FAILURE TO THRIVE y Sign of inadequate growth resulting from inability to obtain or use calories required for growth y No universal

definition y Common parameter: WEIGHT, sometimes height that falls below th 5 percentile for child s age 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. y 3 GENERAL CATEGORIES: y Organic Failure to Thrive y Physical Cause y Congenital heart defects, neurologic lesions, cerebral palsy, microcephaly y Chronic renal failure, gastroesophageal reflux y Malabsorption syndrome, endocrine dysfunction y Cystic fibrosis, 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. 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 Incorrect formula preparations y Neglect, food fads y Excessive juice consumption y Poverty y Behavioral problems affecting eating y 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 immunodeficiency y Defective utilization y Trisomy 21 or 18, congenital infection, metabolic storage diseases y ETIOLOGY multifactorial y Infant organic disease y Dysfunctional parenting behaviors

Subtle neurologic/ behavioral problems Disturbed parent-child interactions FACTORS LEADING TO INADEQUATE FEEDING OF 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 y Psychosocial factors maternal depression, Munchausen syndrome by proxy, 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, poor release of milk, breast surgery augmentation, lack of maternal confidence / support. CLINICAL MANIFESTATIONS: th y Growth Failure 5 percentile in weight only or weight and height y Developmental delays social, motor, adaptive, language y Apathy y Poor hygiene y Withdrawn behavior y Feeding/ eating disorder: vomiting, anorexia, pica, rumination y No fear of strangers (stage when stranger anxiety is normal) y Avoidance of eye contact y Wide-eyed gaze & continual scan of environment (radar gaze) y Stiff & unyielding or flaccid & unresponsive y Minimal smiling DIAGNOSTIC EVALUATION: y Evidence of growth retardation & caloric deprivation y Anthropometric measurements y Onset of FTT is fairly recent: weigh (not th height) is below accepted standards (5 percentile) y Long standing FTT: height and weight depressed; chronic malnutrition y Complete health and dietary history --- history of food consumed over 3-5 day period y Child s activity level, perceived food allergies, dietary restrictions y P.E for evidence of organic causes, developmental assessment y Family assessment parental height, household organizations & mealtime behaviors & rituals y Rule out organic causes y y y

Lead toxicity, anemia, stool-reducing substance, occult blood, ova, parasites y Alkaline phospatase, zinc levels THERAPEUTIC MANAGEMENT: y Directed as reversing the malnutrition & underlying cause y Goal: provide sufficient calories to support catch up growth y Treat any coexisting problems y Multidisciplinary team: physician, nurse, dietitian, gastroenterologist, child-life specialist, social worker or mental health professional y Relieve any additional stresses on family referrals to welfare agencies or supplemental food programs y Family therapy y Behavior modification y Hospitalization indications: y Evidence (anthropometric) of severe acute malnutrition y Child abuse / neglect y Significant dehydration y Caretaker substance abuse or psychosis y Outpatient management that does not result in weight gain NURSING CONSIDERATIONS: y Accurate assessment of initial weight & height and daily weight & recording of all food intake y Feeding behavior is documented & parent-child interaction during feeding y Feeding checklist y Should be placed in a room with noninfectious children of similar age y Structure feeding environment to encourage eating y The child y May exhibit altered behavioral interactions y Display intense interest in inanimate objects (toys) but less in social interactions y Watchful of people at a distance but become distressed as others come closer y Dislike being touched or held & avoid faceto-face contact; when held they protest briefly on being put down& apathetic when left alone y History of difficulty in feeding, vomiting, sleep disturbance, excessive irritability y Crying during feedings, hoarding food in mouth, rumination after feeding, refusing to switch from liquids to solids, aversion behaviors (turning from food, spitting) y Difficult temperament or passive, sleepy, lethargic infant who does not wake up for feedings 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, physical/ mental health problems y Physical and sexual abuse, depression, drug dependence, immaturity y

NUTRITIONAL MANAGEMENT: y 4 Primary Goals in Nutritional management of FTT: y Correct nutritional deficiencies & achieve ideal weight for height  Increase caloric intake in formula fed infants: supplements like Polycose, 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)  Rice cereal & vegetable oil  Multivitamin supplementation zinc and iron  Breast-fed infants: add 1 tsp of 24 kcal/oz formula to 3 oz breast milk  Toddlers: high caloric milk (PediaSure)  Fruit juices minimized in infants < 6 months  Extreme cases: tube feedings or IV therapy  Allow for catch up growth  Restore optimum body composition  Educate parents/ primary caregivers regarding child s nutritional requirements & appropriate feeding methods y Step-by-step directions for formula preparations, 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)  Family-system approach HEMOLYTIC DISEASE OF THE NEWBORN y Erythroblastosis fetalis st y Hyperbilirubinemia in 1 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 y Blood Incompatibility y Antigen / Agglutinogens substance capable of producing an immune response if recognized by the body as foreign y Antigens + Antibodies = agglutination (clumping) y Antibodies in plasma of 1 blood group (except AB group no antibodies) produce agglutination when mixed with antigens of a different blood group y ABO blood group system antibodies occur naturally y Rh system - isoimmunization . Rh Incompatibility y The presence of naturally occurring Rh factor determines the blood type. y Rh (+) presence of antigen y Rh (-) absence of antigen y No problems occur when Rh blood type are same in both mother and fetus or if mother is Rh (+) and infant is Rh (-). y Mother Rh (-) and Infant Rh (+) : problem st y Isoimmunization no effect on 1 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, maternal antibody production is stimulated. y Factors that increase incidence of transpalcental hemorrhage & subsequent isoimmunization: y

Multiple gestation, abruptio placenta, placenta previa, manual removal of placenta, cesarean delivery y No sensitization: if there s strong placental barrier which prevents transfer of fetal blood into maternal circulation y 10-15% of sensitized mothers: no hemolytic reaction in 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, cardiac failure, anasarca, effusions (pleural, pericardial, peritoneal) y Stillborn or in severe respiratory distress y Early intrauterine detection: ultrasound, fetal blood sampling y Management: fetal blood transfusions 2. ABO Incompatibility y Major blood group antigens of fetus are different from those of the mother y Major blood groups: A, B, AB, O y Presence / absence of antibodies & antigens determines whether agglutination will occur y CLINICAL MANIFESTATIONS: st y Anemia (hemolysis of RBCs) jaundice on 1 24 hours; serum bilirubin elevated (result from liver s inability to conjugate & excrete excess bilirubin) y Hepatosplenomegaly, varying degrees of hydrops, 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 abortion y Amniocentesis fetal blood type can lead to infection or leaking y Ultrasonography allow early treatment; used to check amniotic fluid and condition of the placenta y Indirect Coombs Test evaluate rising anti Rh antibody st titers in maternal circulation; done Rh (-) mothers; 1 prenatal visit y Direct Coombs Test detect antibodies attached to the circulating erythrocytes of affected infants ; done to baby; to determine how extensive is the hemolysis y THERAPEUTIC MANAGEMENT: y Postnatal therapy: phototherapy for mild cases, exchange transfusion for severe cases y Prevention of Rh isoimmunization: Rho immune globulin (Rhogam) y Human gamma globulin concentrate of antiD 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, anti-D antibodies & memory cells not formed y Must be administered to unsensitized mothers within 72 hours (possibly as long as st 3-4 weeks) after the 1 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, 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, slows down the progression of bilirubin production y Used in conjunction with phototherapy; decreased necessity for exchange transfusion 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, corrects anemia, prevents cardiac failure y Indications: y Rapidly increasing bilirubin level, hemolysis despite intensive phototherapy y Infant born with hydrops fetalis or sign or cardiac failure 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 y ABO INCOMPATIBILITY y Early detection & implementation of phototherapy st y (+) jaundice within 1 24 hours, increased serum bilirubin levels, RBC spherocytosis, increased ESR: diagnostic of ABO incompatibility y IVIG + phototherapy y Exchange transfusion not commonly required except when phototherapy fails to decrease bilirubin concentration PROGNOSIS: y Severe anemia: result in stillbirth, shock, congestive heart failure, pulmonary/ cerebral complications (cerebral palsy) y With early detection & intrauterine treatment erythroblastic Newborn rare, exchange transfusions for the conditions less common 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 & y

infused, time of each procedure, 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 y Attention on thermoregulation y Hypothermia increase oxygen and glucose consumption metabolic acidosis; (-) binding capacity of albumin & bilirubin & hepatic enzyme reaction kernicterus y Hyperthermia damages donor s RBC, increase free K+, predisposes infant to cardiac arrest y Performed with infant under radiant warmer, with sterile drapes, blood is warmed y After procedure: nurse inspects umbilical vein (for bleeding), catheter may remain in place SUDDEN INFANT DEATH SYNDROME (SIDS) y Sudden death of infant < 1 years old y Unexplained after a complete mortem examination, including an investigation of death scene & review of case history rd y 3 leading cause of death in children between 1 month 1 year ; increased incidence in winter y Incidence: 0.65:1000 live births (1999); males > females y Peak age: 2-4 months; 95% occur by 6 months y Time of death: during sleep y Racial: Native Americans, African Americans, Hispanics y Lower socioeconomic class nd y Risks: Preterm especially low birth weight; multiple births (2 twin, 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 st to 1 born child) y Infants with recent history of mild illness 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 y Lower incidence in breast-fed infants pacifier may be protective against SIDS y Maternal risk: young age, cigarette smoking especially during pregnancy y Poor prenatal care, substance abuse (heroin, methadone, cocaine)

12% of all SIDS death could be prevented with prenatal smoking cessation Maternal smoking decreases infant s ability to arouse to auditory stimuli in mothers who smoke prenatally y ETIOLOGY: y Unknown y Hypothesis: related to brainstem abnormality in neurologic regulation of cardiorespiratory control y Abnormalities: prolonged sleep apnea, increased frequency of brief inspiratory pauses, excessive periodic breathing, impaired arousal responsiveness to increase carbon dioxide or decrease oxygen y Sleep apnea is not the cause of SIDS; genetic predisposition has been postulated as the cause y Autopsies: pulmonary edema & intrathoracic hemorrhages y Should be performed on all infants suspected of dying of 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 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, parental smoking around infant and dangers of sharing an adult bed with infant y Post partum discharge planning, newborn discharge teaching and newborn-care classes y Follow-up visits, well-baby clinic visits, immunization visits y Discuss infant sleep position 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 back to sleep y Avoid soft, moldable mattresses, blankets, pillows y No pillows/ quilts, stuffed toys, towels y Discouraging bed sharing y Encourage breastfeeding y Avoid overheating during sleep y Infants should wear lightclothing, 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; naptime and bedtime, 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, huddled in 1 corner y Frothy, blood-tinged fluid fills the mouth & nostrils, 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, panic, grief y Compassionate, sensitive approach to family 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: this 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, >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, 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, that may or may not be followed by bradycardia, oxygen desaturation and color change y Temporary apnea - <15-20 seconds y Pathologic apnea - > 20 seconds 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 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, 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 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 POSSIBLE CAUSES OF APNEA OF PREMATURITY: y Prematurity y Airway obstruction with mucus or milk, or poor positioning y Anemia, polycythemia y Dehydration y Cooling / overheating y Hypoxemia y Hypercapnia / hypocapnia y Hypoglycemia, hypocalcemia, hyponatremia y Sepsis, meningitis y Seizures y Increased vaga tone (in response to suctioning nasopharynx, gavage tube insertion, reflux of gastric contents, endotracheal intubation) y CNS depression pharmacologic agents y Intraventricular hemorrhage (IVH) y Patent ductus arteriosus (PDA), congestive heart failure (CHF) y Depression following maternal obstetric sedation y Respiratory distress pnemonia, inborn errors of metabolism (hyperammonemia), congenital defects of upper airways CLINICAL MANIFESTATIONS: y Persistent apneic spells y TREATMENT y Observe for apnea y Check for thermal stability y Administration of methylxanthines (theophylline, aminophylline or caffeine) y Reduce frequency of primary apneabradycardia 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 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 NURSING CONSIDERATION: y Monitor respiration and heart rate routinely in all preterm infants y Observe for presence of respirations y Observe color y 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 After breathing is restored: assess for and manage any precipitating factors (temperature instability, abdominal distention, ambient oxygen) use pulse oximetry y Record episodes of apnea - # apneic spells, appearance during and after the episode, did infant self-recover or whether tactile stimulation or other measures were done to restore breathing. y Investigate possible cause of apneic episode y Observe for signs of theophylline or caffeine toxicity; tachycardia (rate 180-190/ min) and later, vomiting, restlessness, irritability Assess skin (with NCPAP) for breakdown, irritation, and nasal septum y AUTISTIC SPECTRUM DISORDER (AUTISM) y Complex developmental disorder of brain function accompanied by intellectual and behavioral deficits y Manifested during early childhood: 18-36 months of age y 1-2 in 500 children; males > females (females more severely affected) y Not related to socioeconomic level, race, parenting style y ETIOLOGY y Unknown y Multiple biologic causes y Abnormal EEG, epileptic seizures, delayed development of hand predominance, persistence of primitive reflexes, metabolic abnormalities (increased serotonin), hypoplasia of vermis of cerebellum y Increased in twins y High risk of recurrence of ASD in families with one affected child y Not caused by thimerosal-containing vaccines y Associated with fragile X syndrome, tuberous sclerosis, metabolic disorder, fetal rubella syndrome, H. influenza meningitis, structural brain anomalies y 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 Higher incidence of neonatal hyperbilirubinemia 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, memory, mathematics, perceptual skills (puzzle building) 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, single word by 16 months, 2-word phrases by 24 months

Sudden deterioration in extant expressive speech is also a red-flag event for further evaluation y DIAGNOSTIC CRITERIA FOR ASD: y Total of 6 (or more) items from (1), (2), (3) with at least two from (1), and one each from (2) & (3) (1) Qualitative impairment in social interaction, as manifested by at least 2 of the following:  Marked impairment in use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, & gestures to regulate social interaction  Failure to develop peer relationships appropriate to developmental level  A lack of spontaneous seeking to share enjoyment, interests, or achievements w/ other people (ex. By a lack of showing, bringing, or pointing out objects of interest)  Lack of social/ emotional reciprocity (2) Qualitative impairments in communication as manifested by at least 1 of the following:  Delay in, or total lack, of the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gesture or mime)  In individuals w/ adequate speech, marked impairment in the ability to initiate or sustain a conversation with others  Stereotyped and repetitive use of language or idiosyncratic language  Lack of varied, spontaneous, make-believe play or social imitative play appropriate to developmental level (3) Restricted repetitive and stereotyped patterns of behavior, interests & activities, as manifested by at least 1 of the following:  Encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus  Apparently inflexible adherence to specific, nonfunctional routines or rituals  Stereotyped & repetitive motor mannerisms (ex. Hand or finger flapping or twisting, or complex whole-body movements)  Persistent preoccupation w/ parts of objects  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  The disturbance is not better accounted for by Rett disorder or childhood disintegrative disorder y PROGNOSIS: y Severely disabling condition y Some improve with acquisition of language skills & communication w/ others y Some achieve independence, but most require lifelong adult supervision y Aggravation of psychiatric symptoms children during adolescence, w/ girls having tendency for continued deterioration y Most favorable for children who develop communicative speech by age, years & have an IQ higher than 50 at time of diagnosis 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, increase social awareness of others, teach verbal communication skills and decrease unacceptable behavior y

y y

Provide a structured routine for the child to follow key management in ASD 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, administering meds, feeding these children may swallow thermometer, gags when eating Family support - counseling