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Pediatric Nursing

I. Health Problems of the Newborn


II. The High Risk Newborn


E. High Risk Related to Infectious Process

Sepsis / Septicemia
Refers to a generalized bacterial infection in the bloodstream, with resulting infection of tissues and organs.

Clinical Manifestations: chills, fever, tachycardia (rapid heart rate), tachypnea (rapid breathing), and a high white-blood-cell count. If left untreated: septic shock, or sepsis syndrome (a potentially fatal condition characterized by a dramatic drop in blood pressure, and damage to or failure of various organs, particularly the kidneys, heart, and lungs).

Sepsis / Septicemia
Prevention: Breast-feeding Strict aseptic technique during delivery Thorough handwashing Proper handling of formula or supplies (gavage tubes)

Diagnostic Evaluation: Laboratory and radiographic examination, Cultures of blood, urine, & CSF. Drug study=signs of anemia, leukocytosis, leukopenia Therapeutic Mgt.: Early recognition & diagnosis. Aggressive Antibiotic therapy Circulatory support, respiratory support

F. High Risk Related to Cardiovascular and Hematologic Complications

Patent Ductus Arteriosus

The ductus arteriosus, a fetal blood vessel that usually closes soon after birth, remains open. In babies with these abnormalities, some of the oxygen-rich blood returning from the lungs is pumped to the lungs again, placing extra strain on the right ventricle and on the blood vessels leading to and from the lung.

Patent Ductus Arteriosus

Occurs in the majority of preterm infants under 2.6 lbs. During fetal life the ductus remains patent through the vasodilatory action of prostaglandins within its tissue. Postnatallly the increase in oxygen tension has a constricting effect on the ductus, but uit may reopen in preterm infants in response to the lowered oxygen tension associated with respiratory impairment.

Clinical Manifestations: Early signs: Pa CO2, PaO2, recurrent apnea. Other signs: bounding peripheral pulses, wide pulse pressure with diastolic pressure, pericardial hyperactivity, cardiomegaly, and a systolic or continuous machinery-type murmur heard loudest in systole Diagnostic evaluation: echocardiography

Patent Ductus Arteriosus

Nursing Care Management: Nursing observation early detection assessment of cardiovascular status Monitoring after implementation of therapy

Therapeutic Management: Careful fluid regulation Respiratory support Diuretic therapy Administration of indomethacin (a prostaglandin synthetase inhibitor that has been successful in constricting the ductus in critically ill preterm infants) Close monitoring for bleeding & renal dysfunction (drug inhibit platelet & renal function). Surgical ligation

Preterm infants tend to develop anemia that is more severe and appears earlier than in more mature infants. It may be a result of hemorrhage during pregnancy or labor and delivery (loss of placental integrity, anomalies of the umbilical cord), hemorrhage during the neonatal period, or blood disorder.

Therapeutic Managment: Iron supplements Packed RBC transfusions Nursing Care Managment: Careful monitoring and recording of all blood drawn for test. Epoetin administration (moderate anemia)

A venous hematocrit of 65% or more. With a hematocrit above 65%, blood flow becomes increasingly sluggish and hyperviscous, resulting in hyperperfusion of organs.

Etiology: Twin-to-twin transfusion and maternal-fetal transfusion Delayed cord clamping Intrapartum asphyxia Clinical Manifestations: Plethora Peripheral cyanosis Respiratory distress Lethargy Seizure activity Hyperbilirubinemia hypoglycemia


Nursing Care Management: Watching for signs Assist in diagnostic tests and therapeutic procedures.

G. High Risk Related to Neurologic Disturbance

Perinatal HypoxicIschemic Brain Injury Most common cause of neurologic impairment observed in term and preterm infants.

The brain damage usually results from asphyxia before, during, or after delivery. Ischemia and hypoxemia may occur simultaneously, or one may precede the other.

Perinatal HypoxicIschemic Brain Injury

Therapeutic Mgt: Aggressive resuscitation at birth Provide adequate ventilation Maintain cerebral perfusion

Clinical Manifestations: Stuporous or comatose Seizures begin after 6 to 12 hours Between 24 & 72 hours, the LOC may deteriorate Hypotonia evidence of disturbances in sucking and swallowing Full-term: hips & shoulders muscular weakness Preterm: lower limb weakness

Nsg. Care Mgt.: Perinatal Hypoxic Careful assessment and Ischemic Brain Injury observation for signs that Prevention: recognize high-risk might indicate cerebral pregnancy, monitor hypoxia/ischemia the fetus, initiate Monitoring of ventilatory & appropriate IV therapy therapy early. Observation & management of seizures General supportive care to infants and parents

In neonates, although manifested in the same ways as those described in Hemorrhage, older children, occurs with excessive discharge different frequencies and of blood from blood vessels, different degrees of caused by severity. Intracranial Hemorrhage
pathological condition of the vessels or by traumatic rupture of one or more vessels.

Intracranial Hemorrhage

Subdural Hemorrhage

A life-threatening collection of blood in the subdural space. It is most often produced by the stretching and tearing of the large veins in the tentorium cerebelli, the dural membrane that separates the cerebrum from the cerebellum.

Intracranial Hemorrhage

Subarachnoid Hemorrhage

The most common. Occurs in full-term infants as a result of trauma and in preterm infants as a result of the same types of events that cause IVH. Small hemorrhages are the most common. Bleeding id of venous origin, and underlying contusion may also occur.

Intracranial Hemorrhage

Intracerebellar Hemorrhage

Is a common finding on postmortem examination of the premature infant and can be a primary hemorrhage in the cerebellum associated with skull compression during abrupt, precipitous delivery. In full-term infant the bleeding may follow a different delivery.

Intracranial Hemorrhage

Nursing Care Management

Reduce the risk of increased intracranial pressure include avoiding interventions that cause crying (such as painful procedures). Monitoring serum blood glucose levels and preventing hypoglycemia are also important factors in keeping the infant neurologically intact. Care includes evaluating manipulations and handling and administering analgesics to reduce discomfort.

Neonatal Seizures Seizures in the neonatal period are usually the clinical manifestation of a serious underlying disease.

Most common causes: (for term and preterm infants): Perinatal asphyxia Although not life threatening as an isolated entity, seizures constitute a medical emergency because they signal a disease process that may produce irreversible brain damage.

Neonatal Seizures
Causes of Neonatal Seizures

Metabolic Hypoglycemia, hyperglycemia Hypernatremia, hyponatremia Hypocalcemia Hypomagnesemia Toxic Uremia Bilirubin encephalopathy Prenatal Infections Toxoplasmosis Syphilis Herpes Simplex Hepatitis

Neonatal Seizures Causes of Neonatal Seizures

Postnatal infections Bacterial meningitis Viral meningoencephalitis Sepsis Brain abscess Trauma at Birth Hypoxic brain injury Intracranial hemorrhage Subarachnoid, subdural hemorrhage Intraventricular hemorrhage

Neonatal Seizures Causes of Neonatal Seizures

Malformations Hydroencephalopathy Tuberous sclerosis Miscellaneous Degenarative disease Narcotics withdrawal

Neonatal Seizures


Slow, rhythmic jerking movements Approx. 1-3/sec Involves face, upper or lower extremities on one side of body May involve neck or trunk Infant is conscious during event May migrate randomly from one part of the body to another Movements may start at different times Extension/stiffening movements Extension of all four limbs (similar to decerebrate rigidity) Upper limbs are maintained in a stiffly flexed position. Sustained posturing of a limb Asymmetric posturing of trunk or neck

Classifications Focal of Neonatal Seizures MultiFocal


Neonatal Seizures


May develop in either full-term or preterm infants but more common in preterm. Often overlooked by inexoerienced observers Signs; Horizontal eye deviation Repetitive blinking or fluttering of the eyelids, staring Sucking or other oral-buccallingual movements Arm movements that resembles rowing or swimming Leg movements described as pedaling Apnea Signs may appear alone or in combination

Classifications of Neonatal Seizures

Neonatal Seizures

Myoclonic Focal

Rapid jerks that involve flexor muscle groups. Involves upper extremity flexor muscle group No electroencephalogram (EEG) discharges observed Asynchronous twitching of several parts of the body No associated EEG discharges observed Bilateral jerks of upper and lower limbs Associated with EEG discharges

Classifications of Neonatal Seizures

Multifocal Generalized

Neonatal Seizures

Diagnostic evaluation

Careful physical examination Pregnancy and family history investigation Blood glucose and electrolyte examination CSF exam Electroencephalography CT and echoencephalography

Neonatal Seizures Therapeutic Management

Prevention of cerebral damage Correction of metabolic derangements Respiratory and cardiovascular support Suppression of the seizure activity Underlying cause is treated

Neonatal Seizures Nursing Care Management

Recognize when the infant is having a seizure so that therapy can be instituted To carry out the therapeutic regimen Observe the response to the therapy Further evidence of seizures or other symptomatology assessment

H. High Risk Related to Maternal Conditions

Infants born to women with Infants of diabetic gestational diabetes Mothers mellitus are at risk for the same complications as Before insulin IDMs. therapy, few women with The single most important diabetes were able factor influencing fetal to conceive; for well-being is the those who did, the euglycemic status of the mortality rate for mother. both mother and
infant was high.

Infants of diabetic Mothers

Effects of Diabetes on the Fetus

High maternal blood glucose levels during fetal life result to macrosomic infants. Hypoglycemia may appear a short time after birth causing serious neurologic damage.

Macrosomic for gestational Infants of diabetic age Mothers Very plump and full faced Liberately coated with Clinical vernix caseosa Manifestations plethoric Larger than average placenta and umbilical cord

Infants of diabetic Mothers

Therapeutic Management

Careful monitoring of serum glucose levels Observation of accompanying complications such as RDS Infant are examined Blood studies If feeding fails to increase glucose levels, IV glucose should be administered Breast milk feeding first hour after birth in stable cardiorespiratory condition infants.

Infants of diabetic Mothers

Nursing Care Management

Early examination for congenital anomalies Signs of possible respiratory and cardiac problems Maintenance of adequate thermoregulation Early introduction of carbohydrate feedings as appropriate Monitoring of serum blood glucose levels

Drug-Exposed Infants
Clinical Manifestations Signs of drug withdrawal
Heroin: 12 24 hrs Methadone: 1-2 days to 2-3 wks or more

*It is important to note that the term addiction is often associated with behaviors whereby the person seeks the drug to experience a high or euphoria, escape from reality, or satisfy a personal need. Newborns are not addicted in a behavioral sense, yet they may experience mild to strong physiologic signs as a result of the mothers drug use. Therefore, the infant is not addicted; drug-exposed newborn is a better term, which implies intrauterine drug exposure.

Drug-Exposed Infants

Signs of Withdrawal in the neonate

Irritability Tachypnea (>60 bpm) Tremors Excoriations (knees, face) Shrill cry Mottling (skin) Hypertonicity of muscles Sneezing Frantic sucking of hands Yawning

Poor feeding Vomiting, often projectile Hyperactivity Temperature instability Perspiring Loose diarrheal stools Fever Seizures Nasal stuffiness Sleep disturbances

Drug-Exposed Infants

Therapeutic Management

Initially consists of modulating the environment to decrease external stimuli. Drug therapies to decrease withdrawal side effects include administration of phenobarbital, morphine, chloramphenicol, diazepam, or methadone

Drug-Exposed Infants Nursing Care Management

Presence of Neonatal Abstinence Syndrome (NAS): Reduce external stimuli (dimming the lights, noise level) Providing adequate nutrition and hydration

Maternal Infections
Human Immunodeficiency Virus

Fetal or Newborn Effect Depressed nasal bridge Mild upward or downward obliquity of eyes Long palpebral fissures with blue sclerae Patulous lips Ocular hypertelorism (wide space between to organs or parts) Prominent vermilion border Transmission Transplacental During vaginal delivery Potentially in breast milk

Maternal Infections Human Immunodeficiency Virus

Nursing Considerations Administer zidovudine (AZT) alone or zidovudine and lamivudineuntil delivery to HIV-positive mother; untreated mother may be treated at delivery with 2dose regimen of nevirapine; administer nevirapine to newborn after delivery CS is recommended to reduce transmission

Maternal Infections

Chickenpox (Varicella-Zoster Virus)

Fetal or Newborn Effect Intrauterine exposure congenital varicella syndrome, limb dysplasia, microcephaly, cortical atrophy, chorioretinitis, cataracts, auditory nerve palsy, mental retardation Severe symptoms (rash, fever) Transmission 1st trimester (fetal varicella syndrome) Perinatal period (infection)

Maternal Infections Chickenpox (Varicella-Zoster Virus)

Nursing Considerations Use varicella zoster immunoglobulin to treat infants born to mother with onset of disease within 5 days before or 2 days after delivery. Institute isolation precaution in newborn up to 21-28 days after birth Prevention: immunization with varicella vaccine

Maternal Infections

Chlamydia Infection

Fetal or Newborn Effect Conjunctivitis Pneumonia Transmission Last trimester or perinatal perios Nursing Considerations Standard ophthalmic prophylaxis Treat with oral erythromycin for 14 days.

Fetal or Newborn Effects Variable manifestation from asymptomatic to severe Microcephaly, cerebral Cytomegalovirus calcifications, chorioretinitis Jaundice, hepatosplenomegaly Petechial or purpuric rash Neurologic sequelae: seizure disorders, sensorimotor, deafness, mental retardation

Maternal Infections

Fetal or Newborn Effects Maternal Throughout pregnancy Infections Nursing Considerations Affected individual excrete virus Cytomegalovirus Virus is detected in urine or tissue by electron microscopy Avoid kissing affected child Pregnant woman should avoid close contact with known cases To treat infection, administer IV antivirals (ganciclovir) to newborn

Fetal or Newborn Effects May be asymptomatic at birth Hepatitis B Virus Acute hepatitis, changes in liver function Transmission Transplacental Contaminated maternal fluids or secretions during delivery Maternal Infections

Nursing Considerations Administer hepatitis b immunoglobulin to infant within 12 hr of birth; Hepatitis B Virus administer hepa B vaccine at separate site Prevention: Immunization to all infants with Hepa B vaccine Maternal Infections

Maternal Infections
Rubella, Congenital (Rubella Virus)

Fetal or Newborn Effects Eye defects: cataracts, microphthalmos, retinitis, glaucoma CNS signs: microcephaly, seizures, severe mental retardation Congenital heart defects: patent ductus arteriosus Auditory: high incidence of delayed hearing loss Intrauterine growth retardation Hyperbilirubinemia, meningitis, thrombocytopenia, hepatomegaly

Maternal Infections
Rubella, Congenital (Rubella Virus)

Transmission 1st trimester Early 2nd trimester Nursing Considerations Pregnant woman should avoid contact with all affected persons Caution women against pregnancy for at least 3 mo after vaccination.

III. Conditions Caused by Defects in Physical Development

A. Malformations of the CNS

Defects of Neural Tube


Definition A congenital malformation in which both cerebral hemispheres are absent. The condition is incompatible with life, and many infants are stillborn. For those who survive, no specific treatment is available.

Defects of Neural Tube Spina Bifida and Myelodysplasia

Definition Myelodysplsia-refers broadly to any malformation of the spinal canal and cord. Spina Bifida-midline defects involving failure of the osseous (bony) spine to close.

Defects of Neural Tube Spina Bifida and Myelodysplasia

Types of Spina Bifida Spina Bifida Occulta Meningocele Spina Bifida Myelomeningocele Spina Bifida

Defects of Neural Tube

Spina Bifida Occulta

The mildest form of spina bifida is called occulta (hidden). There is only a small gap in a few of the vertebrae (bones of the spine) and no obvious opening in the spinal column. The spinal cord may be normal, with no noticeable nerve damage at birth. However, neurological problems may be diagnosed at a later age or in adulthood.

Defects of Neural Tube Meningocele Spina Bifida

A more serious form of spina bifida may develop if the protective coating (called the meninges) around the spinal cord comes through an opening in the spine. A sac containing with fluid can form and protrude from the opening. This condition, called meningocele spina bifida, may not result in nerve damage, but minor disabilities and other problems can develop. About 4 percent of infants diagnosed with spina bifida at birth have this form.

Defects of Neural Tube

Myelomeningocele Spina Bifida

In the most serious type of spina bifida, part of the spinal cord as well as its protective coating come through the opening in the spine. This condition is called myelomeningocele spina bifida, and is what most people think of as spina bifida, accounting for 96 percent of the cases diagnosed in infants. It can result in nerve damage and severe disabilities. The person may be paralyzed with possible loss of sensation below the area of the spine where the cleft occurred. Bowel and bladder control may be affected. In addition, the spinal fluid often cannot drain properly and may collect around the brain.

Defects of Neural Tube


not known combination of genetic and environmental factors may be involved. Diabetes and obesity in the mother may also be risk factors, as is use of certain anti-seizure medications. High temperatures from fevers or hot tub use during pregnancy appear to have some association with spina bifida. Among different racial groups, the incidence of spina bifida is highest in Hispanics, followed by European whites. Lower socio-economic status is also a risk factor.

Defects of Neural Tube


Studies indicate that taking folic acid, a B-vitamin, during pregnancy can reduce the risk of spina bifida and other neural tube defects by as much as 70%. Prenatal screening can often detect serious forms of spina bifida. The opening in the spine leads to increased levels of alphafetoprotein during pregnancy, which may be detected by amniocentesis or a maternal blood test.

Defects of Neural Tube


Infants born with the most severe form of spina bifida usually have surgery within 24 hours to preserve the functions of the spinal cord and protect against infection. However, damaged nerves cannot be repaired or replaced, and some paralysis, muscle weakness, and loss of sensation may be permanent. Therapy, medication, and additional surgery may be needed as a child grows older.

Defects of Neural Tube


People with spina bifida may need braces or crutches to walk, or may use wheelchairs. Problems with bladder and bowel control may require special procedures or medication as well. With proper medical care, many children with spina bifida can grow up to become functioning adults with normal intelligence.

Etiology: Congenital 1. Myelomeningocele 2. Aqueduct stenosis Acquired 1. Intraventricular hemorrhage 2. Tumor 3. CSF infection 4. Head injury

A potentially serious increases in the volume of cerebrospinal fluid (CSF) within the ventricles of the brain. In infants, since their skull plates have not fused, it causes enlargement of the head, and there is a risk of brain damage from CSF pressure on the developing brain.

Ventricular Circulation: Lateral Ventricles Foramen of Monro Third Ventricle (Combines with fluid) Aqueduct of Sylvius Fourth Ventricle Lateral Foramen of Luschka and midline foramen of Magendie Cisterna magna Cerebral and cerebellar subarachnoid spaces Arachnoid villi (absorb)

Hydrocephalus Mechanism of CSF Imbalance

1. Nonobstructive or communicating hydrocephalus Impaired absorption of CSF within the subarachnoid space Obliteration of the subarachnoid cisterns Malfunction of the arachnoid villi


Mechanism of CSF Imbalance

2. Obstructive or noncommunicating hydrocephalus Obstruction to the flow of CSF through the ventricular system

Hydrocephalus Developmental Defects

Chiari Malformation Brain defect involving posterior fossa contents; the type II Chiari malformations, seen in almost exclusively with myelomeningocele, is characterterized by herniation of a small cerebellum, medulla, pons, and fourth ventricle into the cervical spinal canal through an enlarged foramen magnum. The resulting obstruction of CSF flow causes the hydrocephalus.


Clinical Manifestations

3 Factors that Influence Clinical Picture: 1. Acuity of onset 2. Timing of onset 3. Associated structural malformations Infancy bulging fontanels Head enlargement Anterior fontanel is tense, nonpulsatile Scalp veins are dilated

Bones of the skull become Hydrocephalus thin, sutures become palpably separated producing Macewen sign Clinical (cracked-pot sound) Manifestations Sun-setting sign Irritable and lethargic Changes in LOC Opisthotonos Lower extremity spasticity


Clinical Manifestations

Childhood Caused by ICP Headache on awakening Emesis Upright posture Papilledema Strabismus Ataxia: Extrapyramidal Sign (EPS) Irritable Lethargic Apathetic Confused incoherent


Diagnostic Evaluation Therapeutic Management

Ultrasonography Head circumference Neurologic signs CT scan and MRI

1. Relief of ventricular pressure 2. Treatment of the cause of the ventriculomegaly 3. Treatment of associated complications 4. Management of problems related to the effect of the disorder in psychomotor development 5. Surgery: Ventriculoperitolial (VP) shunt Ventriculoatrial (VA) shunt

Hydrocephalus Nursing Care Management

Assessment of ventricular size and ICP Daily head circumference measurement Assessment of the fontanel Shunt function assessment: monitoring signs of ICP Preparing the child for diagnostic tests: sedation Post-Op: position to unoperated side, flat on bed Neurologic assessment, BP, observe abdominal distension

B. Cranial Deformities

Normal cranium
Sutures separated my membraneous seams. Principal sutures: sagittal, coronal, and lambdoid Anterior and Posterior fontanels Ossification of sutures and fontanels: 8 wks-posterior fontanel closed 6 mo-fibrous union of suture lines and interlocking of serrated edges 18 mo-anterior fontanel closed 10-12 yrs-sutures not separated by ICP

Occipitofrontal Circumference greater than 3 standard deviations below the mean for age and sex Reflects a small brain

Primary Autosomal recessive disorder Chromosome abnormality Application of toxic stimulus during period of induction (radiation, maternal infection, chemical agents) Major cell migration in prenatal development Secondary Infection Trauma Metabolic disorders Anoxia Fetal exposure to alcohol and tobacco use

Neurologic Manifestations Decerebration (cerebral dysfunction: coordinating voluntary muscular fxn) Complete unresponsiveness Autistic behavior Educable mental retardation Mild hyperkinesis Nursing Care Management No treatment Supportive Helping parents adjust to rearing a child with cognitive impairment

Premature closure at birth of one or more cranial sutures.

Craniofacial Abnormalities

C. Skeletal Defects

Developmental Dysplasia of the Hip

Congenital Clubfoot

D. Disorders of the GI Tract

Cleft Lip & Cleft Palate

Esophageal Atresia & Tracheosophageal Fistula

Anorectal Malformations

E. Hernias



F. Defects of the GU Tract






IV. Health Problems During Infancy

A. Nutritional Disturbances

Vitamin Disturbances

Protein Energy Malnutrition Kwashiorkor

Protein Energy Malnutrition Marasmus

B. Disorder of Unknown Etiology

Sudden Infant Death Syndrome (SIDS)