The High Risk Infant
A High-Risk Infant is one who is susceptible to illness (morbidity) or even death (mortality) because of
dysmaturity, immaturity, physical disorders, or complications of birth. In most cases, the infant is the
product of a pregnancy involving one or more predictable risk factors, including the following:
 Low socioeconomic level of the mother, poor nutrition
 Exposure to environmental dangers such as toxic chemicals
 Preexisting maternal conditions such as heart disease, diabetes
 Obstetric factors such as age or parity, other premature births
 Medical conditions related to pregnancy such as PIH, Premature rupture of membranes,
infection, etc.
Early identification and prompt management are imperative in treating newborns with complications.
Classification of High Risk Infants
I. Classification According to Gestational Age
A.
Preterm: infants born before completion of 37 weeks gestation.
B.
Term: infants born between the 38 and 42 weeks gestation.
C.
Postterm: infants born after 42 weeks gestation.
II. Classification According to Gestational Age and Birth Weight
A.
Large for Gestational Age (LGA): infant at any week the weight is above the 90th percentile.
B.
Appropriate for Gestational Age (AGA): infant at any week the weight is between the
10th and 90th percentile.
C.
Small for Gestational Age (SGA): infant at any week the weight is below the 10th percentile.
The Premature Infant
The Preterm infant must travel the same complex pathway from intrauterine to extrauterine life as the
term infant. Because of immaturity, the preterm neonate is unable to make this transition as smoothly.
CHARACTERISTICS:
I. Digestive System
A.
Gag and suck reflexes may be weak and poorly developed.
Hypotonic cardiac sphincter. Increase chance of regurgitation and aspiration.
B.
Suck and swallow reflexes may be uncoordinated.
C.
Small stomach capacity - 2ml. in 1200 gm. 15ml. in 2000 gm. baby.
Vomiting more likely to occur.
D.
Poor ability to tolerate fats.
E.
Immature absorption, decreased amounts of HCL.
II. Central Nervous System
A.
Poor muscle tone - muscles appear limp, flaccid, assumes frog-like position at rest.
Muscles weak and underdeveloped.
B.
Cry - weak and feeble.
C.
Reflexes - weak and immature, slow to respond to stimulation.
D.
Susceptibility to brain damage.
E.
Heat regulation unstable.
1.
Body temperature may be normal but it fluctuates; small muscle mass; absent sweat or shiver
response.
2.
Large body surface in proportion to body weight.
3.
Lack of subcutaneous fat.
4.
Poor capillary response to environmental changes.
III. Respiratory System
A.
Insufficient production of surfactant -incomplete aeration of lungs.
B.
Immaturity of alveolar system -smaller lumen, greater collapsibility of respiratory passages.
C.
Immaturity of musculature and insufficient calcification of bony thorax.
D.
Respirations 40-60/min., shallow, irregular, usually diaphragmatic. Prone to Respiratory Distress.
IV. Integumentary System
A.
Skin thin and capillaries easily seen, reddened and translucent.
B.
Little subcutaneous fat.
C.
Lanugo plentiful, widely distributed.
D.
Vernix may cover body is born between 31 and 33 weeks.
E.
Ears - minimal cartilage, pliable, folded over.
V. Immune System
A.
Lack of passive immunity from mother; deficient placental transmission.
B.
Inability to produce own antibodies - immature system.
C.
Skin is thin and offers little protection from disease causing organisms.
D.
Number of WBC’s is decreased and therefore have decreased ability to phagocytise bacteria.
VI. Hepatic System
A.
Poor glycogen stores -increased susceptibility to hypoglycemia.
B.
Inability to conjugate bilirubin - increase hyperbilirubinemia.
C.
Decrease ability to produce clotting factors, low plasma prothrombin levels.
VII.Circulatory System
A.
Capillary fragility increases susceptibility to hemorrhage,
especially intracranial. Leads to increase bilirubin levels.
B.
Prone to anemia - poor iron stores.
VIII. Renal System
A.
Renal function immature - poor ability to concentrate urine.
B.
Fluid and electrolyte and acid-base balance precarious.
C.
Impaired renal clearance of drugs.
Nursing Care Of The Preterm Infant
I. Maintain Respiratory Function
A.
Maintain airway patency through judicious suctioning.
B.
Position with head slightly elevated and neck slightly extended.
C.
Assess for signs of respiratory distress:
1.
Cyanosis - serious sign when generalized.
2.
Tachypnea - sustained respiratory rate > than 60 after first 4
hours of life.
3.
Retractions - subcostal, intercostal, and substernal.
4.
Expiratory grunting, sighing.
5.
Flaring nostrils.
6.
Apneic episodes - stimulate by gently rubbing chest or tapping
foot.
7.
Presence of rales or rhonchi on auscultation.
D.
Administer O2 (warmed and humidified). Analyze oxygen
concentration every hour.
II. Maintain Warmth, Thermoregulation
A.
Increase environmental temperature to maintain thermal
neutrality.
B.
1.
2.
3.
Minimize heat loss and prevent cold stress:
Warm and humidify oxygen.
Maintain skin in dry condition (evaporation)
Keep isoletes, radiant warmers, and cribs away from windows
and cold external walls, radiation.
4.
Use skin probe to monitor infant skin temperature.
5.
Avoid laying on cold surface (conduction).
6.
Use radiant warmers during procedures (convection).
7.
Warm blood for exchange.
8.
Conserve infant’s energy and handle as little as possible.
III. Maintain Nutrition and Hydration
A.
May require I.V. feedings until stabilized. I.V. regulated by
infusion pump to prevent circulatory overload.
B.
Prior to feeding assess:
1.
Respirations (should be < 60).
2.
Abdominal girth for abdominal distention.
3.
Bowel sounds.
4.
Cry, color and tone.
5.
Suck, swallow and gag reflex.
6.
Residual formula in stomach by gavage, if large amounts, then
poor digestion. Usually replace amount before feeding.
C.
Initiate feedings - usually begin with sterile water or glucose
water. Progress to dilute formula and then to concentrated
formulas that provide more calories in less volume.
D.
Evaluate for sign of dehydration:
1.
Early sign (weight loss).
2.
Depressed fontanel, sunken eyeballs.
3.
Poor skin turgor and dry mucus membranes.
4.
Decreased urine output.
E.
Monitor daily weight and I&O.
F.
Observe for fatigue during feedings (if tires, then alternate nipple
feeding with gavage feeding, or even I.V.’s).
G.
Involve parent in feeding.
IV. Prevention of Infection
A.
Maintain aseptic techniques and meticulous handwashing.
B.
Prevent skin breakdown.
C.
Teach and supervise parents’ handwashing and gowning.
D.
Observe for signs of infection (vomiting, jaundice, lack of
appetite, lethargy).
V. Promote Attachment and Mothering
A.
Allow parents to visit baby frequently.
B.
Allow parents to help care for infant to promote parent-infant
attachment. Teach to gently stroke and talk to baby when giving
care.
C.
Answer questions openly. Provide up-to-date information on baby’s
progress.
VI. Be Aware of Complications
A.
Respiratory Distress Syndrome
B.
C.
D.
E.
F.
G.
H.
Cold Stress
Necrotizing Enterocolitis
Hypoglycemia/Hypocalcemia
Retinopathy of Prematurity
Hyperbilirubinemia
Sepsis
PDA
Respiratory Distress Syndrome
PATHOPHYSIOLOGY
The central problem in RDS is atelectasis, which results from the development of a hyaline membrane
within the newborn’s bronchial tree, that is, within the alveolar ducts and the alveoli. These ducts and
alveoli become filled with a sticky exudate, a hyaline material, which prevents aeration. With decrease
perfusion, accompanying problems begin with hypoxemia, metabolic and respiratory acidosis, and
classic lung changes including decreased compliance, capillary damage, and alveolar necrosis.
CAUSE
The cause is still unknown. The alteration in or lack of pulmonary surfactant that prevents alveolar
collapse at the end of expiration has been established as a possible cause.
CLINICAL MANIFESTATIONS
Pulmonary compliance is diminished. The stiffness of the lungs and their distensibility contribute to the
hard work of breathing. Pulmonary vasoconstriction causes increased pulmonary resistance which
causes hypoperfusion of alveolar capillaries; hence, the lungs are ischemic as well as atelectatic. Fetal
circulatory state persists in some states and becomes life-threatening. Pulmonary compliance decreases
and the energy required for the simple act of breathing increases which leads to further impairment of
gas exchange and a vicious cycle that becomes incompatible with life. (For specific signs and symptoms,
see respiratory section)
TREATMENT
1.
Oxygen therapy.
2.
CPAP.
3.
Surfactant replacement.
Bronchopulmonary Dysplasia
A pathogenic process that may develop in the lungs as a sequela to the alveolar damage caused by use
of high oxygen concentrations and the prolonged use of CPAP. There is damage to the alveolar
epithelium causing scarring to severe emphysema. These infants have long-term dependence on oxygen
therapy.
Meconium Aspiration
Aspiration of meconium into bronchial tree causing severe irritation and swelling. Prevention attempted
by suctioning prior to initiating respirations in infant. ECMO may be used for respiratory support.
Retinopathy of Prematurity
An acquired disease in which retinal damage occurs in infants receiving continuous oxygen therapy in
high concentrations. The severity of the disease depends on the concentration of oxygen given and the
immaturity of the eyes at the time when the oxygen is given. Nursing measures to help prevent this is to
monitor oxygen levels. Oxygen levels under 50% have been shown to be safe. Levels between 50%-70%
are questionable. Transcutaneous oxygen tension monitor is a noninvasive devise that provides
continuous readings.
Necrotizing Enterocolitis
An inflammatory disease of the gastrointestinal mucosa frequently complicated with perforation. NEC
develops when there is asphyxia or hypoxia in which cardiac output tends to be directed more toward
the heart and brain and away from the abdominal organs. The intestinal cells become ischemic and
damaged and stop secreting protective mucus infection occurs. Perforation may occur with
overwhelming sepsis.
SIGNS AND SYMPTOMS
Early: Increase amount in gastric aspirate - >5-25 cc. and abdominal
distention. Measure abdominal girth and an increase >1 cm. should
be reported. Assess bowel sounds, abdominal tenderness or
rigidity of abdominal wall.
Subtle: Lethargy, sudden listlessness, temperature instability, decrease
urine output, occult blood in stools, poor color, and apneic periods.
Dramatic:
Massive abdominal distention, vasomotor collapse.
DIAGNOSIS
X-ray examination shows dilatation of small bowel with air in peritoneum. Bubbles or layers of air are
seen in the wall of the bowel. Lab studies show absolute neutropenia.
TREATMENT
Surgery:
Medical:
Resection of necrotic sections and possible temporary
colostomy. This allows bowel to recover.
NPO with NG tube. Peripheral or central hyperalimentation
antibiotic therapy. Continue to monitor for changes in
condition.
Small For Gestational Age Infant
Intrauterine Growth Retardation (IUGR) is used interchangeably with SGA. Many factors may cause an
infant to be SGA such as: undernutrition, diminished uterine blood flow, smoking, low socioeconomic
class, narcotic usage, premature separation of placenta, and etc.
Clinical manifestations of the SGA infant are related to the duration and time of onset of the influence
causing intrauterine growth retardation. Perform a gestational age assessment. Care of the SGA infant
depends on age. Problems associated with IUGR are:
1.
Poor glucose levels
2.
Limited temperature control
3.
Aspiration syndrome
4.
Perinatal asphyxia
5.
Polycythemia
Nursing care of the SGA infant in many ways is similar to that for the premature infant including:
1.
Observe for problems associated with asphyxia
2.
Screen for hypoglycemia
3.
Prevent cold stress and hypothermia
The Postmature Infant
The post mature infant is one whose gestation is 42 weeks or longer and who may show signs of weight
loss with placental insufficiency with intrauterine malnutrition and hypoxia.
CLINICAL MANIFESTATIONS
1.
Reduced subcutaneous tissue (loose skin).
2.
Long fingernails.
3.
Reduced amount of vernix.
4.
Abundant scalp hair.
5.
Wrinkled, macerated skin.
6.
Often meconium stained skin, cord, nails.
NURSING CARE AND MANAGEMENT
1.
Be alert for RDS that may indicate meconium aspiration.
2.
Observe for signs of birth injury (dislocated shoulder, CNS injury,
fractured pelvis, facial paralysis).
3.
Continue with care as with preterm infant.
Hyperbilirubinemia
Hyperbilirubinemia is characterized by elevated serum levels of unconjugated (indirect) bilirubin.
Bilirubin rising more than 0.5 to 1 mg./100 ml. in 1 hour
15 mg. per 100 ml. in a preterm infant; 20 mg. per 100 ml. in a full term infant
ETIOLOGY
1.
Hemolytic disease (Rh and ABO incompatibility)
2.
Extravascular bleed (cephalhematoma)
3.
Bilirubin conjugation defects (breastmilk jaundice, asphyxia)
4.
Hypoalbumin
5.
Physiologic jaundice (occurs after the first 24 hours of birth. Mainly
due to immature liver and lack of glucoronyl transferase).
PATHOPHYSIOLOGY OF HYPERBILIRUBINEMIA
Unconjugated bilirubin is a break-down product of destroyed RBC’s. Unconjugated bilirubin is normally
transferred in the plasma firmly bound to albumin to the liver where conjugation occurs. Conjugated
bilirubin is water soluble and can then be excreted into the bile and eliminated with the feces.
Unconjugated bilirubin is not in excretable form and remains in the circulation causing problems.
The above list are causes of Hyperbilirubinemia. The most common cause is from Hemolytic Disease –
Rh Incompatibility and ABO Incompatibility. The major focus will be on these diseases.
Rh INCOMPATIBILITY
ETIOLOGY AND PATHOPHYSIOLOGY
Rh incompatibility occurs when there is an incompatibility between the blood of a Rh negative mother
and that of a Rh positive fetus. When the fetal Rh positive ANTIGEN (invaders) enter the maternal Rh
negative bloodstream it causes an immunological response – the mother will form ANTIBODIES
(defenders) against the Rh positive antigen.
These antibodies are harmless to the mother. The problem arises when the maternal antibodies cross
the placenta and destroy fetal red blood cells, causing ERYTHBROBLASTOSIS FETALIS. Infants with
erythroblastosis fetalis are anemic from destruction of red blood cells. Severely affected infants may
have HYDROPS FETALIS, a severe anemia that results in heart failure and generalized edema. These
infants seldom survive.
ASSESSMENT
1. Sclerae appearing yellow before skin appears yellow – usually in the
first 24 hours after delivery
2. Skin appearing light to bright yellow – advances from head to toe
3. Lethargy
4. Dark, amber concentrated urine
5. Poor feeding
6. Dark stools
DIAGNOSIS
Coombs Test – may be done on the fetal cord blood (direct Coombs test) or on the maternal blood
(indirect Coombs test). Tests for the presence of maternal antibodies attached on the infant’s red blood
cells. The test is positive if there are maternal antibodies.
Amniocentesis – determine degree of hyperbilirubinemia.
NURSING MANAGEMENT
1.
Careful observation of infant for signs of increased jaundice
2.
Careful observation for and prevention of acidosis/hypoxia and
hypoglycemia, which decrease binding of bilirubin to albumin and
contribute to jaundice.
3.
Maintain adequate hydration
4.
Avoid cold stress
5.
Phototherapy – use of “bili” lights, special fluorescent lamps placed
over the infant or a fiberoptic phototherapy blanket that is placed
against the infant’s skin. During phototherapy, bilirubin in the skin
absorbs the light and changes into water-soluble products. These
products do not require conjugation by the liver and can be excreted
in the bile and urine.
Nursing care while receiving phototherapy centers around:
1. Maintaining a neutral thermal environment
2. Providing optimal nutrition
3. Protecting the eyes
4. Enhancing response to the therapy
5. Promoting mother-infant interaction
Side effects of Phototherapy include:
1. Frequent loose, green stools
2.
3.
4.
5.
Skin rash similar to erytherma toxicum
Increased basal body metabolism
Dehydration
Hyperthermia
6.
Exchange Transfusion – necessary when all else fails to reduce high bilirubin levels quickly
enough. This treatment removes sensitized red blood cells, antibodies, and unconjugated bilirubin in the
blood.
COMPLICATIONS of Phototherapy:
1. Infection
2. Hypervolemia/Hypovolemia
3. Cardiac dysrhythmias
4. Air embolism
PREVENTION of Rh Incompatibility is with – ADMINISTRATION OF RHOGAM:
Who Gets It?
RhoGam is given to the Rh negative mother within 72 hours after delivery of a Rh positive infant or
anytime a Rh negative woman may be exposed to the Rh positive antigen (ie., Abortion, amniocentesis,
chorionic villi sampling, accidental transfusion of Rh positive blood to a Rh negative woman).
Purpose:
Prevent production of maternal Rh antibodies (defenders) against the Rh positive fetal antigens
(invaders) by suppressing the immune reaction. It prevents maternal antibody response and
subsequently prevents hemolytic disease of the newborn of future pregnancies.
ABO INCOMPATIBILITY
The incompatibility occurs when the mother is type O and the baby is type A or B. Type O infants,
because they have no antigenic sites on the RBC’s, are never affected regardless of the mother’s blood
type. The Type A or B infants produce A or B antigens which enter the mother’s bloodstream, causing
the mother to produce A or B antibodies. These antibodies cross back into baby’s bloodstream and
cause hemolysis of the infant’s red blood cells.
COMPLICATION
Kernicterus - results from deposits of unconjugated bilirubin within the brain stem and basal ganglia.
The yellow staining of the brain tissue and necrosis of neurons lead to neurologic damage. Associated
with levels of unconjugated bilirubin over 20 mg. in normal term infants. Preterm infants can develop
kernicterus with levels lower (10 mg.).
Signs and Symptoms of Kernicterus:
1.
Poor feeding
2.
Vomiting
3.
Lethargy
4.
High-pitched cry
5.
Hypotonia
6.
Decreased moro reflex
7.
Opisthotonos
8.
Apnea
9.
Seizures
Infant of Diabetic Mother
An infant of a diabetic mother is at risk and requires close observation the first few hours to the first few
days of life. The severity of infant problems depends on classification of the maternal diabetes. The
infant may have been delivered early (36-38 weeks) and is often delivered by cesarean section.
CLINICAL MANIFESTATIONS
1.
Large in size (macrosomic, LGA)
2.
Plethora
3.
Enlarged liver, spleen, heart
4.
Hypotonic muscle tone, poor suck, lethargy
COMPLICATIONS
1.
Hypoglycemia
2.
Hyperbilirubinemia
3.
Respiratory Distress Syndrome
4.
Birth trauma
5.
Polycythemia
6.
Congenital anomalies
NURSING CARE
1.
Observe for Hypoglycemia (preterm: below 20 mg.; full-term:
below 30 mg.)
2.
Continue with other measure for the high risk infant
Cold Stress
Cold Stress is excessive heat loss resulting in compensatory mechanisms (increased respirations and
nonshivering thermogenesis) to maintain core body temperature. Both preterm and SGA infants are at
risk for cold stress because they have decreased adipose tissue, brown fat stores, and glycogen available
for metabolism.
The metabolic consequences of cold stress can be devastating and potentially fatal to an infant.
NURSING CARE of Cold Stress:
1.
Warm infant slowly
2.
Assess temperature every 15 minutes
3.
Assess for hypoglycemia and metabolic acidosis
Prevention is of the utmost importance and is achieved by careful monitoring and maintenance of a
warm thermal environment.
Infant of Addicted Mother
The newborn of an alcoholic or drug-dependent mother will also be alcohol or drug dependent. After
birth, when an infant=s connection with the maternal blood supply is severed, the neonate suffers
withdrawal. In addition, the drugs ingested by the mother may be teratogenic, resulting in congenital
anomalies.
The greatest risk to the fetus of the dependent mother is:
1.
Intrauterine asphyxia
2.
3.
4.
5.
6.
Intrauterine infection
Alterations in birth weight
Low apgar score
RDS
Congenital anomalies
CLINICAL MANIFESTATIONS
1.
Central nervous system signs: hyperactivity, hyperirritability, exaggerated reflexes, tremors,
sneezing, hiccups, short, nonquiet sleep.
2.
Respiratory signs: tachypnea, excessive secretions.
3.
Gastrointestinal signs: uncoordinated, vigorous suck, vomiting, drooling, diarrhea, sensitive
gag reflex.
4.
Vasomotor signs: stuffy nose, flushing, sweating.
5.
Other signs: excoriated buttocks, facial scratches
NURSING CARE
1.
Reduce stimuli
2.
Small frequent feedings
3.
Assess vital signs every 30 minutes
4.
Careful skin care
5.
Promote mother’s interest in infant
6.
Administer medications - usually paregoric or phenobarbital.
Given time these infants will recover. Some may suffer residual organic brain damage.
Fetal Alcohol Syndrome - refers to a series of malformations frequently found in infants born to women
who have been chronic severe alcoholics.
CLINICAL MANIFESTATIONS
1.
Facial Features:
a. Short palebral fissures (small eye slits)
b. Maxillary hypoplasia (small chin)
c. Low set ears
d. Short upturned nose
2.
Growth deficiencies IUGR
3.
Microcephaly
4.
Poor coordination
5.
Cardiac and Joint Abnormalities
6.
Irritability
7.
Mental Retardation
TREATMENT/NURSING CARE
The long-term prognosis for the FAS infant is less than favorable. Most infants with FAS are growthretarded at birth and few demonstrate catch-up growth. In fact, most infants are failure to thrive. CNS
dysfunctions are the most common and serious problem associated with FAS. The brain is the organ
that is most sensitive to damage from alcohol in the fetus. Most are mentally retarded.
Nursing care is similar to addicted baby.
________________________________________
Infectious Diseases
Many infections affect the newborn. The acronym for the most commonly encountered infections is
TORCHA.
T = TOXOPLASMOSIS
Toxoplasmosis is a protozoan infection caused by Toxoplasma gondii found in raw meat and infected
feces of cats. Placental transmission occurs, and the neonate is born with serious disease.
Most infants are asymptomatic at birth, but the prognosis is poor. The infant may have microcephaly,
hydrocephaly, hypotonia, chorioretinitis, blindness, deafness.
Treated with sulfonamides. These meds do not reverse neuro damage but do control progression.
O= OTHER
SYPHILIS
Transmission of the organism responsible for syphilis can occur during pregnancy. If the mother is not
treated for this disease then the infant will be born with congenital syphilis.
Signs and Symptoms:
1.
Maculopapular rash on soles of feet and palms of hands (copper-colored).
2.
Rhinitis - copious clear mucus discharge and obstructed nasal passageway, snuffles.
3.
Excoriated upper lip - red rash about mouth and anus.
4.
Enlarged organs.
5.
Pseudo paralysis - extremely painful joints.
6.
Irritable, poor feeder.
TREATMENT/NURSING CARE
1.
Penicillin
2.
Strict isolation
3.
Encourage mom to love baby and assist with caretaking activities
HEPATITIS B
Transplacental transmission and passage through birth canal with infected mother.
Infants are most commonly infected during birth by contact with contaminated urine, feces, or vaginal
secretions. Transmission may occur through breast milk.
Diagnosis - culture of amniotic fluid, cord blood.
Neonatal effects are serious. Infants are usually symptom free at birth. Develops hepatitis, cirrhosis of
the liver, or cancer of the liver.
If mother is positive - give infant hepatitis B immune globulin within the first 12 hours of birth and the
vaccine also should be given.
R = RUBELLA
The effect of Rubella on the fetus can be serious, depending on the gestational age at the time of
infection.
Most Common Anomalies:
Heart - pulmonary artery stenosis, PDA
Eyes - cataracts, glaucoma
Ears - deafness
IUGR
Central Nervous System - mental retardation, encephalitis, motor impairment
**There is no treatment for this. Mother may have option to consider termination of the pregnancy
depending on the time that she was exposed to the virus.
C = CYTOMEGALOVIRUS
Infected transplacental or during a vaginal delivery. Mom has no symptoms, will not know had problem
until birth. Prenatal screening is not cost effective because there is no vaccine or treatment for this
disease.
Infants are born with severe brain damage, microcephaly, cerebral palsy, epilepsy, blindness and
possible death. Most common findings are hepatosplenomegaly, jaundice, and a petechial rash.
H = HERPES SIMPLEX TYPE 2
Infected by transplacental infection, ascending infection by way of the birth canal, or direct
contamination with the birth canal.
Signs And Symptoms:
Onset of signs and symptoms may be 6 - 11 days after birth. May see localized lesions in the eyes,
throat, mouth, skin. Neonatal herpes is disseminated, affecting the liver, adrenals, and the central
nervous system.
Treatment:
Treated with Acyclovir.
A = AIDS
Infected transplacental, at time of birth, or in breast milk. Infants immune system is compromised as
evidenced by lower resistance to infection. Pregnant women infected with HIV produce IgG antibodies.
The IgG crosses the placenta to the fetus. Therefore cord blood is positive for antibody when tested.
Every baby born to a mother who is seropositive for HIV will have HIV antibody at birth.
Early symptoms are failure to gain weight, lymphadenopathy, fever, thrust, and respiratory distress.
May not see S & S until 4 - 6 months after birth. See symptoms in pediatrics - lymphoid interstitial
pneumonitis - considered a criterion for diagnosis.
Care - universal precautions, Isolation. Therapy includes gamma globulin, antimicrobial medications,
AZT, cortiosteroids.
Infants many times are placed in foster homes - parents do not keep the child.
Possible Nursing Diagnosis To Consider For Complications Of The Neonate
Hyperbilirubinemia








Impairment of skin integrity rt jaundice, diarrhea
Potential for injury rt phototherapy
Sensory-perceptual alteration; visual rt eye shields
Ineffective thermoregulation rt immaturity, environmental temperature
Fluid volume deficit rt inadequate fluid intake, phototherapy-induced diarrhea
Alteration in parenting rt enforced separation
Alteration in tissue perfusion rt hypo-/hypervolemia during exchange transfusion
Knowledge deficit regarding jaundice, treatment care of neonate
The Premature Infant









Impaired gas exchange rt inefficient ventilation of the alveoli and immaturity of the lungs
Injury, physiological rt Hypoglycemia 2 to decreased intake and decreased energy stores of
brown fat and glycogen
Ineffective thermoregulation rt prematurity, decreased layer of subcutaneous tissue and
immature neuromuscular control
Potential for infection rt lack of normal flora
Alteration in nutrition rt immature sucking reflex, gastrointestinal immaturity
Alteration in sensory stimuli rt maternal deprivation and hospitalization of ill neonate
Alteration in parenting rt the birth of a premature infant
Parental anxiety and grieving rt premature=s illness and the loss of the anticipated perfect baby
Knowledge deficit rt special care necessary for care of the premature infant