Deviations in intrauterine growth patterns not only increase the risk of morbidity and mortality in the early newborn period, but may also have long-term implications for altered growth and development and for altered CNS function and learning disabilities in childhood.
This general plan of care is designed to facilitate optimal nursing management of the infant with deviations in intrauterine growth and is to be used in conjunction with the CPs: The Neonate at Two Hours to Two Days of Age, and The Preterm Infant, as appropriate. Growth deviations are classified as SGA, intrauterine growth retardation/restriction (IUGR), and LGA.
SGA/IUGR: Any newborn whose birth weight falls at or below the 10th percentile on classification charts, considering local factors (e.g., ethnicity, altitude).
LGA/Macrosomic: Any newborn whose birth weight is at or above the 90th percentile on classification charts, considering local population at any week in gestation (with special attention to determining appropriate gestational age), or who at birth weighs more than 4000 g (8 lb 13 oz).
NEONATAL ASSESSMENT DATA BASE
Activity level may be excessive, with vigorous cry/hungry suck attributable to chronic intrauterine hypoxia.
Excessive/strenuous exercise program
Resides at high altitude
Heart/lung disease; bleeding, severe anemia or sickle cell anemia; chronic hypertension or PIH
Abdomen may appear scaphoid or concave.
Pyelonephritis, chronic renal disease
All body parts may be below expected size for gestational age but in proportion/symmetrical to each other (suggests a chronic or prolonged problem throughout gestation).
Disproportionate weight as compared to length and head circumference (appears long and thin with normal head circumference) suggests episodic vascular insufficiency in third trimester.
Sunken abdomen; absence of subcutaneous tissue.
Decreased muscle mass, especially in the cheeks, buttocks, and thighs.
May demonstrate metabolic instability associated with hypoglycemia/hypocalcemia.
Malnutrition/poor nutritional intake (chronic or during third trimester); history of eating disorders
Advanced diabetes mellitus (class D or above); PKU
Skull suture and fontanels appear widened; bulging of fontanels caused by inadequate bone growth may be evident.
Small head with protruding forehead, sunken nasal bridge, short upturned nose, thin upper lip, receding chin (indicative of fetal alcohol syndrome [FAS]).
Muscle tone may appear tight with flexion of upper and lower extremities, minor joint/limb abnormalities, and restricted movement (suggests FAS).
Wide-eyed appearance (associated with chronic hypoxia in utero).
Signs of respiratory distress may be present (especially in presence of meconium aspiration syndrome [MAS], polycythemia, or infection).
Mucus may be green-tinged.
Dry, cracked, and peeling skin present, with loose skin fold; sparse scalp hair.
Meconium staining may be evident with greenish stains on fingernails and at base of umbilical cord.
Umbilical cord may have single artery and/or be thin, slightly yellow, dull, dry.
Congenital anomalies/malformations or infection may be present.
Irradiation and use of medications with teratogenic side effects (e.g., antimetabolites, anticonvulsants, trimethadione)
Collagen disease; maternal infections such as rubella, syphilis, cytomegalovirus, toxoplasmosis; uterine tumors
Females tend to be smaller than males at birth.
Adolescent or advanced maternal age (younger than age 16 or older than age 40)
Primiparity, grand multiparity
Placenta previa/separation, insufficiency, infarction, fibrosis, thrombosis, hemangioma, abnormal cord insertion and single umbilical artery with vascular anastomoses (twin-to-twin)
Evidence of congenital malformations may involve the heart, CNS, kidney, lungs, GI tract.
Long, hard nails extending beyond ends of toes and fingers.
Absence of vernix caseosa/lanugo; desquamation or epidermis.
Higher incidence in males
Birth of previous LGA infant
Cesarean birth because of cephalopelvic disproportion or oxytocin-induced labor related to diabetes/fetal distress/prolonged pregnancy
Slow to orient to maternal face/voice (generally improves within 48 hr)
May be preterm/postterm by clinical assessment
May be postterm (42 wk or more) because of postconceptional bleeding, leading to a miscalculation of dates/prolonged pregnancy associated with menstrual cycle longer than 28 days.
Dextrostix Glucose Estimations: Less than 40 mg/dl in LGA infant or 25 mg/dl in SGA infant during first 3 days indicates hypoglycemia.
Serum Glucose: Verifies Dextrostix value <40 mg/dl in LGA infant,25 mg/dl in SGA infant.
Chest X-Ray and ABGs: Help determine cause/severity of respiratory distress if present, e.g., pneumonia, MAS, RDS.
CBC: May reveal central venous Hct elevated above 65%; central venous Hb 20 g/dl associated with polycythemia/hyperviscosity.
WBC Count: May be elevated or depressed.
Platelet Count: May be depressed if mother was pre-eclamptic or if infant was born with a congenital viral infection.
Coagulation Studies (prothrombin time [PT], partial thromboplastin time [PTT], fibrinogen, fibrin split products [FSP]): May indicate DIC, especially in the presence of polycythemia or asphyxia.
Blood Type for ABO Group, Rh Factor, and Crossmatch: Plasma exchange may be necessary if Rh incompatibility exists.
Serum Electrolytes (including ionized calcium): Assesses for hypocalcemia (level 7 mg/dl [3.5 mEq/L] or less in first 3 days of life); inappropriate antidiuretic hormone secretion, and instability related to metabolic complications.
Bilirubin: May be elevated secondary to polycythemia and resorption of bleeding associated with birth injury, e.g., intracranial hemorrhage, cephalhematoma.
Urinalysis on/after Second Voided Specimen, Including Specific Gravity and Sugar/Acetone: Assesses homeostasis, renal involvement.
Bacterial and Viral Cultures: Rule out/diagnose infectious process.
Electrocardiography (ECG), Echocardiography, Ultrasonography, Angiography, and Genetic Studies: As appropriate with suspected FAS, congenital defects, and/or complications.
Maintain physiological homeostasis.
Prevent and/or treat complications.
Identify/minimize effects of birth trauma.
Provide family with appropriate information/strategies for meeting short- and long-term needs associated with growth deviation.
NURSING DIAGNOSIS: GAS EXCHANGE, impaired
May Be Related To: Alveolar capillary membrane changes (decreased surfactant levels, retained pulmonary fluid, meconium aspiration), altered oxygen supply (diaphragmatic paralysis/phrenic nerve paralysis, increased intracranial pressure)
CRITERIA—NEONATE WILL: respiratory effort with rate of 30–50/min; and ABGs WNL.
Be free of apnea and complications of hypoxia/lung disease.
Review history for abnormal prenatal growth Low-birth-weight infant or infant with IUGR
patterns and/or reduced amounts of amniotic suffers chronic intrauterine asphyxia, resulting in
fluid, as detected by ultrasonography/fundal hypoxia/malnutrition. Fetal contribution to the
changes. amniotic pool is reduced in the stressed infant.
Macrosomia can be related to maternal diabetes,
prolonged pregnancy, heredity, and inappropriate
nutrition. Macrosomia in IDM results from excess
release of growth hormone (thyroid stimulation),
increasing the number of cells and/or organ size
throughout the body.
Note type of delivery and intrapartal events Infant with chronic hypoxia will be more
indicative of hypoxia. susceptible to acidosis/respiratory
depression/persistent fetal circulation (PFC) after
delivery. Cesarean birth increases risk of excess
mucus because thoracic compression by the birth
canal does not occur as in a vaginal delivery.
Note time/onset of breathing and Apgar scores. The infant with intrapartal asphyxia may present
Observe ensuing respiratory patterns. with a delayed onset of respirations and altered
respiratory pattern. Apgar scores aid in evaluation of
the degree of depression or asphyxia of the newborn
at birth and are directly correlated with serum
pH/degree of infant acidosis.
Assess respiratory rate, depth, effort. Observe Infant with altered growth is more susceptible to
and report signs and symptoms of respiratory respiratory distress associated with chronic asphyxia
distress, distinguishing from symptoms associated in SGA infant, inadequate surfactant levels in IDM,
with polycythemia. perinatal asphyxia, aspiration of meconium or
amniotic fluid, and PFC. Diminished lung
compliance may occur as a result of polycythemia.
Auscultate breath sounds regularly. Presence of crackles/rhonchi reflect respiratory
congestion and need for intervention.
Suction nasopharynx/endotracheal tube as Ensures patency of airway, removes excess mucus.
needed, after first providing supplemental oxygen. Supplemental oxygen reduces hypoxic effect of
Auscultate apical pulse; note presence of cyanosis. Tachypnea, bradycardia, and cyanosis may occur in
response to altered oxygen levels.
Prevent iatrogenic complications associated with Such complications increase metabolic demands
cold stress, metabolic imbalance, and caloric and oxygen needs.
Ensure availability of resources in the event Equipment for oxygenation, suction, intubation,
complications occur. assisted ventilation, resuscitation, and chest tube
placement must be readily available in the event of
severe/prolonged respiratory distress.
Serum pH; Detects possible metabolic acidosis occurring from
inadequate oxygen intake/respiratory acidosis and
anaerobic metabolism with acid end products. Note:
Normal pH values range from 7.35–7.44; HCO3 is
19–22 mEq/L (bicarbonate reflects buffering capacity
of the blood).
ABGs; Indicate degree of hypoxia/hypercapnia, as well as
therapy needs/effectiveness. Note: Normal newborn
arterial Po2 ranges from 50–70 mm Hg, arterial Pco2
from 35–45 mm Hg.
Hct. Polycythemia, which occurs in 50% of SGA infants
related to excess RBC production in response to
chronic intrauterine hypoxia, typically increases
capillary/venous Hct levels to greater than 60%, with
resultant respiratory distress associated with
diminished lung compliance.
Administer warm, humidified oxygen; provide Corrects/prevents hypoxia, hypercapnia, and
assisted ventilation, as indicated. respiratory acid-base imbalances.
Review chest x-rays. May confirm meconium aspiration pneumonia,
common in SGA or postterm infant, or RDS, in IDM.
Provide chest physiotherapy, as indicated. Percussion and postural drainage promote
mobilization of secretions, enhancing airway patency
and gas exchange, especially in the presence of MAS.
Note: Contraindicated in preterm infant.
Administer medications as indicated:
Sodium bicarbonate; Corrects metabolic imbalances/acidosis resulting
from prolonged respiratory acidosis.
Xanthine derivatives, e.g., aminophylline, Sympathomimetic bronchodilators may be useful
theophylline; in treating apnea of prematurity.
Tolazoline HCl (Priscoline); Potent vasodilator that relaxes smooth muscle to
maximize circulatory effort/oxygenation in cases of
Dopamine. May be required to counteract hypotensive effect of
NURSING DIAGNOSIS: NUTRITION: altered, less than body requirements
May Be Related To: Decreased nutritional stores, increased insulin production and/or hyperplasia of the pancreatic beta cells
DESIRED OUTCOMES/EVALUATION Ingest and digest adequate nutrients for weight
CRITERIA—NEONATE WILL: gain (or to prevent weight loss of 2% or more).
Display serum glucose >40 mg/dl, and other associated laboratory studies WNL.
PARENT(S) WILL: Identify/treat/prevent short- and long-term complications of malnutrition.
Compare weight in relation to gestational age Identifies presence, degree, and risk of altered
and size. Document on growth chart. Weigh daily. growth pattern. LGA infant with excess extracellular
fluid experiences a postdelivery diuresis, resulting in
a loss of up to 15% of birth weight. SGA infant may
have already lost weight in utero or may suffer from
reduced fat/glycogen stores.
Maintain thermoneutral environment, including The SGA infant does not have adequate adipose
use of incubator/radiant warmer, as indicated. tissue for insulation and has a large body surface
Monitor heat controls, temperature of infant and area compared to body weight. Brown adipose
environment frequently, noting hypothermia/ tissue stores may be inadequate to maintain
hyperthermia. thermoregulation. Both hypothermia and
hyperthermia increase metabolic demands,
necessitating increased intake in an already
compromised infant. Note: Thermal instability may
be iatrogenically induced by improperly operated
heating equipment used to maintain thermogenesis
in dysmature infant. (Refer to CP: The Preterm Infant;
ND: Thermoregulation, ineffective.)
Initiate early and frequent feedings and Assists in maintaining fluid/electrolyte balance
advance as tolerated. and meeting caloric needs to support metabolic
process. Helps prevent hypoglycemia associated with
inadequate body stores in SGA infant or continued
pancreatic secretion of insulin in IDM.
Assess tolerance to feedings. Note stool color, Advances in amount and caloric composition of
consistency, and frequency; presence of reducing feedings are dependent on tolerance. Evidence of
substances; abdominal girth; vomiting, and reducing substances (increased glucose) in stool
gastric residuals. suggests inability to digest formula because of
obstruction and/or disease process present. Note:
Poor sucking reflex and recurrent vomiting or
persistent regurgitation may be seen in FAS,
requiring further evaluation/intervention. (Refer to
CP: The Infant of an Addicted Mother.)
Monitor intake and output. Calculate daily Provides information about actual intake in
caloric and electrolyte consumption. relation to estimated needs for use in readjustment of
Assess hydration level, noting fontanels, skin Increased metabolic demands of the SGA infant
turgor, urine specific gravity, condition of may increase fluid requirements. Hyperglycemic
mucous membranes, and weight fluctuations. states may produce diuresis in the infant. IV
administration of fluids may be required to meet
increased demands but must be conscientiously
managed to avoid fluid excess.
Monitor Dextrostix levels immediately after birth Hypoglycemia may occur after birth because of
and routinely until serum glucose is stabilized. limited glucose stores in the SGA infant and from
hyperplasia/continued release of insulin in the LGA
infant. Symptoms in the SGA infant usually appear
between 24 and 72 hr of age, but may begin as early as
3 hr or as late as 7 days; the IDM may be symptomatic
within 1–3 hr of birth. Hyperglycemia may result from
inappropriate infusion of solutions containing glucose.
Observe for signs of hypoglycemia, e.g., tachypnea Because glucose is a major source of fuel for the
and irregular respirations, apnea, lethargy, flaccidity, brain, deficits may cause permanent CNS damage.
cyanosis, temperature fluctuations, diaphoresis, Hypoglycemia significantly increases morbidity
poor feeding, jitteriness, high-pitched cry, tremors, and mortality rates, and severity of long-term
eye rolling, seizure activity. effects is dependent on duration of such episodes.
Untreated symptomatic infants have a higher
incidence of neurological abnormalities and/or lower
mean IQ later in childhood than treated infants.
Note signs of hypocalcemia, e.g., neuromuscular Peak incidence of early hypocalcemia is during
irritability (tremors, twitching, seizing, clonus), first 48–72 hr of life and is often related to
hypotonia, vomiting, high-pitched cry, cyanosis, temporary abdominal distension, neonatal
apnea, and cardiac dysrhythmias with prolonged hypoparathyroidism in premature infant, or
Q-T interval. prenatal asphyxia in SGA infant or IDM. Late
hypocalcemia (at 6–10 days) may be caused by
ingestion of milk formulas containing a higher ratio
of phosphorus to calcium.
Discuss long-term complications of malnutrition Chronic protein deficiencies in the SGA infant
in SGA infant and obesity in LGA infant; review make child prone to learning difficulties and
importance of protein during phase II of brain cerebral dysfunction, characterized by short
growth. attention span, poor fine-motor coordination,
hyperactivity behavior problems, and speech defects.
Excess fat cells in the LGA/macrosomic infant may
create lifelong problems associated with obesity (e.g.,
diabetes, cardiovascular disease, stroke). Adequate
protein during hyperplasia/hypertrophy phase of
brain growth during the first 6 mo of life helps to
overcome insults that occurred in early gestational
period of brain development.
Monitor laboratory studies as indicated:
Serum glucose; Hypoglycemia may occur as early as 1–3 hr after
birth. In the SGA infant, glycogen reserves are
quickly depleted and gluconeogenesis is inadequate
because of reduced stores of muscle protein and fat,
while the IDM has decreased ability to release
glucagon and catecholamines needed to stimulate
glucagon breakdown/facilitate release of glucose.
Calcium; Frequency of screening is dependent on this risk
group, i.e., IDM, intrapartal asphyxia, or preterm
infants. Levels 7 mg/dl require further
Sodium, potassium, chloride, phosphorus, Electrolyte instability may be a consequence of
and magnesium; deviations in growth, inadequate placental transfer,
or altered maternal mineral balance. Note:
Hypomagnesemia/hyperphosphatemia are usually
associated with hypocalcemia.
BUN, creatinine, serum/urine osmolality, Detects altered kidney function associated with
urine electrolytes; reduced nutrient stores and fluid levels resulting
from acute malnutrition/asphyxia.
Triglyceride/cholesterol levels, and liver Useful in determining nutritional deficits and
function tests. therapy needs/effectiveness.
Establish intravascular access as indicated. IV access allows for fluid and electrolyte
administration. Intra-arterial access allows for ease in
obtaining samples for monitoring laboratory values.
Administer glucose-containing solutions/ The severely compromised infant with deviations in
parenteral nutrition. intrauterine growth may be unable to consume
adequate fluids and nutrients via an enteral route. IV
glucose (i.e., infusion of D5W) may be required when
serum glucose cannot be maintained at or above 40
mg/dl, or seizure activity occurs.
Provide electrolyte supplementation as indicated, Metabolic instability in the SGA/LGA infant may
e.g., 10% calcium gluconate. necessitate supplements to maintain homeostasis,
especially calcium, sodium, and occasionally
NURSING DIAGNOSIS: TISSUE PERFUSION, risk for altered
Risk Factors May Include: Interruption of arterial or venous blood flow (hyperviscosity associated with polycythemia)
Possibly Evidenced By: [Not applicable; presence of signs/symptoms establishes an actual diagnosis]
DESIRED OUTCOMES/EVALUATION Maintain normal vital signs, with adequate
CRITERIA—NEONATE WILL: peripheral pulses and Hct WNL.
Be free of complications associated with polycythemia.
Note risk factors for/presence of polycythemia. Maternal fetal or infant transfusion (during gestation
or at birth), twin gestation (twin-to-twin transfusion),
chronic fetal distress associated with maternal PIH,
placenta previa; chromosomal anomalies, endocrine
disorders; and residing at altitudes over 5000 ft place
the infant at risk for developing increased blood
volume. Polycythemia resulting from increased
erythropoietin production in response to chronic
intrauterine hypoxia may occur in both the SGA/LGA
infant. In many cases, infants of diabetic mothers are
polycythemic. Although the pathophysiology of the
hyperviscosity is not fully understood, it may be
related to decreased extracellular fluid volume or
increased bone marrow stimulation associated with
Monitor temperature, intake/output, and urine Prevention or correction of dehydration decreases
specific gravity. Note skin turgor, condition of the risks of hyperviscosity.
mucous membranes, and fontanels.
Observe skin color for ruddiness or pallor. Note Helps detect/promotes prompt intervention to
presence of hyperthermia, respiratory distress, prevent possible complications of polycythemia,
hypertension or hypotension, tachycardia, e.g., myocardial, cerebral, and renal ischemia;
decreased pulses, oliguria, hematuria, or altered cardiopulmonary congestion; hyperbilirubinemia;
neurological findings. thromboembolism, and convulsions.
Monitor central/peripheral Hct/Hb and bilirubin. Indicates degree of polycythemia/hyperviscosity.
Send blood for type, crossmatch, and Rh. (Refer to Hyperbilirubinemia often results from
CP: Newborn: Hyperbilirubinemia.) polycythemia (central Hct is >65%; Hb is 22 g/dl) as
excess RBCs break down.
Establish intravascular access, preferably through Provides for fluid administration to correct
umbilical catheterization. hyperviscosity and exchange transfusion, if
Prepare for/assist with exchange transfusion Fresh frozen plasma, 5% albumin or 9% saline,
as indicated. replaces infant’s blood in equal amounts, thereby
diluting infant’s remaining blood volume to
prevent/correct polycythemia and hyperviscosity.
Usually 10% of the infant’s blood volume is
removed/exchanged at one time.
Monitor for complications of procedure, including Provides for early detection/intervention.
transfusion reactions, overload (CHF), catheter
complications, cardiac dysrhythmias, hypovolemia,
anemia, and hepatitis.
Possibly Evidenced By: [Not applicable; presence of signs/symptoms establishes an actual diagnosis]
DESIRED OUTCOMES/EVALUATION Be free of complications.
Inspect all LGA infants for birth injuries. Note Because of disproportion between fetal size and
bulging/tense fontanels; muscle spasticity, maternal pelvis, LGA infants have a high
twitching, or flaccidity; high-pitched, weak, incidence of birth injuries/trauma, such as
constant cry; tremors or seizure activity; changes IICP/CNS damage, cervical/brachial plexus palsy,
in pupil size/reaction; or asymmetrical chest fractured clavicle/humerus, diaphragmatic
movement. paralysis, and cephalhematoma.
Observe invasive sites, urine/stool, NG drainage, Early recognition promotes timely intervention.
and pulmonary secretions for signs of bleeding. Septicemia, congenital syphilis, cytomegalic
Note petechiae/bruising, changes in inclusion disease, and rubella may result in DIC,
responsiveness/activity level or muscle resulting in pulmonary, cerebral, or IVH.
tone, nystagmus, opisthotonic posturing, or
Measure occipital frontal circumference, as Hydrocephalus may develop following IVH.
Monitor vital signs. Observe peripheral capillary Hypotension, bradycardia, apnea, hypothermia,
refill and color and temperature of skin. delayed capillary refill, and pallor reflect developing
shock related to blood loss, requiring prompt
Assess home situation for abusive relationships. Maternal abuse during pregnancy is a significant risk
factor for development of SGA infant. Releasing
infant into potentially unsafe environment increases
risk of abuse/neglect and FTT.
Monitor for signs and symptoms of infection (e.g., Poor resistance to infection, cracks in epidermis,
changes in temperature, color, muscle tone and and possible exposure to infectious agents in utero
activity, feeding tolerance, cardiopulmonary status; place the SGA/postterm infant at risk for
or presence of petechiae, rash, jaundice). infection, which may be life-threatening, especially if
not detected in its earliest phases. (Refer to CP: The
Preterm Infant; ND: Infection, risk for.)
Discuss with parents the potential of conditions that Enhances early identification and promotes
may have long-term sequelae, such as birth injury optimal management of long-term effects of
or fetal malnutrition hypoxia (significant role in injury/condition.
late or subnormal CNS functioning), which may
result in convulsions or altered reflex responses.
Monitor laboratory studies as indicated:
CBC with differential; Dropping Hct may reflect hemorrhage; a shift of the
differential may suggest infection.
Coagulation studies: PTT/activated PTT Alterations in clotting times, presence of FSP
(APTT), PT, fibrinogen levels, FSP, platelets; reflect developing coagulopathies.
Blood type, crossmatch, and Rh factor; Blood replacement may be required.
Bacterial viral cultures and sensitivities. Verifies presence, etiology, severity of infectious
Provide supplemental oxygen, CPAP, and/or Aids in correcting hypoxia, acidemia, and
mechanical ventilation, as needed. (Refer to ND: hypotension; reduces risk of IVH/increased ICP.
Gas Exchange, impaired.)
Administer blood products, albumin, and Replaces losses/enhances circulating volume; may
coagulants, as necessary. help control bleeding.
Administer anticonvulsants (e.g., phenobarbital), May be necessary to quiet cerebrum and reduce
as indicated. electrical stimuli that precipitate seizure activity.
Assist with diagnostic studies, as indicated, e.g., Bloody spinal fluid indicates IVH. Scans are useful
lumbar puncture, CT, or ultrasound scan. in identifying site/extent of cerebral hemorrhage.
Refer family to appropriate community resources/ Provides support/guidance for dealing with
support groups. possible long-term effects of condition.
NURSING DIAGNOSIS: INFANT BEHAVIOR, risk for disorganized
May Be Related To: Functional limitations related to growth deviations (restricting neonate’s opportunity to seek out, recognize, and interpret stimuli), electrolyte imbalance, and psychological stress, immaturity or CNS damage (low threshold for stress), low energy reserves, poor organizational ability, limited ability to control environment
Possibly Evidenced By: [Not applicable; presence of signs/symptoms establishes an actual diagnosis]
DESIRED OUTCOMES/EVALUATION Exhibit organized behaviors that allow the
CRITERIA—NEONATE WILL: achievement of optimal potential for growth and development as evidenced by modulation of physiological, motor, state, and attentional-interactive functioning.
Identify appropriate responses (including environmental modifications) to infant cues.
Verbalize readiness to assume caregiving independently.
Determine infant’s capacity for stimulation, Allows provision of stimuli consistent with
noting behavioral responses involving gross and infant’s capabilities and with cues reflecting
fine motor movement, presence of irritability, sensory overload.
restlessness, crying, eye contact, and facial
Provide stimuli consistent with chronological and Size of the infant with deviations in growth may
developmental capabilities. be a false indicator of capacity for stimulation.
Monitor environmental stimulation. Minimize/ Control of stressors can reduce infant’s energy
remove inappropriate or hazardous stimuli. demands, aiding in maintenance of homeostasis
(promotes rest, weight gain).
Provide parents with information regarding the Parents who are informed of their newborn’s
newborn’s capabilities/needs. capabilities can provide appropriate stimulation to
optimize the newborn’s development.
Encourage parental involvement in identification Fosters continued support of the infant’s capacities
of coping strategies/deficits of infant, including in the acute care setting and transition to home.
control of behavioral state and temperament. Identifies role for parents in providing coregulation
to the infant.
Promote ongoing assessment of neurodevelopmental Prevents/minimizes complications and optimizes
gains/deficits. Plan future interventions accordingly. growth and development.
Suggest/refer to early stimulation program if Optimizes infant development/interactional skills
available/indicated. (affective, cognitive, social).
Refer for long-term neurodevelopmental Sequelae of morbidity associated with deviations
assessment and intervention as indicated. in intrauterine growth may affect long-term coping.
(Refer to CP: The Preterm Infant; ND: Infant Behavior, risk for disorganized.)
May Be Related To: Lack of exposure, misinterpretations, unfamiliarity with resources
Possibly Evidenced By: Verbalization of problem, misconception, request for information
DESIRED OUTCOMES/EVALUATION Identify newborn’s short- and long-term needs.
CRITERIA—PARENT(S) WILL: List available resources.
Participate in discharge planning.
Provide appropriate anticipatory guidance Malnutrition in SGA infant may result in
regarding implications of growth deviations. subnormal CNS/intellectual development as well as
hearing/speech deficits. LGA infant is susceptible to
malnutrition problems associated with obesity. (Refer
to ND: Nutrition: altered, less than body
Review short- and long-term needs for care of Provides information for parents to understand
the SGA/LGA infant. Assist with follow-up in need for ongoing physical, neurodevelopmental,
discharge planning. and psychosocial assessment needed for long-term
follow-up. (Refer to CP: The Parents of a Child with
Special Needs; NDs: Knowledge deficit [Learning
Need]; Family Coping: ineffective, risk for
Identify community/governmental resources Presence of specific needs such as feeding
as appropriate. problems, resolving complications, or congenital
anomalies require ongoing monitoring and problem
solving to foster optimal growth and development.