± acquired in perinatal period y Direct contact with organisms from maternal GIT & GUT y Group B streptococcus (GBS). enterococci. Kleibsiella. coagulase-negative staphylococci ± Very Low Birth Weight infants y Gonococci. Herpes Simplex Virus II. Chlamydia y Late Sepsis (1-3 weeks after birth) ± nosocomial y Staphylococci. Pseudomonas y Coagulase-negative staphylococci ± Extremely Low Birth Weight. influenza. E. Very Low Birth Weight Infants .

urinary. pharynx. personnel. nervous. mucous membranes of the eyes. internal systems (respiratory. object in the environment . nose. ear.SEPSIS / SEPTICEMIA y SOURCES OF INFECTION: y Bacterial Invasion: umbilical stump. GIT) y Postnatal Infection: cross-contamination from other infants.

dyspnea. Hepatomegaly. grunting. ³not doing well´. vomiting. poor feeding. nonspecific y General: Fever. edema y GI System: poor feeding. vague. Apnea/tachypnea. cyanosis y Renal System: Oliguria . flaring. diarrhea/ decreased stooling. abdominal distention. hemoccult-positive stools y Respiratory System: irregular respirations. Temperature instability. retractions.SEPSIS / SEPTICEMIA y SIGNS AND SYMPTOMS: y Systemic Infections ± subtle.

hyporeflexia. High-pitched cry.SEPSIS / SEPTICEMIA y SIGNS AND SYMPTOMS: y Cardiovascular System/ Circulatory: Pallor/ cyanosis/ mottling. purpura. irregular heartbeat : Tachycardia/ Bradycardia. splenomegaly. coma y Increased activity ± irritability. pallor. seizures y Full fontanelle. cold clammy skin. abnormal eye movements y Hematologic System: Jaundice. edema y CNS: diminished activity ± lethargy. petechiae. hypotension. ecchymosis . increased/ decreased tone. tremors.

SEPSIS / SEPTICEMIA y DIAGNOSIS: y Based on suspicion of presenting clinical signs and symptoms y Laboratory and radiographic examination ± definitive diagnosis y Blood/ urine/ CSF cultures ± 10% will have negative cultures y CBC: anemia. and if with altered mental status or meningeal signs . leukocytosis/ leucopenia y Leucopenia ± ominous sign y C-reactive protein serial measurements y Chest x-ray y Lumbar puncture if < 28 days old.

discontinue in 3 days if culture is negative & infant is asymptomatic (thru IV infusion) y Antifungal/ antiviral therapies . thermoregulation y Aggressive administration of antibiotics. immunotherapy y Antibiotics X7-10 days if cultures are positive. respiratory y y y y y y Respiratory distress/ hypoxia : Oxygen therapy IVF regulation Correct electrolytes and acid-base balance NPO temporarily Blood transfusions for anemia and shock Vital signs.SEPSIS / SEPTICEMIA y THERAPEUTIC MANAGEMENT: y SUPPORTIVE THERAPY: Circulatory.

SEPSIS / SEPTICEMIA y PROGNOSIS y Variable y ELBW/ VLBW infants: Early onset sepsis severe neurologic & respiratory sequelae y Late-onset sepsis & meningitis: poor outcome .

.SEPSIS / SEPTICEMIA y NURSING CONSIDERATIONS: y Recognize existing problem: ³something is wrong´ y Awareness of potential modes of infection transmission y Knowledge of the side effects of specific antibiotic & proper regulation & administration of drug are vital y Prolonged antibiotic therapy ± (+) growth of resistant organisms & superinfection from fungal/ mycotic agents (Candida albicans) y Nystatin oral suspension swabbed on oral mucosa ± prophylaxis y Avoid fully flexed position for obtaining spinal fluid.

SEPSIS / SEPTICEMIA y NURSING CONSIDERATIONS: y Continual cardiorespiratory & pulse oximetry monitoring provides an ongoing assessment of infant¶s condition y Decrease additional physiologic or environmental stress y Thermoregulated environment y Anticipate potential problems ± dehydration. stool) y Adequate housekeeping y Observe for signs of complications ± meningitis. septic shock . use disposable equipment y Proper disposal of excretions (vomitus. hypoxia y Precautionary measures: proper hand washing.


NECROTIZING ENTEROCOLITIS y Acute inflammatory disease of the bowel y Seen primarily in premature infants. although. described in full-term neonates as well y Occurs several weeks after birth y ETIOLOGY: y Precise Cause: unknown y Prematurity: risk factor .

mucosa permeable to toxins Gas-forming bacteria invasion (+) pneumatosis intestinalis (air in submucosa / subserosa) .NECROTIZING ENTEROCOLITIS y ETIOLOGY: y 3 FACTORS THAT PLAY ROLE IN DEVELOPMENT OF NEC: y Intestinal Ischemia ± vascular compromise on GIT Diminished Blood Supply Cell death No secretion of protective. lubricating mucus Thin unprotected wall attacked by proteolytic enzyme Bowel wall swell and break down Unable to synthesize IgM.

poor feeding. jaundice . hypotension y Unstable temperature.NECROTIZING ENTEROCOLITIS y ETIOLOGY: y 3 FACTORS THAT PLAY ROLE IN DEVELOPMENT OF NEC: y Colonization by pathogenic bacteria y Substrate (formula feeding) in intestinal lumen ± stress on ischemic bowel y SIGNS AND SYMPTOMS: y Nonspecific Clinical Signs: y Lethargy. hypotension y Vomiting. oliguria.

y Air in portal vein. blood in stools/gastric content y Gastric retention.³soapsuds´ or bubbly appearance of thickened bowel wall & ultralumina.NECROTIZING ENTEROCOLITIS y SIGNS AND SYMPTOMS: y Specific Signs: y Distended (often shiny) abdomen. free air under the diaphragm (perforation) . bilious vomitus y Localized abdominal wall erythema/ induration y DIAGNOSIS: y Abdominal x-ray: Sausage-shaped dilation of intestine distended loops of bowel. ³pneumatosis intestinalis´ --.

NECROTIZING ENTEROCOLITIS y DIAGNOSIS: y y y y Occult blood in the stool Blood culture ± bacteremia / septicemia CBC: anemia. electrolyte imbalance y TREATMENT: y Begins with prevention y NPO x 24-48 hours ± infants who have suffered birth asphyxia. VLBW infants y Breast milk y Minimal enteral feedings ± trophic feeding. ELBW. GIT priming . leucopenia/ leukocytosis Metabolic acidosis.

failure to thrive . fat malabsorption. colonic stricture with obstruction.NECROTIZING ENTEROCOLITIS y TREATMENT: y Confirmed NEC: y y y y Discontinue all oral feedings Place NGT ± for decompression IV fluids. IV antibiotics Surgery in extreme cases y PROGNOSIS: y Sequelae of surgical intervention: shirt-gut syndrome.

y Vital signs including blood pressure y Avoid rectal temperatures (danger of perforation) y Avoid pressure on distended abdomen y Infants are left undiapered & positioned supine or on the side y Conscientious attention to nutritional and hydration needs. administration of antibiotics y Oral feedings: started 7-10 days after diagnosis & treatment using human milk.NECROTIZING ENTEROCOLITIS y NURSING CONSIDERATIONS: y Prompt recognition of early warning signs of NEC: abdominal listen for presence of bowel sounds distention. elemental formula y Sterile water may be given initially y Strict hand washing . residual gastric contents before feedings. absent bowel sounds y Measure abdominal girth.


sometimes height that falls below 5th percentile for child¶s age inability to obtain or use calories required for growth y Weight for age (height) z value of less than -2. .0 y Weight curve (loss) that crosses >2 percentile lines on National Center for Health Statistics (NCHS) growth after previous achievement of a stable growth pattern.FAILURE TO THRIVE y Sign of inadequate growth resulting from y No universal definition y Common parameter: WEIGHT.

cerebral palsy.y 3 GENERAL CATEGORIES: y Organic Failure to Thrive y Physical Cause y y y y FAILURE TO THRIVE Congenital heart defects. endocrine dysfunction Cystic fibrosis. microcephaly Chronic renal failure. . acquired immunodeficiency syndrome (AIDS) y Nonorganic Failure to Thrive (NFTT) y Unrelated to disease y Result of psychosocial factors ± inadequate nutritional information by parent y Deficiency of maternal care of disturbance in maternal-child attachment y Disturbance in child¶s ability to separate from parent leading to food refusal to maintain attention y Idiopathic Failure to Thrive ± unexplained by usual organic and environmental etiologies but may also be classified as NFTT. neurologic lesions. gastroesophageal reflux Malabsorption syndrome.

y Some experts suggest that classifications are
too simplistic because most cases of growth failure have mixed causes.
y FTT be classified according to pathophysiology for
the following categories:
y Inadequate Caloric Intake
y y y y y y
Incorrect formula preparations Neglect, food fads Excessive juice consumption Poverty Behavioral problems affecting eating CNS problems affecting intake

y Inadequate absorption
y Cystic fibrosis, celiac disease, vitamin/ mineral deficiencies,
biliary atresia, hepatic disease

y Increase metabolism
y Hyperthyroidism, congenital heart defects, chronic

y Defective utilization
y Trisomy 21 or 18, congenital infection, metabolic storage

y ETIOLOGY ± multifactorial
y y y y
Infant organic disease Dysfunctional parenting behaviors Subtle neurologic/ behavioral problems Disturbed parent-child interactions

INFANT y Poverty ± dilute formula to extend available supply; no
insurance y No primary care practitioner; homelessness

y Health or childbearing beliefs ± fad diets, excessive concern
with obesity, hypercholesterolemia, nursing caries y Strict use of scheduled feedings y Inappropriate food source; excessive juice intake

y Inadequate nutritional knowledge ± cultural confusion
(immigrant to USA); cognitive impairments

y Family Stress ± overwhelming involvement with another
chronically ill child y Financial, marital, excessive parenting & employment
responsibilities y Single parent employed full time, depression, substance abuse, acute grief

poor release of milk.FAILURE TO THRIVE y Psychosocial factors ± maternal depression. breast surgery augmentation. Munchausen syndrome by proxy. lack of maternal confidence / support. . child temperament y Feeding resistance ± oral tactile hypersensitivity y Infant receiving nonoral nutritional therapy early in life or exclusively fed with feeding tubes y Insufficient breast milk ± fatigue.

motor. pica. language Apathy Poor hygiene Withdrawn behavior Feeding/ eating disorder: vomiting. anorexia.FAILURE TO THRIVE y CLINICAL MANIFESTATIONS: y Growth Failure ± 5th percentile in weight only or weight and y y y y y y y y y y height Developmental delays ± social. rumination No fear of strangers (stage when stranger anxiety is normal) Avoidance of eye contact Wide-eyed gaze & continual scan of environment (radar gaze) Stiff & unyielding or flaccid & unresponsive Minimal smiling . adaptive.

chronic malnutrition y Complete health and dietary history --.history of food consumed y y y y over 3-5 day period Child¶s activity level. ova. anemia.FAILURE TO THRIVE y DIAGNOSTIC EVALUATION: y Evidence of growth retardation & caloric deprivation y Anthropometric measurements y Onset of FTT is fairly recent: weigh (not height) is below accepted standards (5th percentile) y Long standing FTT: height and weight depressed. zinc levels . perceived food allergies. occult blood. stool-reducing substance.E for evidence of organic causes. household organizations & mealtime behaviors & rituals Rule out organic causes y Lead toxicity. parasites y Alkaline phospatase. developmental assessment Family assessment ± parental height. dietary restrictions P.

social worker or mental health professional Relieve any additional stresses on family ± referrals to welfare agencies or supplemental food programs .FAILURE TO THRIVE y THERAPEUTIC MANAGEMENT: y Directed as reversing the malnutrition & underlying y y y y cause Goal: provide sufficient calories to support ³catch up´ growth Treat any coexisting problems Multidisciplinary team: physician. child-life specialist. nurse. gastroenterologist. dietitian.

FAILURE TO THRIVE y THERAPEUTIC MANAGEMENT: y Family therapy y Behavior modification y Hospitalization indications: y y y y y Evidence (anthropometric) of severe acute malnutrition Child abuse / neglect Significant dehydration Caretaker substance abuse or psychosis Outpatient management that does not result in weight gain .

FAILURE TO THRIVE y NURSING CONSIDERATIONS: y Accurate assessment of initial weight & height and daily y y y y weight & recording of all food intake Feeding behavior is documented & parent-child interaction during feeding Feeding checklist Should be placed in a room with noninfectious children of similar age Structure feeding environment to encourage eating .

FAILURE TO THRIVE y NURSING CONSIDERATIONS: y The child y May exhibit altered behavioral interactions y Display intense interest in inanimate objects (toys) but less in y y y y y social interactions Watchful of people at a distance but become distressed as others come closer Dislike being touched or held & avoid face-to-face contact. aversion behaviors (turning from food. vomiting. sleep disturbance. lethargic infant who does not wake up for feedings . spitting) Difficult temperament or passive. excessive irritability Crying during feedings. hoarding food in mouth. sleepy. rumination after feeding. when held they protest briefly on being put down& apathetic when left alone History of difficulty in feeding. refusing to switch from liquids to solids.

depression.FAILURE TO THRIVE y NURSING CONSIDERATIONS: y The parent y Increased risk for altered parent-infant interactions because: y Isolation and social crisis y Inadequate support systems y Poor / absent parenting role models when they were children y Lack of education. drug dependence. immaturity . physical/ mental health problems y Physical and sexual abuse.

medium chain triglycerides may be added slowly ± in 2kcal/oz increments q2-3 days to yield up 28-30 kcal/oz y Carbohydrate additives (8 kcal/tsp) .FAILURE TO THRIVE y NUTRITIONAL MANAGEMENT: y 4 Primary Goals in Nutritional management of FTT: y Correct nutritional deficiencies & achieve ideal weight for height y Increase caloric intake in formula fed infants: supplements like Polycose.

FAILURE TO THRIVE y NUTRITIONAL MANAGEMENT: y Rice cereal & vegetable oil y Multivitamin supplementation ± zinc and iron y Breast-fed infants: add 1 tsp of 24 kcal/oz formula to 3 oz breast milk y Toddlers: high caloric milk (PediaSure) y Fruit juices ± minimized in infants < 6 months y Extreme cases: tube feedings or IV therapy y Allow for catch up growth y Restore optimum body composition .

written schedule of feeding times y Juices should be avoided in children with growth failure until adequate weight gain has been achieved (should not exceed 4oz/day) y Family-system approach .FAILURE TO THRIVE y NUTRITIONAL MANAGEMENT: y Educate parents/ primary caregivers regarding child¶s nutritional requirements & appropriate feeding methods y Step-by-step directions for formula preparations.


HEMOLYTIC DISEASE OF THE NEWBORN y Erythroblastosis fetalis y Hyperbilirubinemia in 1st 24 hrs of life y Abnormally rapid rate of RBC destruction y Anemia caused by this destruction (+) production of RBCs increased # cells for hemolysis y Major causes: isoimmunization (primarily Rh) & ABO incompatibility .

isoimmunization y y y y .HEMOLYTIC DISEASE OF THE NEWBORN y Blood Incompatibility y Antigen / Agglutinogens ± substance capable of producing an immune response if recognized by the body as foreign Antigens + Antibodies = agglutination (clumping) Antibodies in plasma of 1 blood group (except AB group ± no antibodies) produce agglutination when mixed with antigens of a different blood group ABO blood group system ± antibodies occur naturally Rh system .

HEMOLYTIC DISEASE OF THE NEWBORN 1. Mother Rh (-) and Infant Rh (+) : problem y y y y . Rh (+) ± presence of antigen Rh (-) ± absence of antigen No problems occur when Rh blood type are same in both mother and fetus or if mother is Rh (+) and infant is Rh (-). Rh Incompatibility y The presence of naturally occurring Rh factor determines the blood type.

maternal antibody production is stimulated. .HEMOLYTIC DISEASE OF THE NEWBORN Fetal RBCs (with antigens foreign to mother) Enters maternal circulation Mother produces anti-Rh antibodies y Isoimmunization ± no effect on 1st pregnancy y Initial sensitization to Rh antigens rarely occurs before the onset of labor y With increased risk of fetal blood transferred to maternal circulation during placental separation.

cesarean delivery hemorrhage & subsequent isoimmunization: y Multiple gestation.HEMOLYTIC DISEASE OF THE NEWBORN Subsequent pregnancy with Rh (+) fetus Previously formed maternal antibodies to Rh (+) blood cells enter fetal circulation Attack and destroy fetal RBCs y Factors that increase incidence of transpalcental removal of placenta. manual . placenta previa. abruptio placenta.

HEMOLYTIC DISEASE OF THE NEWBORN Fetus compensate for hemolysis and anemia Increase rate of erythropoiesis (+) erythroblasts in circulation Erythroblastosis fetalis y Sensitization may occur during 1st pregnancy if woman had previously received an Rh (+) blood transfusion .

cardiac failure.HEMOLYTIC DISEASE OF THE NEWBORN y No sensitization: if there¶s strong placental barrier y 10-15% of sensitized mothers: no hemolytic reaction in which prevents transfer of fetal blood into maternal circulation Newborn y Some Rh (-) women even though exposed to Rh (+) fetal blood are unable to produce antibodies to foreign antigen y Most severe form: hydrops fetalis y Fetal hypoxia. peritoneal) y Stillborn or in severe respiratory distress y Early intrauterine detection: ultrasound. pericardial. fetal blood sampling y Management: fetal blood transfusions . anasarca. effusions (pleural.

ABO Incompatibility y Major blood group antigens of fetus are different from those of the mother Major blood groups: A. AB. B.HEMOLYTIC DISEASE OF THE NEWBORN 2. O Presence / absence of antibodies & antigens determines whether agglutination will occur y y .


HEMOLYTIC DISEASE OF THE NEWBORN Antibodies in plasma of 1 blood group (except type AB) + Antigens of a different blood group = agglutination (clumping) hemolysis Release large amounts of bilirubin into circulation .

HEMOLYTIC DISEASE OF THE NEWBORN y Most common: mother ± type O and infant ± type A or B Naturally occurring anti-A or anti-B antibodies Present in maternal circulation cross placenta Attack fetal RBC y May occur in 1st pregnancy and subsequent pregnancy. Hemolysis (less severe than Rh incompatibility) .


varying degrees of hydrops. done to baby. used to check amniotic fluid and condition of the placenta Indirect Coombs Test ± evaluate rising anti Rh antibody titers in maternal circulation.HEMOLYTIC DISEASE OF THE NEWBORN y CLINICAL MANIFESTATIONS: y Anemia (hemolysis of RBCs) jaundice on 1st 24 hours. 1st prenatal visit Direct Coombs Test ± detect antibodies attached to the circulating erythrocytes of affected infants . sign of hypovolemic shock y Hypoglycemia ± due to pancreatic cell hyperplasia y DIAGNOSTIC EVALUATION: y Genetic testing y Chorionic Villus Sampling ± determine fetal group and type can lead to y y y y abortion Amniocentesis ± fetal blood type can lead to infection or leaking Ultrasonography ± allow early treatment. to determine how extensive is the hemolysis . done Rh (-) mothers. serum bilirubin elevated (result from liver¶s inability to conjugate & excrete excess bilirubin) y Hepatosplenomegaly.

HEMOLYTIC DISEASE OF THE NEWBORN y THERAPEUTIC MANAGEMENT: y Postnatal therapy: phototherapy for mild cases. anti-D antibodies & memory cells not formed . exchange transfusion for severe cases y Prevention of Rh isoimmunization: Rho immune globulin (Rhogam) y Human gamma globulin concentrate of anti-D to all unsensitized Rh (-) mothers after delivery or abortion of an Rh-positive infant or fetus y Destroys (by phagocytosis & agglutination) fetal RBCs passing into maternal circulation before they can be recognized by mother¶s immune system immune response is blocked.

slows down the progression of bilirubin production y Used in conjunction with phototherapy.HEMOLYTIC DISEASE OF THE NEWBORN y THERAPEUTIC MANAGEMENT: y Must be administered to unsensitized mothers within 72 hours (possibly as long as 3-4 weeks) after the 1st delivery or abortion & repeated after subsequent ones y Administration of RhIg at 26-28 weeks AOG reduces risk of Rh isoimmunization y Administered thru IM to Rh (-) sensitized women. decreased necessity for exchange transfusion . never to newborn or father y Intravenous immunoglobulin (IVIG) ± decreased severity of RBC destruction (hemolysis) in HDN & subsequent development of jaundice y Attacks maternal cells that destroy neonatal RBCs.

hemolysis despite intensive phototherapy y Infant born with hydrops fetalis or sign or cardiac failure . corrects anemia.HEMOLYTIC DISEASE OF THE NEWBORN y THERAPEUTIC MANAGEMENT: y Intrauterine transfusion ± infuse blood into umbilical vein of fetus y Infuse Rh O-negative packed RBCs to raise fetal hematocrit to 40-50% every 2 weeks until fetus reaches 37-38 weeks y Exchange transfusion ± infant¶s blood removed in small amounts (5-10ml at a time) & replaced with compatible blood (Rh ± negative blood) y Removes sensitized RBCs. lowers serum bilirubin. prevents cardiac failure y Indications: y Rapidly increasing bilirubin level.

HEMOLYTIC DISEASE OF THE NEWBORN y THERAPEUTIC MANAGEMENT: y Fresh whole blood typed & crossmatched to mother¶s serum y Amount of donor blood is double the blood volume of infant (85ml/kgBW) but not >500ml y Sterile surgical procedure: catheter umbilical vein inferior vena cava y 5-10 ml withdrawn within 15-20 secs same volume x 60-90 secs .

RBC spherocytosis.HEMOLYTIC DISEASE OF THE NEWBORN y THERAPEUTIC MANAGEMENT: y ABO INCOMPATIBILITY y Early detection & implementation of phototherapy y (+) jaundice within 1st 24 hours. increased serum bilirubin levels. increased ESR: diagnostic of ABO incompatibility y IVIG + phototherapy y Exchange transfusion ± not commonly required except when phototherapy fails to decrease bilirubin concentration .

pulmonary/ cerebral complications (cerebral palsy) y With early detection & intrauterine treatment ± erythroblastic Newborn rare. shock.HEMOLYTIC DISEASE OF THE NEWBORN y PROGNOSIS: y Severe anemia: result in stillbirth. exchange transfusions for the conditions less common . congestive heart failure.

cumulative record of total volume exchanged y Vital signs monitored y (+) signs of cardiac/ respiratory problems: procedure stopped temporarily & resumed once stable y Observe for transfusion reaction .HEMOLYTIC DISEASE OF THE NEWBORN y NURSING CONSIDERATIONS: y Initial nursing responsibility ± recognizing jaundice y Thru prenatal & perinatal history y Exchange transfusion: prepare infant and family assist practitioner with procedure y Document blood volume exchanged: amount of blood volume withdrawn & infused. time of each procedure.

catheter may remain in place . blood is warmed y After procedure: nurse inspects umbilical vein (for bleeding). (-) binding capacity of albumin & bilirubin & hepatic enzyme reaction kernicterus y Hyperthermia ± damages donor¶s RBC. predisposes infant to cardiac arrest y Performed with infant under radiant warmer.HEMOLYTIC DISEASE OF THE NEWBORN y NURSING CONSIDERATIONS: y Attention on thermoregulation y Hypothermia ± increase oxygen and glucose consumption metabolic acidosis. increase free K+. with sterile drapes.


65:1000 live births (1999).SUDDEN INFANT DEATH SYNDROME (SIDS) y Sudden death of infant < 1 years old y Unexplained after a complete mortem examination. Hispanics . African Americans. including an investigation of death scene & review of case history y 3rd leading cause of death in children between 1 month ± 1 year . 95% occur by 6 months y Time of death: during sleep y Racial: Native Americans. increased incidence in winter females y Incidence: 0. males > y Peak age: 2-4 months.

multiple births (2nd twin.SUDDEN INFANT DEATH SYNDROME (SIDS) y Risks: Preterm especially low birth weight. male twin & small-for-date twin) y Newborn with low APGAR score y Infants with CNS disturbances & respiratory disorder (bronchopulmonary dysplasia/ chronic lung disease) y Increased birth order (subsequent siblings as opposed to 1st born child) y Infants with recent history of mild illness .

SUDDEN INFANT DEATH SYNDROME (SIDS) y Sleep in prone position y Cause oropharyngeal obstruction or affect thermal balance or arousal state y Rebreathing of carbon dioxide by prone infant & impaired arousal from active & quiet sleep y Side-lying position no longer recommended ± tends to turn to prone position y Use of soft bedding ± not able to move their heads to the side suffocation and lethal rebreathing y Overheating (thermal stress). co-sleeping with adult especially on sofa y Adult beds/ sofas are not designed for infants & may carry risk of accidental entrapment & suffocation .

. cigarette smoking especially during pregnancy y Poor prenatal care. methadone.SUDDEN INFANT DEATH SYNDROME (SIDS) y Lower incidence in breast-fed infants ± pacifier may be protective against SIDS y Maternal risk: young age. substance abuse (heroin. cocaine) y 12% of all SIDS death could be prevented with prenatal smoking cessation y Maternal smoking decreases infant¶s ability to arouse to auditory stimuli in mothers who smoke prenatally.

impaired arousal responsiveness to increase carbon dioxide or decrease oxygen y Sleep apnea is not the cause of SIDS. excessive periodic breathing. increased frequency of brief inspiratory pauses. genetic predisposition has been postulated as the cause y Autopsies: pulmonary edema & intrathoracic hemorrhages SIDS y Should be performed on all infants suspected of dying of .SUDDEN INFANT DEATH SYNDROME (SIDS) y ETIOLOGY: y Unknown y Hypothesis: related to brainstem abnormality in neurologic regulation of cardiorespiratory control y Abnormalities: prolonged sleep apnea.

SUDDEN INFANT DEATH SYNDROME (SIDS) y INFANTS AT RISK FOR SIDS: y Infants with 1 or more ALTEs requiring cardiopulmonary resuscitation (CPR) or vigorous stimulation y Preterm infants who continue to have apnea at the time of hospital discharge y Siblings of 2 or more SIDS victim y Infants with certain types of disease or conditions ± central hypoventilation y Home monitoring and/or use of respiratory stimulant drugs recommended y No diagnostic tests exist to predict which infants will survive .

SUDDEN INFANT DEATH SYNDROME (SIDS) y NURSING CONSIDERATIONS: y Educate families in prevention of SIDS y Risk of prone sleeping position in infant births ± 6 months y Use of appropriate beddings. newborn discharge teaching and newborn-care classes y Follow-up visits. immunization visits y Discuss infant sleep position . well-baby clinic visits. parental smoking around infant and dangers of sharing an adult bed with infant y Post partum discharge planning.

stuffed toys. pillows y No pillows/ quilts. moldable mattresses.SUDDEN INFANT DEATH SYNDROME (SIDS) y NURSING CONSIDERATIONS: y Psychologic intervention ± loss of child y Practices that may reduce the risk of SIDS y Avoid smoking during pregnancy and near the infant y Encouraging supine sleeping position y ³back to sleep´ y Avoid soft. towels y Discouraging bed sharing y Encourage breastfeeding . blankets.

naptime and bedtime.SUDDEN INFANT DEATH SYNDROME (SIDS) y NURSING CONSIDERATIONS: y Avoid overheating during sleep y Infants should wear light-clothing. huddled in 1 corner . comfortable room temperature y Infant¶s head position should be varied to prevent flattening of the skull y Use of pacifier ± protective against occurrence of SIDS. no sweetened coating y Finding the infant y it¶s always the mother who finds child dead in crib y Child is in disheveled bed w/ blankets over head.

lying face down in secretions (bled to death) y Diaper is wet and full of stool ± cataclysmic type of death y Parents must deal with his/her initial shock. grief y Compassionate. blood-tinged fluid fills the mouth & nostrils. panic.SUDDEN INFANT DEATH SYNDROME (SIDS) y NURSING CONSIDERATIONS: y Frothy. sensitive approach to family .

SUDDEN INFANT DEATH SYNDROME (SIDS) y NURSING CONSIDERATIONS: y Arriving at emergency department y No attempt at resuscitation y Parents are asked only factual questions ± when they found the infant. how he/she looked y No misguided statements: ³this looks like suffocation´ (guilt) y Discuss possible autopsy y Compassionate care ± allow them to say good-bye to their child .


APNEA OF PREMATURITY (AOP) y Preterm infants. rare: full-term y Apneic spells increase in prevalence the younger the gestational age y 1/3 infants <33 weeks AOG. that may or may not be followed by bradycardia.> 20 seconds .<15-20 seconds y Pathologic apnea . >1/2 healthy infants < 30 weeks AOG y Resolves as infant reaches 37 weeks postmenstrual age y Preterms are periodic breathers ± periods of rapid respirations separated by periods of very slow breathing. oxygen desaturation and color change y Temporary apnea . often short periods with no visible or audible respirations y Apnea ± extension of periodic breathing y Lapse of spontaneous breathing for 20 seconds or longer.

APNEA OF PREMATURITY (AOP) y Classification according to origin: y Central Apnea ± absence of diaphragmatic and other respiratory effort y Occurs when CNS does not transmit signals to the respiratory muscle y Obstructive Apnea ± air flow ceases because of upper airway obstruction yet chest or abdominal wall movement is present y Mixed Apnea: combination of central and obstructive apnea y Most common apnea seen in preterm infants .

have fewer dendritic associations than those of more mature infants y Respiratory reflexes less mature ± contributing factor in etiology y Weakness of muscles of thorax. diaphragm and upper airway ± contribute to apneic episodes .APNEA OF PREMATURITY (AOP) y PATHOPHYSIOLOGY: y Reflects the immature and poorly refined neurologic and chemical respiratory control mechanism in premature infants y Not responsive to hypercarbia and hypoxemia.

APNEA OF PREMATURITY (AOP) y PATHOPHYSIOLOGY: y Apnea ± observed during periods of REM sleep y Precipitated/ worsened by a variety of factors: y Infection y Intracranial hemorrhage y PDA y Secondary causes: investigated in infants with newonset apnea or when there¶s significant change in frequency or severity of apneic episodes y Apnea in full-term: consider secondary cause .

or poor positioning Anemia. inborn errors of metabolism (hyperammonemia). endotracheal intubation) CNS depression ± pharmacologic agents Intraventricular hemorrhage (IVH) Patent ductus arteriosus (PDA). congestive heart failure (CHF) Depression following maternal obstetric sedation Respiratory distress ± pnemonia. hypocalcemia. congenital defects of upper airways . hyponatremia Sepsis. reflux of gastric contents. polycythemia Dehydration Cooling / overheating Hypoxemia Hypercapnia / hypocapnia Hypoglycemia.APNEA OF PREMATURITY (AOP) y POSSIBLE CAUSES OF APNEA OF PREMATURITY: y y y y y y y y y y y y y y y y Prematurity Airway obstruction with mucus or milk. gavage tube insertion. meningitis Seizures Increased vaga tone (in response to suctioning nasopharynx.

aminophylline or caffeine) y Reduce frequency of primary apnea-bradycardia spells in newborn y CNS stimulants to breathing y Observe for symptoms of toxicity y Caffeine ± fewer side effects . once daily dosing y Monitor weight and urine output .APNEA OF PREMATURITY (AOP) y CLINICAL MANIFESTATIONS: y Persistent apneic spells y TREATMENT y Observe for apnea y Check for thermal stability y Administration of methylxanthines (theophylline.

APNEA OF PREMATURITY (AOP) y TREATMENT: y Nasal continuous positive airway pressure (NCPAP) and intermittent positive pressure ventilation y CPAP acts to maintain airway patency y More effective for obstructive/ mixed apnea .

APNEA OF PREMATURITY (AOP) y NURSING CONSIDERATION: Monitor respiration and heart rate routinely in all preterm infants Observe for presence of respirations Observe color Provide gentle tactile stimulation ± rubbing the back/ chest gently. turning infant to supine position y If tactile stimulation fails to reinstitute respiration ± flow by oxygen and suctioning of nose and mouth y Apply artificial ventilation with bag-valve mask and with sufficient pressure to lift rib cage y If breathing does not begin y Raise chin gently to open airway y Infant is never shaken y y y y .

did infant self-recover or whether tactile stimulation or other measures were done to restore breathing. Investigate possible cause of apneic episode Observe for signs of theophylline or caffeine toxicity. and nasal septum . tachycardia (rate 180-190/ min) and later. abdominal distention. irritation. ambient oxygen) ± use pulse oximetry Record episodes of apnea .APNEA OF PREMATURITY (AOP) y NURSING CONSIDERATION: y After breathing is restored: assess for and manage any y y y y precipitating factors (temperature instability. irritability Assess skin (with NCPAP) for breakdown. vomiting.# apneic spells. appearance during and after the episode. restlessness.


race. parenting .AUTISTIC SPECTRUM DISORDER (AUTISM) y Complex developmental disorder of brain function accompanied by intellectual and behavioral deficits age y Manifested during early childhood: 18-36 months of y 1-2 in 500 children. males > females (females more severely affected) style y Not related to socioeconomic level.

structural brain anomalies Perinatal events: higher incidence of maternal uterine bleeding during pregnancy y Lower incidence of maternal vaginal infections during pregnancy y Decreased maternal use of contraceptives y Higher incidence of neonatal hyperbilirubinemia . persistence of primitive reflexes. delayed development of hand y y y y y predominance. H. epileptic seizures. influenza meningitis. tuberous sclerosis. hypoplasia of vermis of cerebellum Increased in twins High risk of recurrence of ASD in families with one affected child Not caused by thimerosal-containing vaccines Associated with fragile X syndrome. metabolic abnormalities (increased serotonin). fetal rubella syndrome. metabolic disorder.AUTISTIC SPECTRUM DISORDER (AUTISM) y ETIOLOGY y Unknown y Multiple biologic causes y Abnormal EEG.

perceptual skills (puzzle building) .AUTISTIC SPECTRUM DISORDER (AUTISM) y CLINICAL MANIFESTATIONS AND DIAGNOSTIC EVALUATION: y Hallmark: inability to maintain eye contact with another person y Display limited functional play and may interact with toys in an unusual manner y Deficits in social development: primary feature of illness y Majority have some degree of mental retardation y Females tend to have very low intelligence scores y Savants ± children with ASD who excel in particular areas: art. music. mathematics. memory.

2-word phrases by 24 months y Sudden deterioration in extant expressive speech is also a red-flag event for further evaluation . single word by 16 months.AUTISTIC SPECTRUM DISORDER (AUTISM) y Speech and language delays y Immediate evaluation of any child who does not display such language skills as babbling or gesturing by 12 months.

bringing. as manifested by at least 2 of the following: y Marked impairment in use of multiple nonverbal behaviors such as eye-to-eye gaze. and one each from (2) & (3) (1) Qualitative impairment in social interaction.AUTISTIC SPECTRUM DISORDER (AUTISM) y DIAGNOSTIC CRITERIA FOR ASD: y Total of 6 (or more) items from (1). (2). facial expression. or achievements w/ other people (ex. & gestures to regulate social interaction y Failure to develop peer relationships appropriate to developmental level y A lack of spontaneous seeking to share enjoyment. interests. (3) with at least two from (1). body postures. or pointing out objects of interest) y Lack of social/ emotional reciprocity . By a lack of showing.

of the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gesture or mime) y In individuals w/ adequate speech. spontaneous.AUTISTIC SPECTRUM DISORDER (AUTISM) (2) Qualitative impairments in communication as manifested by at least 1 of the following: y Delay in. make-believe play or social imitative play appropriate to developmental level . or total lack. marked impairment in the ability to initiate or sustain a conversation with others y Stereotyped and repetitive use of language or idiosyncratic language y Lack of varied.

nonfunctional routines or rituals y Stereotyped & repetitive motor mannerisms (ex. Hand or finger flapping or twisting.AUTISTIC SPECTRUM DISORDER (AUTISM) (3) Restricted repetitive and stereotyped patterns of behavior. as manifested by at least 1 of the following: y Encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus y Apparently inflexible adherence to specific. interests & activities. or complex whole-body movements) y Persistent preoccupation w/ parts of objects y Delays or abnormal functioning in at least 1 of the following areas with onset before age 3 years y Social interaction y Language as used in social communication y Symbolic or imaginative play y The disturbance is not better accounted for by Rett disorder or childhood disintegrative disorder .

years & have an IQ higher than 50 at time of diagnosis . but most require lifelong adult supervision y Aggravation of psychiatric symptoms ± ½ children during adolescence.AUTISTIC SPECTRUM DISORDER (AUTISM) y PROGNOSIS: y Severely disabling condition y Some improve with acquisition of language skills & communication w/ others y Some achieve independence. w/ girls having tendency for continued deterioration y Most favorable for children who develop communicative speech by age.

AUTISTIC SPECTRUM DISORDER (AUTISM) y NURSING CARE MANAGEMENT: y No cure for ASD but there are numerous therapies y Highly structured & intensive behavior modification programs y Promote positive reinforcement. teach verbal communication skills and decrease unacceptable behavior y Provide a structured routine for the child to follow ± key management in ASD . increase social awareness of others.

feeding these children ± may swallow thermometer. gags when eating y Family support . administering meds.AUTISTIC SPECTRUM DISORDER (AUTISM) y NURSING CARE MANAGEMENT: y Hospitalized child with ASD: dcrease stimulation y Place child in private room y Avoid extraneous auditory & visual distraction y Encourage parents to bring in possessions to which child is attached y Minimum holding & eye contact y Care must be taken when performing procedures.counseling .


MAJOR STRESSORS OF HOSPITALIZATION y SEPARATION ANXIETY y Middle infancy ± preschool age y STAGES: y PROTEST PHASE: y y y y y Cry and scream Cling to parent Avoids/ rejects contact with strangers Verbally and physically attack strangers Attempts to escape and find parents .

drink.MAJOR STRESSORS OF HOSPITALIZATION y DESPAIR PHASE: y y y y y Crying stops. evidence of depression Less active Uninterested in food Withdraws from others Child¶s physical condition may deteriorate from refusal to eat. resignation and not contentment Child becomes more interested in the surroundings Forms new but superficial relationship May have serious attachment to parent after separation . or move y DETACHMENT PHASE: y y y y Denial.

they react with negativism y Results from altered routines and rituals .MAJOR STRESSORS OF HOSPITALIZATION y LOSS OF CONTROL y INFANTS y Trust y Consistent. loving caregivers y Attempts to control their environment through emotional expressions y TODDLERS y Autonomy y When their egocentric pleasures meet with obstacles.

rather than from the specific to the general . y y y y and enforced dependency Egocentric and magical thinking typical of age May view illness and hospitalization as punishment for misdeed PREOPERATIONAL THOUGHT ± explanations are understood only in terms of real events TRANSDUCTIVE REASONING ± deduct from the particular to particular.MAJOR STRESSORS OF HOSPITALIZATION y PRESCHOOLERS y Suffer loss of control by physical restriction. altered routines.

MAJOR STRESSORS OF HOSPITALIZATION y SCHOOL AGE y Striving for independence and productivity y Altered family roles. lack of productivity y Boredom y ADOLESCENTS y Struggle for independence. physical disability. frustration Voluntarily isolate themselves from age mates until they can feel they can compete Need for information about their condition . abandonment. fears of death. self assertion and liberation ± y y y y personal identity Separation from peer group May respond with anger. permanent injury. loss of peer acceptance.

thrashing y Loud crying y Facial expressions of discomfort ± most consistent indicator of stress y No understanding of the relationship between stimuli and subsequent pain.MAJOR STRESSORS OF HOSPITALIZATION y FEARS OF BODILY INJURY AND PAIN y Common fear among children y May persist into adulthood and result in avoidance of needed care y YOUNG INFANT¶S RESPONSE TO PAIN: <6 months y Generalized response of rigidity. .

needs restraints Clings to parent.MAJOR STRESSORS OF HOSPITALIZATION y OLDER INFANT¶S RESPONSE TO PAIN: (6months ± 1year) y y y y Withdrawal from painful stimuli Loud crying Facial grimace Physical resistance y YOUNG CHILD¶S RESPONSE TO PAIN: (toddlers) y y y y y y y Loud crying. ³ouch´. nurse. screaming Verbalization. ³it hurts´ Thrashing of limbs Attempts to push away stimulus Uncooperative. or other significant person Request emotional support . ³ow´.

MAJOR STRESSORS OF HOSPITALIZATION y SCOOL-AGE CHILD¶S RESPONSE TO PAIN y Stalling behavior ± ³wait a minute´. less motor activity y Increased muscle tension and body control y More verbalization (³It hurts´. You¶re hurting me!´) . ³I¶m not ready´ y Muscle rigidity y May use all behaviors of young child y ADOLESCENT¶S RESPONSE TO PAIN y Less vocal protest.

Frequent .INDIVIDUAL RISK FACTORS THAT INCREASE VULNERABILITY TO STRESSES OF HOSPITALIZATION y ³Difficult´ temperament y Lack of fit between child and parent y Age (especially between 6 months and 5 years old) y Male gender y Below average intelligence y Multiple and continuing stresses (ex.

BENEFICIAL EFFECT OF HOSPITALIZATION y Recovery from illness y Increase coping skills y Master stress and feel competent in coping y New socialization experiences .

PREVENTING OR MINIMIZING SEPARATION y Primary nursing goal y Especially for children < 5 years old y Family-centered care y Parents are not ³visitors´ y Familiar items from home .

if possible y Time structuring y Self-care (age appropriate) y School work y Friends and visitors .NORMALIZING THE HOSPITAL ENVIRONMENT y Maintain child¶s routine.

. or death. y Preparation of children for painful procedures y Use of bandages y Repeatedly stress the reason for a procedure y Adolescents may express concern about the actual procedure but more anxious about the resulting scar. bodily intrusion.PREVENTING OR MINIMIZING FEAR OF BODILY INJURY y All children fear bodily injury from mutation. body-image change. disability. decreases their fears.

PAIN FACTS AND FALLACIES y FACT: Children are under treated for pain. y FACT: Analgesia is withheld for fear of the child becoming addicted y FALLACY: Analgesia should be withheld because it may cause respiratory depression in children y FALLACY: Infants do not feel pain. .

y Question the child ± verbal & description of pain. y Secure parent¶s involvement. y Use pain rating scale. y Take action and evaluate result.PRINCIPLE OF PAIN ASSESSMENT IN CHILDREN: QUESTT y Question the child. y Evaluate behavioral & physiologic changes. . y Take the cause of pain into account. y Use of Pain Rating Scale ± provide a quantitative self-reporting measure of pain. Ask child to point where it hurts.

PAIN RATING SCALES y Not all pain rating scale are reliable or appropriate for children y Should be age appropriate y Consistent use of same scale by all staff. y Familiarize child with scale .

A.PAIN RATING SCALE F. relaxed position. ACTIVITY. CONSOLABILITY 0 FACE No particular expression or smile Normal. whimpers. CRY.L. rigid or jerking Crying steadily. frequent complaints Difficult to console or comfort LEGS ACTIVITY CRY CONSOLABILITY Content. disinterested Uneasy. tense. shifting back and forth Moans. quivering chin Arched. occasional complaint Reassured by occasional touching. moves easily No cry (awake or asleep) 1 Occasional grimace or frown. screams or sobs. relaxed . hugging or talking to 2 Frequent to constant frown. withdrawn. clenched jaw.C (FACE. LEGS.C. restless.

concrete phenomenon as cause of illness y CONTAGION ± perceives cause of illness as proximity between 2 events that occur by magic .CHILDREN¶S DEVELOPMENTAL CONCEPT OF ILLNESS y PREOPERATIONAL THOUGHT (2-7years) y PHENOMENISM ± perceives an external. unrelated.

object.CHILDREN¶S DEVELOPMENTAL CONCEPT OF ILLNESS y CONCRETE OPERATIONAL THOUGHT (7-10years) y CONTAMINATION ± perceives cause as a person. or action external to the child that is ³bad´ or ³harmful´ to the body y INTERNALIZATION ± perceives illness as having an external cause but as being located inside the body .

CHILDREN¶S DEVELOPMENTAL CONCEPT OF ILLNESS y FORMAL OPERATIONAL THOUGHT (13yrs & above) y PHYSIOLOGIC ± perceives cause as malfunctioning or nonfunctioning organ or process. can explain illness in sequence of events y PSYCHOPHYSIOLOGIC ± realizes that psychologic actions and attitudes affect health and illness. .

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